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disease states, the concept of gene therapy has been extremely appealing. However, despite intensive work in this field of medicine, gene therapy has yet to make a major impact on the treatment of patients. Many technical challenges exist that must be overcome before gene therapy can be put into widespread practice. The gene delivery system (vector) encounters extracellular and intracellular barriers, must be nontoxic and nonimmunogenic, and must allow sufficient expression of the gene of interest. Many vectors have been created in attempts to overcome these problems; however, the ideal expression vector for use in humans has yet to be identified. Both inherited and acquired diseases may potentially benefit from gene therapy. X-linked severe combined immunodeficiency-X1 is an inherited disease in which gene therapy is not only being actively pursued as a potentially curative treatment, but some exciting progress has been made in recent years. In addition, acquired diseases, such as cancer, often have defined genetic alterations and, thus, are potential candidates for treatment with gene therapy. For example, malignant melanoma, a tumor that is notoriously chemoresistant, may avoid immune recognition by progressive loss of cell surface MHC class I molecules. Allovectin-7® is a DNA plasmid containing the gene encoding human MHC class I HLA-B7. Early phase I\u002FII studies of Allovectin-7® in patients with metastatic melanoma have shown some encouraging results. It is one of many examples of how gene therapy may affect cancer treatment in the near future.",{"EN":443},"Current Status and Future Prospects of Gene Therapy",{"VOID":445},"10.2165\u002F00024669-200504030-00001",[66],"https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.2165\u002F00024669-200504030-00001",[449,467,482],{"id":450,"sortIndex":134,"researcher":20,"roles":451,"affiliations":452,"properties":462},"9c3af0f2-b1b3-4a6f-8344-2e69ef352910",[],[453],{"id":20,"sortIndex":21,"affiliation":454,"properties":20},{"id":455,"createTime":456,"updateTime":456,"relativeEntities":457,"slug":458,"properties":459,"entityType":84,"verifyStatus":19,"verifyTime":20,"verifyNote":20,"syncStatus":19,"languages":20,"translateLanguages":20,"viewCount":21},"ec3bd151-75c0-4153-ae78-c366c842fd2f","2024-04-11T06:44:12.480+00:00",[],"Cutaneous-Oncology-Program-University-of-Colorado-Cancer-Center-Anschutz-Cancer-Aurora-USA",{"title":460},{"EN":461},"Cutaneous Oncology Program, University of Colorado Cancer Center, Anschutz Cancer, Aurora, USA",{"title":463,"email":465},{"EN":464},"Rene Gonzalez",{"VOID":466},"rene.gonzalez@uchsc.edu",{"id":468,"sortIndex":71,"researcher":20,"roles":469,"affiliations":470,"properties":479},"62d11bdb-a86b-4d48-96b0-d3bf5ea2e3ef",[],[471],{"id":20,"sortIndex":21,"affiliation":472,"properties":20},{"id":473,"createTime":474,"updateTime":474,"relativeEntities":475,"slug":20,"properties":476,"entityType":84,"verifyStatus":19,"verifyTime":20,"verifyNote":20,"syncStatus":19,"languages":20,"translateLanguages":20,"viewCount":21},"adabcf17-45ef-4ddb-a183-29cb4bd841bf","2023-12-10T07:42:37.634+00:00",[],{"title":477},{"VI":478},"Exempla Saint Joseph Hospital, Denver, USA",{"title":480},{"EN":481},"Tahl N. Humes",{"id":483,"sortIndex":21,"researcher":20,"roles":484,"affiliations":485,"properties":491},"311342c2-ca2b-49da-a39b-6e14458d43d4",[],[486],{"id":20,"sortIndex":21,"affiliation":487,"properties":20},{"id":455,"createTime":456,"updateTime":456,"relativeEntities":488,"slug":458,"properties":489,"entityType":84,"verifyStatus":19,"verifyTime":20,"verifyNote":20,"syncStatus":19,"languages":20,"translateLanguages":20,"viewCount":21},[],{"title":490},{"EN":461},{"title":492},{"EN":493},"Karl D. 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Androgen deprivation therapy using finasteride and low dose flutarnide to treat PSA failure following therapy for clinically localized adenocarconoma of the prostate [abstract]. J Urology 1999; 161: 299\nOrnstein DK, Rao GS, Johnson B, et al. Combined finasteride and flutarnide therapy in men with advanced prostate cancer. Urology 1996; 48: 901–5\nTannock IF, Osoba D, Stacker MR, et al. Chemotherapy with rnitoxantrone plus prednisone or prednisone alone for symptomatic hormone-resistant prostate cancer: a Canadian randomized trial with palliative end points. J Clin Oncol 1996; 14: 1756–64\nKantoff PW, Halabi S, Conaway M, et al. Hydrocortisone with or without mitoxantrone in men with hormone refractory prostate cancer: results of the Cancer and Leukemia Group B. J Clin Oncol 1999; 17: 2506–13\nHudes G, Einhorn L, Ross E, et al. Vinblastine versus vinbiastine plus oral estrarnustine phosphate for patients with hormone-refractory prostate cancer: a Hoosier Oncology Group and Fox Chase Network phase III trial. J Clin Oncol 1999; 17(10): 3160–6\nHudes GR, Nathan FE, Khater C, et al. Phase II Trial of 96 hour paclitaxel plus estramustine in metastatic hormone-refractory metastatic prostate cancer. J Clin Oncol 1997; 15: 3156–63\nHudes GR, Manola J, Conroy J, et al. Phase II study of weekly paclitaxel (P) by 1-hour infusion plus reduced dose oral estrarnsutine (EMP) in metastatic hormone-refractory prostate carcinoma: a trial of the Eastern Cooperative Oncology Group. Proc Am Soc Clin Oncol 2001; 20: 697a\nPetryiak DP, Macarthur RB, O’Connor J, et al. Phase I trial of docetaxel with estrarnustine in androgen-independent prostate cancer. J Clin Oncol 1999; 17(3): 958–67\nHussain M, Petryiak D, Fisher E, et al. Docetaxel and estrarnustine versus rnitoxantrone and prednisone for hormone-refractory prostate cancer: scientific basis and design of Southwest Oncology Group Study 9916. Sernin Oncol 1999; 26(5 Suppl. 17): 55–60",{"EN":625},"The treatment of metastatic prostate cancer is based upon the principle that prostate cancer growth is stimulated by androgens. Androgen ablation therapy is an effective treatment for metastatic prostate cancer. The timing of initiation of androgen ablation and the role of combined androgen blockade have been investigated. The utilization of intermittent androgen suppression offers the potential for improved quality of life. Intermittent therapy for metastatic disease is being compared with continuous therapy in an ongoing cooperative group trial. Recent studies have defined the evolving role of cytotoxic chemotherapy in hormone-refractory disease.",{"EN":627},"Metastatic Prostate Cancer",{"VOID":629},"10.2165\u002F00024669-200302020-00002","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.2165\u002F00024669-200302020-00002",[632,648,673],{"id":633,"sortIndex":134,"researcher":20,"roles":634,"affiliations":636,"properties":645},"f372a9c4-8157-4959-afc2-48cb34d570ef",[635],"AUTHOR",[637],{"id":20,"sortIndex":21,"affiliation":638,"properties":20},{"id":639,"createTime":640,"updateTime":640,"relativeEntities":641,"slug":20,"properties":642,"entityType":84,"verifyStatus":19,"verifyTime":20,"verifyNote":20,"syncStatus":19,"languages":20,"translateLanguages":20,"viewCount":21},"2d476b7e-c341-499a-934c-bb67f0a244fe","2024-01-24T09:42:26.564+00:00",[],{"title":643},{"VI":644},"Division of Urology Department of Surgery, University of Pennsylvania School of Medicine, Philadelphia, USA",{"title":646},{"VI":647},"Bruce S. Malkowicz",{"id":649,"sortIndex":71,"researcher":20,"roles":650,"affiliations":651,"properties":670},"93e3681f-2762-4f99-8337-ebf0e7d29ee1",[635],[652,662],{"id":653,"sortIndex":71,"affiliation":654,"properties":661},"4288ae80-fbf7-41be-8d9c-070e87834bc2",{"id":655,"createTime":656,"updateTime":656,"relativeEntities":657,"slug":20,"properties":658,"entityType":84,"verifyStatus":19,"verifyTime":20,"verifyNote":20,"syncStatus":19,"languages":20,"translateLanguages":20,"viewCount":21},"ab433a15-fd0e-4a0b-a17a-e5757eb1316d","2024-01-26T11:46:58.895+00:00",[],{"title":659},{"VI":660},"Abramson Cancer Center of the University of Pennsylvania, Philadelphia, USA",{},{"id":20,"sortIndex":21,"affiliation":663,"properties":20},{"id":664,"createTime":665,"updateTime":665,"relativeEntities":666,"slug":20,"properties":667,"entityType":84,"verifyStatus":19,"verifyTime":20,"verifyNote":20,"syncStatus":19,"languages":20,"translateLanguages":20,"viewCount":21},"7c649985-367e-44e4-a155-f52ab30f85b6","2024-01-17T23:31:55.854+00:00",[],{"title":668},{"VI":669},"Division of Hematology\u002FOncology, Department of Medicine and the Abramsom Cancer Center, University of Pennsylvania School of Medicine, Philadelphia, USA",{"title":671},{"VI":672},"David J. Vaughn",{"id":674,"sortIndex":21,"researcher":20,"roles":675,"affiliations":676,"properties":682},"ccfbb1b5-824c-4dc9-803f-9bc08ed8ba42",[635],[677],{"id":20,"sortIndex":21,"affiliation":678,"properties":20},{"id":639,"createTime":640,"updateTime":640,"relativeEntities":679,"slug":20,"properties":680,"entityType":84,"verifyStatus":19,"verifyTime":20,"verifyNote":20,"syncStatus":19,"languages":20,"translateLanguages":20,"viewCount":21},[],{"title":681},{"VI":644},{"title":683},{"VI":684},"Brian M. Levin",{"url":630,"publisher":686,"properties":701},{"id":6,"createTime":7,"updateTime":8,"relativeEntities":687,"slug":10,"properties":688,"entityType":18,"verifyStatus":19,"verifyTime":20,"verifyNote":20,"syncStatus":19,"languages":20,"translateLanguages":20,"viewCount":21,"subjectFields":692,"manageAffiliations":693,"indexDatabases":694,"url":20,"thumbnailPath":20,"statistic":20,"gsStatistic":20,"type":20,"analyzePriority":20},[],{"issn":689,"title":690,"url":691},{"VOID":13},{"EN":15},{"VOID":17},[],[],[695],{"id":26,"indexDatabase":696,"url":39,"indexYears":40,"academicFieldIds":20,"indexDatabaseRanking":41},{"id":28,"createTime":29,"updateTime":30,"relativeEntities":697,"label":698,"description":699,"key":36,"publicationTags":700,"standard":20},[],{"EN":33,"VI":33},{"EN":33,"VI":35},[38],{"volume":702,"pages":703},{"VOID":130},{"VOID":704},"87-94",{"id":706,"createTime":707,"updateTime":708,"relativeEntities":709,"slug":710,"properties":711,"entityType":62,"verifyStatus":63,"verifyTime":708,"verifyNote":64,"syncStatus":19,"languages":20,"translateLanguages":20,"viewCount":21,"primaryUrl":720,"fullTextUrl":20,"authors":721,"publicationType":107,"publisherRelationship":812,"citationCount":20,"citationInfo":20,"publishDate":510,"publishYear":511,"citationAnalyzeStatus":19,"lastCitationAnalyze":20,"indexDatabases":20,"openAccess":20,"references":20,"isForceReanalyzing":430},"765f7a4a-7be1-4c51-834f-0f4e863467a0","2024-02-08T02:57:12.368+00:00","2024-12-05T23:28:13.958+00:00",[],"Pain-control-with-zoledronic-acid-in-patients-with-breast-cancer-and-metastatic-bone-disease",{"references":712,"abstract":714,"title":716,"doi":718},{"VOID":713},"Fitzgibbon D. Cancer pain: management. In: Loeser JD, editor. Bonica’s management of pain. 3rd ed. Philadelphia (PA): Lippincott-Williams & Wilkins, 2001\nRipamonti C, Dickerson ED. Strategies for the treatment of cancer pain in the new millennium. Drugs 2001; 61(7): 955–77\nDaut RL, Cleeland CS. The prevalence and severity of pain in cancer. Cancer 1982; 50: 1913–8\nJanjan N. Bone metastases: approaches to management. Semin Oncol 2001; 28Suppl. 2: 28–34\nPons F, Fuster D. Under-utilization of radionuclide therapy in metastatic bone pain palliation. Nucl Med Commun 2002; 23(4): 301–2\nColeman RE. Skeletal complications of malignancy. Cancer 1997; 80(8 Suppl.): 1588–94\nBerruti A, Dogliotti L, Bitossi R, et al. Incidence of skeletal complications in patients with bone metastatic prostate cancer and hormone refractory disease: predictive role of bone resorption and formation markers evaluated at baseline. J Urol 2000; 164: 1248–53\nMercadante S. Malignant bone pain: pathophysiology and treatment. Pain 1997; 69: 1–18\nLucas LK, Lipman AG. Recent advances in pharmacotherapy for cancer pain management. Cancer Pract 2002; 10Suppl. 1: 14–20\nBerenson JR, Rosen LS, Howell A, et al. Zoledronic acid reduces skeletal-related events in patients with osteolytic metastases. Cancer 2001; 91: 1191–200\nGreen JR. Antitumor effects of bisphosphonates. Cancer 2003; 97(3 Suppl.): 840–7\nWellington K, Goa KL. Zoledronic acid: a review of its use in the malignancy of bone metastases and hypercalcaemia of malignancy. Drugs 2003; 63(4): 417–37\nHortobagyi GN, Theriault RL, Lipton A, et al. Long-term prevention of skeletal complications of metastatic breast cancer with pamidronate: Protocol 19 Aredia Breast Cancer Study Group. J Clin Oncol 1998; 16: 2038–44\nHortobagyi GN, Theriault RL, Porter L, et al. Efficacy of pamidronate in reducing skeletal complications in patients with breast cancer and lytic bone metastases: Protocol 19 Aredia Breast Cancer Study Group. N Engl J Med 1996; 335: 1785–91\nConte PF, Latreille J, Mauriac L, et al. Delay in progression of bone metastases in breast cancer patients treated with intravenous pamidronate: results from a multinational randomised controlled trial. The Aredia Multinational Cooperative Group. J Clin Oncol 1996; 14: 2552–9\nHillner BE, Ingle JN, Berenson JR, et al. American Society of Clinical Oncology guideline on the role of bisphosphonates in breast cancer. J Clin Oncol 2000; 18(6): 1378–91\nGreen JR, Muller K, Jaeggi KA. Preclinical pharmacology of CCP 42,446, a new potent, heterocyclic bisphosphonate compound. J Bone Miner Res 1994; 9: 745–51\nRosen LS, Gordon D, Kaminski M, et al. Zoledronic acid versus pamidronate in the treatment of skeletal metastases in patients with breast cancer or osteolytic lesions of multiple myeloma: a phase III, double-blind comparative trial. Cancer J 2001; 7(5): 377–87\nSaad F, Gleason DM, Murray R, et al. A randomised, placebo-controlled trial of zoledronic acid in patients with hormone-refractory metastatic prostate carcinoma. J Natl Cancer Inst 2002; 94(19): 1458–68\nColeman RE. Evaluation of bone disease in breast cancer. Breast 1993; 3: 73–8\nSimon R. Optimal two-stage designs for phase II clinical trials. Control Clin Trials 1989; 10(1): 1–10\nPavlakis N, Stockler M. Bisphosphonates for breast cancer. Cochrane Database Systematic Review 2002 (1): CD003474\nZojer N, Keck AV, Pecherstorfer M. Comparative tolerability of drug therapies for hypercalcaemia of malignancy. Drug Saf 1999; 21: 389–406\nDesHarnais Castel L, Bajwa K, Markle JP, et al. A microcosting analysis of zoledronic acid and pamidronate therapy in patients with metastatic bone disease. Support Care Cancer 2001; 9: 545–51\nWalker K, Medhurst SJ, Kidd BL, et al. Disease modifying and anti-nociceptive effects of the bisphosphonate, zoledronic acid in a model of bone cancer pain. Pain 2002; 100: 219–29\nNeville-Webbe HL, Holen I, Coleman RE. The anti-tumour activity of bisphosphonates. Cancer Treat Rev 2002; 28(6): 305–19\nPickering LM, Mansi JL. The role of bisphosphonates in breast cancer management: review article. Curr Med Res Opin 2002; 18(5): 284–95\nJagdev SP, Coleman RE, Shipman CM, et al. The bisphosphonate, zoledronic acid, induces apoptosis of breast cancer cells: evidence for synergy with paclitaxel. Br J Cancer 2001; 84(8): 1126–34\nTassone P, Forciniti S, Galea E, et al. Growth inhibition and synergistic induction of apoptosis by zoledronate and dexamethasone in human myeloma cell lines. Leukemia 2000; 14: 841–4",{"EN":715},"Effective management of pain associated with metastatic bone disease is paramount in the care of cancer patients. Bisphosphonates are recommended in treating skeletal complications and there is evidence that they also control pain. To investigate the effects of zoledronic acid, a potent nitrogen-containing bisphosphonate, in reducing pain in patients with advanced breast cancer and bone metastases. Thirty-two patients (age range 37–79 years, median 56 years) with histologically proven breast cancer and bone metastases received a 15-minute infusion of zoledronic acid 4mg every 4 weeks for a mean of eight cycles (range 1–13) in a phase II pilot study. The primary efficacy endpoint was the control of pain as determined by changes in pain and analgesic scores. Zoledronic acid substantially reduced pain scores compared with baseline, with over 80% of patients reporting mild or no pain at the end of the trial (82% had moderate to very severe pain on entry). The percentage of patients requiring no analgesics increased from 9% to 35% following zoledronic acid treatment. At baseline, 47% of patients required opioids to control pain, whereas 27% required opioids at the end of the trial. Zoledronic acid appeared to be well tolerated, with no patients reporting serious adverse events. These results support previous data indicating that zoledronic acid is effective in patients with breast cancer and painful bone metastases. Follow-up controlled trials are required to further investigate the role of zoledronic acid in the management of cancer patients with metastatic disease.",{"EN":717},"Pain control with zoledronic acid in patients with breast cancer and metastatic bone disease",{"VOID":719},"10.2165\u002F00024669-200403040-00005","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.2165\u002F00024669-200403040-00005",[722,738,750,762,774,787,799],{"id":723,"sortIndex":724,"researcher":20,"roles":725,"affiliations":726,"properties":735},"7729f4de-ef1d-4bf6-8861-935c4fd19794",4,[635],[727],{"id":20,"sortIndex":21,"affiliation":728,"properties":20},{"id":729,"createTime":730,"updateTime":730,"relativeEntities":731,"slug":20,"properties":732,"entityType":84,"verifyStatus":19,"verifyTime":20,"verifyNote":20,"syncStatus":19,"languages":20,"translateLanguages":20,"viewCount":21},"12dfed97-81a2-49fb-ac23-d9b524e9606e","2024-02-08T02:57:12.450+00:00",[],{"title":733},{"VI":734},"Oncologia Medica, Azienda Sanitaria Dispedaciera San Giovanni Battista, Turin, Italy",{"title":736},{"VI":737},"Marinella Mistrangelo",{"id":739,"sortIndex":21,"researcher":20,"roles":740,"affiliations":741,"properties":747},"259d04d9-9504-4ca7-b565-3c2099c2eb1f",[635],[742],{"id":20,"sortIndex":21,"affiliation":743,"properties":20},{"id":729,"createTime":730,"updateTime":730,"relativeEntities":744,"slug":20,"properties":745,"entityType":84,"verifyStatus":19,"verifyTime":20,"verifyNote":20,"syncStatus":19,"languages":20,"translateLanguages":20,"viewCount":21},[],{"title":746},{"VI":734},{"title":748},{"VI":749},"Cinzia Nigro",{"id":751,"sortIndex":134,"researcher":20,"roles":752,"affiliations":753,"properties":759},"eb97209c-ee26-4a50-b3a1-a2ad72f81dbe",[635],[754],{"id":20,"sortIndex":21,"affiliation":755,"properties":20},{"id":729,"createTime":730,"updateTime":730,"relativeEntities":756,"slug":20,"properties":757,"entityType":84,"verifyStatus":19,"verifyTime":20,"verifyNote":20,"syncStatus":19,"languages":20,"translateLanguages":20,"viewCount":21},[],{"title":758},{"VI":734},{"title":760},{"VI":761},"Mara Ardine",{"id":763,"sortIndex":131,"researcher":20,"roles":764,"affiliations":765,"properties":771},"3552844c-9585-4ebf-80e7-8851a8780c71",[635],[766],{"id":20,"sortIndex":21,"affiliation":767,"properties":20},{"id":729,"createTime":730,"updateTime":730,"relativeEntities":768,"slug":20,"properties":769,"entityType":84,"verifyStatus":19,"verifyTime":20,"verifyNote":20,"syncStatus":19,"languages":20,"translateLanguages":20,"viewCount":21},[],{"title":770},{"VI":734},{"title":772},{"VI":773},"Zaira Coccorullo",{"id":775,"sortIndex":776,"researcher":20,"roles":777,"affiliations":778,"properties":784},"f66afb54-0505-4568-a100-34c666b928c0",6,[635],[779],{"id":20,"sortIndex":21,"affiliation":780,"properties":20},{"id":729,"createTime":730,"updateTime":730,"relativeEntities":781,"slug":20,"properties":782,"entityType":84,"verifyStatus":19,"verifyTime":20,"verifyNote":20,"syncStatus":19,"languages":20,"translateLanguages":20,"viewCount":21},[],{"title":783},{"VI":734},{"title":785},{"VI":786},"Oscar Bertetto",{"id":788,"sortIndex":71,"researcher":20,"roles":789,"affiliations":790,"properties":796},"a0693e8a-5e9f-4308-acc9-14d799048bbb",[635],[791],{"id":20,"sortIndex":21,"affiliation":792,"properties":20},{"id":729,"createTime":730,"updateTime":730,"relativeEntities":793,"slug":20,"properties":794,"entityType":84,"verifyStatus":19,"verifyTime":20,"verifyNote":20,"syncStatus":19,"languages":20,"translateLanguages":20,"viewCount":21},[],{"title":795},{"VI":734},{"title":797},{"VI":798},"Michela Donadio",{"id":800,"sortIndex":801,"researcher":20,"roles":802,"affiliations":803,"properties":809},"577905d0-296c-43c2-acd6-5416852a9022",3,[635],[804],{"id":20,"sortIndex":21,"affiliation":805,"properties":20},{"id":729,"createTime":730,"updateTime":730,"relativeEntities":806,"slug":20,"properties":807,"entityType":84,"verifyStatus":19,"verifyTime":20,"verifyNote":20,"syncStatus":19,"languages":20,"translateLanguages":20,"viewCount":21},[],{"title":808},{"VI":734},{"title":810},{"VI":811},"Alessandra Beano",{"url":720,"publisher":813,"properties":828},{"id":6,"createTime":7,"updateTime":8,"relativeEntities":814,"slug":10,"properties":815,"entityType":18,"verifyStatus":19,"verifyTime":20,"verifyNote":20,"syncStatus":19,"languages":20,"translateLanguages":20,"viewCount":21,"subjectFields":819,"manageAffiliations":820,"indexDatabases":821,"url":20,"thumbnailPath":20,"statistic":20,"gsStatistic":20,"type":20,"analyzePriority":20},[],{"issn":816,"title":817,"url":818},{"VOID":13},{"EN":15},{"VOID":17},[],[],[822],{"id":26,"indexDatabase":823,"url":39,"indexYears":40,"academicFieldIds":20,"indexDatabaseRanking":41},{"id":28,"createTime":29,"updateTime":30,"relativeEntities":824,"label":825,"description":826,"key":36,"publicationTags":827,"standard":20},[],{"EN":33,"VI":33},{"EN":33,"VI":35},[38],{"volume":829,"pages":831},{"VOID":830},"3",{"VOID":832},"257-263",{"id":834,"createTime":835,"updateTime":836,"relativeEntities":837,"slug":838,"properties":839,"entityType":62,"verifyStatus":63,"verifyTime":847,"verifyNote":64,"syncStatus":19,"languages":20,"translateLanguages":20,"viewCount":21,"primaryUrl":848,"fullTextUrl":20,"authors":849,"publicationType":107,"publisherRelationship":877,"citationCount":20,"citationInfo":20,"publishDate":898,"publishYear":511,"citationAnalyzeStatus":19,"lastCitationAnalyze":20,"indexDatabases":20,"openAccess":20,"references":20,"isForceReanalyzing":430},"c3ea09c2-85a6-4884-a0e0-0d29d491583a","2024-01-29T11:58:04.263+00:00","2025-01-23T22:53:14.847+00:00",[],"Gemcitabine",{"references":840,"abstract":842,"title":844,"doi":845},{"VOID":841},"Shore S, Raraty MG, Ghaneh P, et al. Review article: chemotherapy for pancreatic cancer. Aliment Pharmacol Ther 2003Dec; 18(11–12): 1049–69\nAmerican Cancer Society. Cancer facts and figures 2005. Atlanta: American Cancer Society [online]. Available from URL: http:\u002F\u002Fwww.cancer.org [Accessed 2005 Sep 21]\nBurris III HA, Moore MJ, Andersen J, et al. Improvements in survival and clinical benefit with gemcitabine as first-line therapy for patients with advanced pancreas cancer: a randomized trial. J Clin Oncol 1997Jun; 15: 2403–13\nKulke MH. Recent developments in the pharmacological treatment of advanced pancreatic cancer. Expert Opin Investig Drugs 2003Jun; 12(6): 983–92\nKo AH. Cancer of the pancreas [online]. Available from URL: http:\u002F\u002Fwww.cancersupportivecare.com\u002Fpancreas.html [Accessed 2005 Nov 11]\nGunzburg WH, Lohr M, Salmons B. Novel treatments and therapies in development for pancreatic cancer. Expert Opin Investig Drugs 2002Jun; 11(6): 769–86\nNoble S, Goa KL. Gemcitabine: a review of its pharmacology and clinical potential in non-small cell lung cancer and pancreatic cancer. Drugs 1997Sep; 54: 447–72\nPlunkett W, Huang P, Xu YZ, et al. Gemcitabine: metabolism, mechanisms of action, and self-potentiation. Semin Oncol 1995Aug; 22(4 Suppl. 11): 3–10\nEli Lilly and Company Limited. Gemzar 200mg powder for solution for infusion: summary of product characteristics [online]. Available from URL: http:\u002F\u002Femc.medicines.org.uk [Accessed 2005 Jul 1]\nShewach DS, Lawrence TS. Radiosensitization of human solid tumor lines with gemcitabine. Semin Oncol1996 1996; 23: 65–71\nPlate JM, Plate AE, Short S, et al. Effect of gemcitabine on immune cells in subjects with adenocarcinoma of the pancreas. Cancer Immunol Immunother 2005Sep; 54(9): 915–25\nNowak AK, Robinson BW, Lake RA. Synergy between chemotherapy and immunotherapy in the treatment of established murine solid tumors. Cancer Res 2003; 63: 4490\nAbbruzzese JL, Grunewald R, Weeks EA, et al. A phase I, clinical, plasma and cellular pharmacology study of gemcitabine. J Clin Oncol 1991Mar; 9: 491–8\nEli Lilly and Company. Gemzar(r) (Gemcitabine HCL) for injection prescribing information [online]. Available from URL: http:\u002F\u002Fpi.lilly.com\u002Fus\u002Fgemzar.pdf [Accessed 2005 Sep 19]\nGrunewald R, Abbruzzese JL, Tarassoff P, et al. Saturation of 2′-2-difluorodeoxycitidine 5′-triphosphate accumulation by mononuclear cells during a phase I trial of gemcitabine. Cancer Chemother Pharmacol 1991Jan; 27: 258–62\nHochster HS. Newer approaches to gemcitabine-based therapy of pancreatic cancer: fixed-dose-rate infusion and novel agents. Int J Radiat Oncol Biol Phys 2003; 56(4 Suppl): 24–30\nTempero M, Plunkett W, Ruiz vanHaperen V, et al. Randomized phase II comparison of dose-intense gemcitabine: thirty-minute infusion and fixed dose rate infusion in patients with pancreatic adenocarcinoma. J Clin Oncol 2003Sep 15; 21(18): 3402–8\nShamseddine AI, Khalifeh MJ, Mourad FH, et al. Comparative pharmacokinetics and metabolic pathway of gemcitabine during intravenous and intra-arterial delivery in unresectable pancreatic cancer patients. Clin Pharmacokinet 2005; 44(9): 957–67\nVenook A, Egorin MJ, Rosner GL, et al. Phase I and pharmacokinetic trial of gemcitabine in patients with hepatic or renal dysfunction: Cancer and Leukemia Group B 9565. J Clin Oncol 2000; 18: 2780–7\nCorreale P, Cerretani D, Marsili S, et al. Gemcitabine increases systemic 5-fluorouracil exposure in advanced cancer patients. Eur J Cancer 2003Jul; 39(11): 1547–51\nBramhall SR, Rosemurgy A, Brown PD, et al. Marimastat as first-line therapy for patients with unresectable pancreatic cancer: a randomized trial. J Clin Oncol 2001; 19: 3447–55\nCantore M, Fiorentini G, Luppi G, et al. Gemcitabine versus FLEC regimen given intra-arterially to patients with unresectable pancreatic cancer: a prospective, randomized phase III trial of the Italian Society for Integrated Locoregional Therapy in Oncology. J Chemother 2004Dec; 16(6): 589–94\nCheverton P, Friess H, Andras C, et al. Phase III results of exatecan (DX-8951f) versus gemcitabine in chemotherapy-naive patients with advanced pancreatic cancer [abstract no. 4005]. J Clin Oncol 2004; 22(14 Suppl.): 4005. Plus oral presentation at the 40th Annual Meeting of the American Society of Clinical Oncology: Late Breakers: 6; 2004 Jun 5–8; New Orleans (LA)\nMoore MJ, Hamm J, Dancey J, et al. Comparison of gemcitabine versus the matrix metalloproteinase inhibitor BAY 12-9566 in patients with advanced or meta-static adenocarcinoma of the pancreas: a phase III trial of the National Cancer Institute of Canada Clinical Trials Group. J Clin Oncol 2003Sep 1; 21(17): 3296–302\nBerlin ID, Catalano P, Thomas JP, et al. Phase III study of gemcitabine in combination with fluorouracil versus gemcitabine alone in patients with advanced pancreatic carcinoma: Eastern Cooperative Oncology Group trial E2297. J Clin Oncol 2002Aug 1; 20: 3270–5\nColucci G, Giuliani F, Gebbia V, et al. Gemcitabine alone or with cisplatin for the treatment of patients with locally advanced and\u002For metastatic pancreatic carcinoma: a prospective, randomized phase III study of the Gruppo Oncologico dell'Italia Meridionale. Cancer 2002Feb 15; 94: 902–10\nUnningham D, Chau I, Stocken D, et al. Phase III randomised comparison of gemcitabine (GEM) versus gemcitabine plus capecitabine (GEM-CAP) in patients with advanced pancreatic cancer [abstract no. PS11]. Eur J Cancer Supplements 2005Oct; 3(4): 4. Plus oral presentation at the 13th European Cancer Conference; 2005 Oct 30–Nov 3; Paris\nHeinemann V, Quietzsch D, Gieseler F, et al. A phase III trial comparing gemcitabine plus cisplatin vs. gemcitabine alone in advanced pancreactic carcinoma [abstract no. 1003]. Proc Am Soc Clin Oncol 2003; 22: 250. Plus oral presentation at the 39th Annual Meeting of the American Society of Clinical Oncology; 2003 May 31–Jun 3; Chicago (IL)\nHerrmann R, Bodoky G, Ruhstaller T, et al. Gemcitabine (G) plus capecitabine (C) versus G alone in locally advanced or metastatic pancreatic cancer: a randomized phase III study of the Swiss Group for Clinical Cancer Research (SAKK) and the Central European Cooperative Oncology Group (CECOG) [abstract no. 4010]. J Clin Oncol 2005; 23Suppl. 16: 1092. Plus oral presentation at the 41st Annual Meeting of the American Society of Clinical Oncology; 2005 May 13–17; Orlando (FL)\nLouvet C, Labianca R, Hammel P, et al. Gemcitabine in combination with oxaliplatin compared with gemcitabine alone in locally advanced or metastatic pancreatic cancer: results of a GERCOR and GISCAD phase III trial. J Clin Oncol 2005May 20; 23(15): 3509–16\nOettle H, Richards D, Ramanathan RK, et al. A phase III trial of pemetrexed plus gemcitabine versus gemcitabine in patients with unresectable or metastatic pancreatic cancer. Ann Oncol 2005; 16: 1639–45\n'Reilly EM, Abou-Alfa GK, Letourneau R, et al. A randomized phase III trial of DX-8951f (Exatecan mesylate; DX) and gemcitabine vs. gemcitabine alone in advanced pancreatic cancer [abstract no. 4006]. J Clin Oncol 2004Jul 15; 22Suppl. 14: 315. Plus oral presentation at the 40th Annual Meeting of the American Society of Clinical Oncology; 2004 Jun 5–8; New Orleans (LA)\nReni M, Cordio S, Milandri C, et al. Gemcitabine versus cisplatin, epirubicin, fluorouracil, and gemcitabine in advanced pancreatic cancer: a randomised controlled multicentre phase III trial. Lancet Oncol 2005Jun; 6(6): 369–76\nRiess M, Helm A, Niedergethmann I, et al. 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A phase I trial of weekly gemcitabine and concurrent radiotherapy in patients with locally advanced pancreatic cancer. Br J Cancer 2002May 20; 86(10): 1551–4\nPoggi MM, Kroog GS, Russo A, et al. Phase I study of weekly gemcitabine as a radiation sensitizer for unresectable pancreatic cancer. Int J Radiat Oncol Biol Phys 2002Nov 1; 54: 670–6\nHoffman JP, McGinn CJ, RossE, et al. A phase I trial of preoperative gemcitabine and radiotherapy followed by postoperative gemcitabine for patients with localized, resectable pancreatic adenocarcinoma. 16th Chemotherapy Foundation Symposium; 1998 Nov 11; New York (NY)\nPipas JM, Mitchell SE, Barth RJ, et al. Phase I study of twice-weekly gemcitabine and concomitant external-beam radiotherapy in patients with adenocarcinoma of the pancreas. Int J Radiat Oncol Biol Phys 2001Aug 1; 50: 1317–22\nBlackstock AW, Tepper J, Kachnic L, et al. Adjuvant gemcitabine and concurrent radiation for resected pancreatic cancer: a phase II study. Proc Am Soc Clin Oncol 2003; 22: 266\nMcGinn CJ, Zalupski MM, Shureiqi I, et al. Phase I trial of radiation dose escalation with concurrent weekly full-dose gemcitabine in patients with advanced pancreatic cancer. J Clin Oncol 2001Nov 15; 19: 4202–8\nAristides M, Lees M, Botwood N, et al. Economic evaluation of gemcitabine in the treatment of pancreatic cancer in the UK. Eur J Health Econ 2003Sep; 4(3): 216–21\nWard S, Morris E, Bansback N, et al. A rapid and systematic review of the clinical effectiveness and cost-effectiveness of gemcitabine for the treatment of pancreatic cancer. Health Technol Assess 2001; 5(24): 1–70\nRagnarson-Tennvall G, Wilking N. Treatment of locally advanced pancreatic carcinoma in Sweden: a health economic comparison of palliative treatment with best supportive care versus palliative treatment with gemcitabine in combination with best supportive care. Pharmacoeconomics 1999Apr; 15: 377–84\nTrippoli S, Messori A. Cost-effectiveness of gemcitabine as first-line therapy for patients with advanced pancreatic cancer. Value Health 1999Jan 28; 2: 22\nKozuch P, Petryk M, Bruckner HW. A comprehensive update on the use of chemotherapy for metastatic pancreatic adenocarcinoma. Hematol Oncol Clin North Am 2002Feb; 16: 123–38\nIshii H, Furuse J, Nagase M, et al. Impact of gemcitabine on the treatment of metastatic pancreatic cancer. J Gastroenterol Hepatol 2005Jan; 20(1): 62–6\nIshii H, Furuse J, Kinoshita T, et al. Treatment cost of pancreatic cancer in Japan: analysis of the difference after the introduction of gemcitabine. Jpn J Clin Oncol 2005Sep; 35(9): 526–30\nMcGinn CJ, Lawrence TS, Zalupski MM. On the development of gemcitabine-based chemoradiotherapy regimens in pancreatic cancer. Cancer 2002Aug 15; 95Suppl. 4: 933–40\nNeoptolemos JP, Cunningham D, Friess H, et al. Adjuvant therapy in pancreatic cancer: historical and current perspectives. Ann Oncol 2003May; 14(5): 675–92\nJacobs AD, Burris HA, Rivkin S, et al. A randomized phase III study of rubitecan (ORA) vs. best choice (BC) in 409 patients with refractory pancreatic cancer report from a North-American multi-center study [abstract no. 4013]. J Clin Oncol 2004Jul 15; 22(14 Suppl.): 4013. Plus oral presentation at the 40th Annual Meeting of the American Society of Clinical Oncology; 2004 Jun 5–8; New Orleans (LA)\nNational Cancer Institute. U.S. National Institutes of Health [online]. Available from URL: http:\u002F\u002Fwww.cancer.gov [Accessed 2005 Oct 18]\nNio Y, Hashimoto K, Yano S, et al. Phase II study on low dose gemcitabine plus oral chemotherapy with uracil-tegafur and cyclophosphamide in combination with radiotherapy against recurrent and advanced pancreatic cancer. Oncol Rep 2005Aug; 14(2): 401–8\nBanu E, Oudard S, Banu A, et al. Cumulative meta-analysis of randomized trials comparing gemcitabine-based chemotherapy versus gemcitabine alone in patients with advanced or metastatic pancreatic cancer [abstract no. 4101]. J Clin Oncol 2005Jun 1; 23(16 Pt 2): 4101. Plus oral presentation presented at the 41st Annual Meeting of the American Society of Clinical Oncology; 2005 May 13–17; Orlando (FL)\nUS Food and Drug Administration. FDA approves Tarceva in combination with gemcitabine for first-line treatment of patients with locally advanced, unresectable or metastatic pancreatic cancer, [online]. Available from URL: http:\u002F\u002Fwww.fda.gov\u002Fcder\u002F [Accessed 2005 Nov 8]\nHeinemann V, Hoehler T, Scipelt G, et al. Randomized comparison of capecitabine plus oxaliplatin (CapOx) versus capecitabine plus gemcitabine (CapGem) versus gemcitabine plus oxaliplatin (GemOx) in advanced pancreatic cancer [abstract no. 735]. Eur J Cancer Supplements 2005Oct; 3(2): 209. Plus oral presentation at the 13th European Cancer Conference; 2005 Oct 30–Nov 3; Paris\nNeoptolemos JP, Stocken DD, Friess H, et al. A randomized trial of chemoradiotherapy and chemotherapy after resection of pancreatic cancer. New Engl J Med 2004Mar 18; 350: 1200–10\nStocken DD, Buchler MW, Dervenis C, et al. Meta-analysis of randomized adjuvant therapy trials for pancreatic cancer. Br J Cancer 2005Apr 25; 92(8): 1372–81",{"EN":843},"Gemcitabine (Gemzar®), an intravenously administered deoxycitidine analog, is approved in the US and several European countries for the treatment of locally advanced (unresectable) or metastatic adenocarcinoma of the pancreas, including fluorouracil-refractory disease. Although gemcitabine demonstrates only modest activity against pancreatic tumors (like most other cytotoxic agents), and rarely prolongs median survival beyond 7 months, it has a relatively mild toxicity profile, which is particularly important in the context of palliative treatment. Gemcitabine was superior to fluorouracil in alleviating tumor-related symptoms and extending survival in a randomized, multicenter trial; it was at least as effective as other single agents (e.g. exatecan and marimastat), but less effective than a four-drug combination (fluorouracil, leucovorin, epirubicin plus carboplatin [FLEC]) in prolonging survival in similar studies. There is the suggestion that survival outcomes with the drug may be enhanced using an extended, slow infusion rate, as opposed to a short, standard infusion rate. Adding another anticancer agent to gemcitabine, however, has to date yielded mostly disappointing results relative to gemcitabine alone in phase III trials. Of the doublet combinations tested, only gemcitabine plus capecitabine and gemcitabine plus erlotinib significantly increased survival (preliminary data), while only gemcitabine plus oxaliplatin significantly improved symptom alleviation, relative to gemcitabine alone; however, a four-drug regimen of cisplatin plus epirubicin, fluorouracil, and gemcitabine (PEFG) significantly improved both outcomes. Administering gemcitabine concurrently with radiotherapy is being evaluated in the setting of locally advanced, unresectable disease. Additionally, gemcitabine and\u002For gemcitabine-based chemoradiotherapy are being investigated as (neo)adjuvant treatments in patients with resectable disease; disease-free survival was improved relative to observation in the first randomized trial of adjuvant gemcitabine (preliminary data). In conclusion, systemic gemcitabine monotherapy has been widely investigated in the treatment of patients with advanced, inoperable pancreatic cancer, and is well tolerated and moderately effective in these individuals. Research is ongoing into ways of maximising treatment outcomes with gemcitabine; these approaches include combining the drug with novel chemotherapeutic agents, integrating it into chemoradiotherapy regimens, using it in patients with resectable disease, and administering it by intra-arterial infusion. Pending confirmation of promising preliminary results with certain gemcitabine-based combination chemotherapies, gemcitabine monotherapy remains the widely accepted standard of care for advanced, nonresectable pancreatic cancer. Gemcitabine is a deoxycitidine analog prodrug that inhibits DNA synthesis through the self-potentiating actions of its active diphosphate and triphosphate derivatives, which are formed after the uptake and intracellular phosphorylation of the parent drug by nucleoside kinases. Gemcitabine demonstrates linear pharmacokinetics over the dose range 53–1000 mg\u002Fm2; the recommended dosage is 1000 mg\u002Fm2once weekly, administered by a 30-minute intravenous infusion. The maximum concentration of gemcitabine triphosphate in peripheral blood mononuclear cells (PBMCs) was attained within 30 minutes of the end of the infusion and increased in proportion to the gemcitabine dose (up to 350 mg\u002Fm2). Gemcitabine triphosphate formation within PBMCs was saturable at higher gemcitabine doses, although this phenomenon can be overcome using an extended, slow infusion rate (i.e. 10 mg\u002Fm2\u002Fmin). Gemcitabine systemic exposure was significantly reduced with intra-arterial as opposed to intravenous administration of the drug. Plasma protein binding of gemcitabine is minimal, and the drug is not extensively distributed into tissues after short infusions (\u003C70 minutes). Gemcitabine is rapidly deaminated intracellularly; up to 98% of the administered dose is excreted in the urine within 1 week. Unchanged parent drug (\u003C10%) and the inactive 2′-deox-y-2′,2′-difluorouridine metabolite account for 99% of the excreted dose. The terminal elimination half-life of gemcitabine after short infusions ranges from 42–94 minutes depending on age and sex; however, dosage adjustments are not necessary on the basis of these characteristics. In a pivotal, randomized, multicenter trial, the recommended dosage regimen of gemcitabine was superior to the previous standard of care fluorouracil (given as an intravenous bolus) in the first-line treatment of patients with advanced, inoperable pancreatic cancer. Gemcitabine was more effective than fluorouracil in alleviating three common debilitating, tumor-related signs and symptoms (pain, functional impairment, weight loss), and conferred a small survival advantage. Relative to other single agents (exatecan, marimastat, BAY 12-9566), gemcitabine had a similar or superior effect on overall survival in randomized, multicenter, phase III studies in patients with locally advanced (unresectable) or metastatic pancreatic cancer. Systemic gemcitabine was, however, inferior to combination chemotherapy with FLEC, administered intra-arterially, in this regard. As a second-line treatment, gemcitabine demonstrated useful palliative efficacy in patients with fluorouracil-refractory pancreatic cancer in a pivotal noncomparative, multicenter trial. The strategy of adding other cytotoxic or targeted anticancer agents (e.g. fluorouracil [with or without folinic acid], pemetrexed, cisplatin, oxaliplatin, irinotecan, exatecan, marimastat, tipifarnib, G17DT, virulizin, or LY293111) to gemcitabine has largely produced disappointing results in terms of improving overall survival relative to gemcitabine monotherapy in randomized, multicenter, phase II or III studies in patients with locally advanced (unresectable) or metastatic pancreatic cancer (n = 92–688). However, preliminary reports indicate that, when used as the second drug in a gemcitabine-containing doublet, capecitabine (in the larger of two studies) and erlotinib confer a survival advantage over gemcitabine alone. Similarly, combination chemotherapy with PEFG significantly improved survival relative to gemcitabine monotherapy (and was superior for the primary endpoint of progression-free survival at 4 months). Gemcitabine monotherapy did not prolong median survival beyond 7.3 months in pivotal and phase III clinical trials. However, survival may be enhanced using an extended, slow infusion of the drug as opposed to the standard (30-minute) infusion. In the only prospective, randomized studies reported to date, gemcitabine-based chemoradiotherapy was superior to fluorouracil-based chemoradiotherapy, and gemcitabine plus doxifluridine-based chemoradiotherapy was similar to paclitaxel plus doxifluridine-based chemoradiotherapy, in the treatment of patients with locally advanced, unresectable pancreatic cancer. According to preliminary results of a randomized, multicenter, phase III study, adjuvant chemotherapy with gemcitabine significantly increased the median duration of disease-free survival (relative to observation) in previously untreated patients with resected pancreatic cancer, regardless of whether the resection margin was positive or negative, or whether lymph nodes were involved. Gemcitabine, either as monotherapy or in combination with other anticancer agents, was generally well tolerated when administered as a first-line treatment for locally advanced (unresectable) or metastatic pancreatic cancer. Fewer than 5% of patients receiving the recommended gemcitabine dosage regimen discontinued treatment because of adverse events (e.g. fever, pain, asthenia, nausea\u002Fvomiting) in a large-scale investigational new drug (compassionate use) treatment program (n = 3023). Myelosuppression was the primary dose-limiting toxicity in clinical trials, with grade 3 or 4 neutropenia occurring in up to 41% of patients, and grade 3 or 4 leukopenia, thrombocytopenia and anemia each occurring in up to 16% of patients with advanced pancreatic cancer who typically received the recommended gemcitabine dosage regimen in phase III studies (n = 107–668). Myelosuppression was increased with an extended, slow infusion of gemcitabine relative to a standard 30-minute infusion of the drug in a randomized, multicenter, phase II trial, although the number of consequent dose reductions and omissions were similar for both protocols. Compared with gemcitabine monotherapy, the incidence of some grade 3 or 4 adverse events (e.g. hematological toxicities) was significantly increased with four-drug regimens containing (PEFG) or not containing (FLEC) gemcitabine, and with pemetrexed, exatecan, or oxaliplatin as the second drug in a gemcitabine-containing doublet. The incidence of neutropenia and thrombocytopenia in patients receiving gemcitabine plus capecitabine was numerically higher than that in patients receiving gemcitabine alone, and the incidence of diarrhea and rash in patients receiving gemcitabine plus erlotinib was numerically higher than that in patients receiving gemcitabine plus placebo, although statistical analyses were not provided. Similar tolerability profiles for gemcitabine-based chemoradiotherapy versus fluorouracil-based chemoradiotherapy (the current standard of care) and gemcitabine plus doxifluridine-based chemoradiotherapy versus paclitaxel plus doxifluridine-based chemoradiotherapy were seen in small, randomized trials in patients with advanced pancreatic cancer. Economic models incorporating clinical outcome and resource use data from a randomized, single-blind study of gemcitabine versus fluorouracil suggest that first-line treatment of advanced pancreatic cancer with gemcitabine, as opposed to fluorouracil or best supportive care only, is cost effective in relation to other accepted healthcare interventions in the UK from a national healthcare payer’s perspective, and in Sweden from a societal perspective. These analyses took into account direct costs only; the impact of indirect or intangeable costs (e.g. quality of life) was not assessed.",{"EN":838},{"VOID":846},"10.2165\u002F00024669-200504060-00006","2025-01-23T22:53:14.846+00:00","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.2165\u002F00024669-200504060-00006",[850,865],{"id":851,"sortIndex":21,"researcher":20,"roles":852,"affiliations":853,"properties":862},"17c409d2-2bf0-43d9-bcfb-9aa14e2ff1a9",[635],[854],{"id":20,"sortIndex":21,"affiliation":855,"properties":20},{"id":856,"createTime":857,"updateTime":857,"relativeEntities":858,"slug":20,"properties":859,"entityType":84,"verifyStatus":19,"verifyTime":20,"verifyNote":20,"syncStatus":19,"languages":20,"translateLanguages":20,"viewCount":21},"989f8144-7f07-4786-9052-505db2945096","2024-01-30T21:16:22.024+00:00",[],{"title":860},{"VI":861},"Adis International Inc., Yardley, USA",{"title":863},{"VI":864},"James E. Frampton",{"id":866,"sortIndex":71,"researcher":20,"roles":867,"affiliations":868,"properties":874},"36683d72-3b9a-483f-8eed-a9d488be370e",[635],[869],{"id":20,"sortIndex":21,"affiliation":870,"properties":20},{"id":856,"createTime":857,"updateTime":857,"relativeEntities":871,"slug":20,"properties":872,"entityType":84,"verifyStatus":19,"verifyTime":20,"verifyNote":20,"syncStatus":19,"languages":20,"translateLanguages":20,"viewCount":21},[],{"title":873},{"VI":861},{"title":875},{"VI":876},"Antona J. Wagstaff",{"url":848,"publisher":878,"properties":893},{"id":6,"createTime":7,"updateTime":8,"relativeEntities":879,"slug":10,"properties":880,"entityType":18,"verifyStatus":19,"verifyTime":20,"verifyNote":20,"syncStatus":19,"languages":20,"translateLanguages":20,"viewCount":21,"subjectFields":884,"manageAffiliations":885,"indexDatabases":886,"url":20,"thumbnailPath":20,"statistic":20,"gsStatistic":20,"type":20,"analyzePriority":20},[],{"issn":881,"title":882,"url":883},{"VOID":13},{"EN":15},{"VOID":17},[],[],[887],{"id":26,"indexDatabase":888,"url":39,"indexYears":40,"academicFieldIds":20,"indexDatabaseRanking":41},{"id":28,"createTime":29,"updateTime":30,"relativeEntities":889,"label":890,"description":891,"key":36,"publicationTags":892,"standard":20},[],{"EN":33,"VI":33},{"EN":33,"VI":35},[38],{"volume":894,"pages":896},{"VOID":895},"4",{"VOID":897},"395-416","2012-08-09",{"id":900,"createTime":901,"updateTime":902,"relativeEntities":903,"slug":904,"properties":905,"entityType":62,"verifyStatus":63,"verifyTime":902,"verifyNote":64,"syncStatus":19,"languages":913,"translateLanguages":20,"viewCount":21,"primaryUrl":914,"fullTextUrl":20,"authors":915,"publicationType":107,"publisherRelationship":945,"citationCount":20,"citationInfo":20,"publishDate":510,"publishYear":511,"citationAnalyzeStatus":19,"lastCitationAnalyze":20,"indexDatabases":20,"openAccess":20,"references":961,"isForceReanalyzing":430},"116fc4f6-72e4-4e2e-81c3-95d563adbf95","2024-04-11T05:20:01.952+00:00","2024-09-21T22:48:36.782+00:00",[],"Postmenopausal-Metastatic-Breast-Cancer",{"keywords":906,"abstract":907,"title":909,"doi":911},{"EN":439},{"EN":908},"Endocrine therapy and chemotherapy play important roles in the management of postmenopausal women with metastatic breast cancer. This paper specifically reviews the indications and options for first-line treatment of metastatic breast cancer and recent advances are highlighted, with particular attention to randomized, controlled, phase III clinical trials. Until recently, tamoxifen was standard first-line endocrine treatment for patients with metastatic breast cancer. Now, potent third generation aromatase inhibitors, such as letrozole and anastrozole, have shown superiority to tamoxifen as first-line endocrine treatment and provide an alternative for postmenopausal women. The most active chemotherapy agents for patients with advanced breast cancer have, until recently, been the anthracyclines, doxorubicin and epirubicin. However, their increasing use in the adjuvant setting has resulted in a need for novel active non-cross-resistant cytotoxic drugs for metastatic breast cancer. Real progress has been made with the introduction of the taxanes, paclitaxel and docetaxel. Other developments include the use of single agent cytotoxics such as vinorelbine, the oral fluoropyrimidine capecitabine and gemcitabine, all of which have some activity following either taxanes or anthracyclines, along with a low toxicity profile. Bisphosphonates are bone-specific palliative treatments that have been instituted on the basis of their impact on symptoms and skeletal related morbidity. Finally, the era of biological therapy in the clinic for patients with breast cancer has been heralded with the development and introduction of trastuzumab, a humanized monoclonal antibody which targets the cell surface growth factor receptor HER2\u002Fneu. Importantly, each of these new treatment options has provided an incremental improvement in efficacy over previous standard first-line therapies.",{"EN":910},"Postmenopausal Metastatic Breast Cancer",{"VOID":912},"10.2165\u002F00024669-200302020-00003",[66],"https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.2165\u002F00024669-200302020-00003",[916,931],{"id":917,"sortIndex":21,"researcher":20,"roles":918,"affiliations":919,"properties":928},"24829bbf-3667-4936-b210-e310c9b4c516",[],[920],{"id":20,"sortIndex":21,"affiliation":921,"properties":20},{"id":922,"createTime":923,"updateTime":923,"relativeEntities":924,"slug":20,"properties":925,"entityType":84,"verifyStatus":19,"verifyTime":20,"verifyNote":20,"syncStatus":19,"languages":20,"translateLanguages":20,"viewCount":21},"a0bd705e-8898-4a6e-938d-116a8c98c5f4","2024-01-16T14:49:47.587+00:00",[],{"title":926},{"VI":927},"Breast Unit, Royal Marsden Hospital London, UK",{"title":929},{"EN":930},"Laura Assersohn",{"id":932,"sortIndex":71,"researcher":20,"roles":933,"affiliations":934,"properties":940},"d24eeca8-43a4-427f-92da-6ddda2dc6ab7",[],[935],{"id":20,"sortIndex":21,"affiliation":936,"properties":20},{"id":922,"createTime":923,"updateTime":923,"relativeEntities":937,"slug":20,"properties":938,"entityType":84,"verifyStatus":19,"verifyTime":20,"verifyNote":20,"syncStatus":19,"languages":20,"translateLanguages":20,"viewCount":21},[],{"title":939},{"VI":927},{"title":941,"email":943},{"EN":942},"Stephen R.D. Johnston",{"VOID":944},"stephen@icr.ac.uk",{"url":20,"publisher":946,"properties":20},{"id":6,"createTime":7,"updateTime":8,"relativeEntities":947,"slug":10,"properties":948,"entityType":18,"verifyStatus":19,"verifyTime":20,"verifyNote":20,"syncStatus":19,"languages":20,"translateLanguages":20,"viewCount":21,"subjectFields":952,"manageAffiliations":953,"indexDatabases":954,"url":20,"thumbnailPath":20,"statistic":20,"gsStatistic":20,"type":20,"analyzePriority":20},[],{"issn":949,"title":950,"url":951},{"VOID":13},{"EN":15},{"VOID":17},[],[],[955],{"id":26,"indexDatabase":956,"url":39,"indexYears":40,"academicFieldIds":20,"indexDatabaseRanking":41},{"id":28,"createTime":29,"updateTime":30,"relativeEntities":957,"label":958,"description":959,"key":36,"publicationTags":960,"standard":20},[],{"EN":33,"VI":33},{"EN":33,"VI":35},[38],[962,964,966,968,970,972,974,976,978,980,982,984,986,988,990,992,994,996,998,1000,1002,1004,1006,1008,1010,1012,1014,1016,1018,1020,1022,1024,1026,1028,1030,1032,1034,1036,1038,1040,1042,1044,1046,1048,1050,1052,1054,1056,1058,1060,1062,1064,1066,1068,1070,1072,1074,1076,1078,1080,1082,1084,1086,1088,1090,1092,1094,1096,1098,1100,1102,1104,1106,1108,1110,1112,1114,1116,1118,1120,1122,1124,1126,1128,1130,1132,1134,1136,1138,1140,1142,1144,1146,1148,1150,1152,1154,1156,1158,1160,1162],{"id":20,"text":963,"url":20,"identifiers":20},"Office for National Statistics. Mortality statistics: review of the Register General on deaths by sex and age, England and Wales, 1999. London: The Stationery Office, 2000",{"id":20,"text":965,"url":20,"identifiers":20},"Cancer Research Campaign. Cancer Research Campaign, CRC Cancer Stats; Mortality UK, London. Available from URL: http:\u002F\u002Fwww.crc.org.uk\u002Fcancer\u002Fpageimages\u002Fcsmortality.pdf [Accessed 2002 Jul 19]",{"id":20,"text":967,"url":20,"identifiers":20},"Greenberg P, Hortobagyi G, Smith T, et al. Long-term follow-up of patients with complete remission following combination chemotherapy for metastatic breast cancer. J Clin Oncol 1996; 14: 2197–205",{"id":20,"text":969,"url":20,"identifiers":20},"Early Breast Cancer Trialists’ Collaborative Group. Polychemotherapy for early breast cancer: an overview of the randomised trials. Lancet 1998; 352: 930–42",{"id":20,"text":971,"url":20,"identifiers":20},"Early Breast Cancer Trialists’ Collaborative Group. 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Endocrine manipulation in advanced breast cancer: recent advances with SERM therapies. Clin Cancer Res 2001; 7Suppl. 1: 4376s–87s",{"id":20,"text":991,"url":20,"identifiers":20},"Gradishar W, Giusman J, Vogel C, et al. Raloxifene HCL, a new endocrine agent, is active in estrogen receptor positive (ER+) metastatic breast cancer. Breast Cancer Res Treat 1997; 46: 53",{"id":20,"text":993,"url":20,"identifiers":20},"Curnrnings S, Eckert S, Krueger K, et al. The effect of raloxifene on risk of breast cancer in posmtenopausal women: results from the multiple outcomes of raloxifene evaluation (MORE) randomized trial. JAMA 1999; 281: 2189–97",{"id":20,"text":995,"url":20,"identifiers":20},"Fisher B, Costantino J, Wickerham D, et al. Tamoxifen for prevention of breast cancer: report of the National Surgical Adjuvant Breast and Bowel Project P-1 study. J Natl Cancer Inst 1998; 90(18): 1371–88",{"id":20,"text":997,"url":20,"identifiers":20},"Brodie A, Njar V. Aromatase inhibitors and breast cancer. Semin Oncol 1996; 23(4 Suppl. 9): 10–20",{"id":20,"text":999,"url":20,"identifiers":20},"Miller WR. Aromatase inhibitors. Endocr Relat Cancer 1996; 3(1): 65–79",{"id":20,"text":1001,"url":20,"identifiers":20},"Geisler J, Haynes B, Anker G, et al. Influence of letrozoie and anastrozole on total body arorealization and plasma estrogen levels in postmenopausal breast cancer patients evaluated in a randomized, cross-over study. J Clin Oncol 2002: 20; 751–57",{"id":20,"text":1003,"url":20,"identifiers":20},"Buzdar A, Jonat W, Howell A, et al. Anastrozole, a potent and selective aromatase inhibitor, versus megestrol acetate in post-menopausal women with advanced breast cancer: results of overview analysis of 2 phase III trials. J Clin Oncol 1996; 14: 2000–11",{"id":20,"text":1005,"url":20,"identifiers":20},"Buzdar A, Jonat W, Howell A, et al. Anastrozoie vs megestrol acetate in the treatment of postmsnopausal women with advanced breast carcinoma: results of a survival update based on a combined analysis of data from two mature phase III trials. Cancer 1998; 83: 1142–52",{"id":20,"text":1007,"url":20,"identifiers":20},"Dombernowsky P, Smith I, Falkson G, et al. Letrozoie, a new oral aromatase inhibitor for advanced breast cancer: doubie-blind randomized trial showing a dose effect and improved efficacy and tolerability compared with megestrol acetate. J Clin Oncol 1998; 16(2): 453–61",{"id":20,"text":1009,"url":20,"identifiers":20},"Buzdar A, Douma J, Davidson N, et al. Phase III, multicenter, double-blind, randomized study of letrozole, an aromatase inhibitor, for advanced breast cancer versus megestrol acetate. J Clin Oncol 2001; 19(14): 3357–66",{"id":20,"text":1011,"url":20,"identifiers":20},"Kvinnsiand S, Anker G, Dirix L, et al. High activity and tolerability demonstrated for exemestane in postmenopausai women with metastatic breast cancer who had previously failed on tamoxifen treatment. Eur J Cancer 2000; 36: 976–82",{"id":20,"text":1013,"url":20,"identifiers":20},"Lonning P, Bajetta E, Murray R, et al. Activity of exemestane in metastatic breast cancer after failure of nonsteroidal aromatase inhibitors: a phase II trial. J Clin Oncol 2000; 18(11): 2234–44",{"id":20,"text":1015,"url":20,"identifiers":20},"Thurlimann B, Paridaens R, Serin D, et al. Third-line hormonal treatment with exemestane in postmenopausai patients with advanced breast cancer progressing on aminogiutethimide: a phase II multicentre multinational study: Exemestane Study Group. Eur J Cancer 1997; 33(11): 1767–73",{"id":20,"text":1017,"url":20,"identifiers":20},"Kaufmann M, Bajetta E, Dirix L, et al. Exemestane is superior to megestrol acetate after tamoxifen failure in postmenopausai women with advanced breast cancer: results of a phase III randomized double-blind trial. J Clin Oncol 2000; 18(7): 1399–411",{"id":20,"text":1019,"url":20,"identifiers":20},"Nabhoitz J, Buzdar A, Pollak M, et al. Anastrozole is superior to tamoxifen as first-line therapy for advanced breast cancer in postraenopausal women: results of a North American multicenter randomized trial. J Clin Oncol 2000; 18(22): 3758–67",{"id":20,"text":1021,"url":20,"identifiers":20},"Bonneterre J, Thurlimann B, Robertson J, et al. Anastrozoie versus tamoxifen as first-line therapy for advanced breast cancer in 668 postmenopausal women: results of the tamoxifen or Arimidex randomized group efficacy and tolerability study. J Clin Oncol 2000; 18(22): 3748–57",{"id":20,"text":1023,"url":20,"identifiers":20},"Mouridsen H, Gershanovich M, Sun Y, et al. Superior efficacy of letrozoie versus tamoxifen as first-line therapy for postmenopausai women with advanced breast cancer: results of a phase III study of the International Letrozoie Breast Cancer Group. J Clin Oncol 2001; 19(10): 2596–606",{"id":20,"text":1025,"url":20,"identifiers":20},"Dirix L, Piccart M, Lohrisch C, et al. Efficacy of and tolerance to exemestane versus tamoxifen in first line hormone therapy of postmenopausal metastatic breast cancer patients: a European Organisation for the Research and Treatment of cancer (EORTC Breast Group) Phase II trial with Pharmacia and Upjohn. Proc Am Soc Clin Oncol 2001; 20: 114a",{"id":20,"text":1027,"url":20,"identifiers":20},"Buzdar A, Nabhoitz J, Robertson J, et al. Anastrozole (Arimidex) versus tamoxifeu as first-line therapy for advanced breast cancer (ABC) in postmenopausal (PM) women — combined analysis from two identically designed multicenter trials [abstract 609D]. 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Or what we know and what we still need to learn about anthracycline dose per course, dose density and cumulative dose in the treatment of breast cancer. Ann Oncol 1997; 8: 1177–82",{"id":20,"text":1051,"url":20,"identifiers":20},"Buzdar A, Hortobagyi G, Prye D, et al. Second-line chemotherapy for metastatic breast cancer including quality of life issues. Breast 1996; 5: 312–7",{"id":20,"text":1053,"url":20,"identifiers":20},"Sjostrom J, Biomqvist C, Mouridsen H, et al. Docetaxei compared with sequential methotrexate and 5-fluorouracil in advanced breast cancer after anthracycline failure: a randomised phase III study with cross-over on progression by the Scandinavian Breast Cancer Group. Eur J Cancer 1999; 35: 1194–201",{"id":20,"text":1055,"url":20,"identifiers":20},"Nabholtz J, Senn J, Beswoda W, et al. Prospective randomised trial of docetaxel vs mitomycin plus vinbiastine in patients with metastatic breast cancer progressing despite previous anthracyciine-containing chemotherapy. J Clin Oncol 1999; 17: 1413–24",{"id":20,"text":1057,"url":20,"identifiers":20},"Bonneterre J, Roche H, Monnier A, et al. Taxoiere vs 5-FU and Naveibine as second-line chemotherapy in patients wiith metastatic breast cancer. Proc Am Soc Clin Oncol 1997; 16: A564",{"id":20,"text":1059,"url":20,"identifiers":20},"Chan S, Friedrichs K, Noel D, et al. Prospective randomised phase III triai of docetaxel vs doxorubicin in patients with metastatic breast cancer. J Clin Oncol 1999; E7: 2341–54",{"id":20,"text":1061,"url":20,"identifiers":20},"Sledge GW, Neuberg D, Bernando P, et al. Phase III trial of doxorubicin vs paclitaxel vs doxorabicin + paclitaxel as front-line chemotherapy for metastatic breast cancer; an intergroup trial [abstract]. J Clin Oncol 2003; 21: 588–92",{"id":20,"text":1063,"url":20,"identifiers":20},"Paridaens R, Biganzoli L, Broiling P, et al. Paclitaxel vs doxorabicin as first-line single agent chemotherapy for metastatic breast cancer; a European Organisation for Research and Treatment of Cancer randomised study with cross-over. J Clin Oncol 2000; 18: 724–33",{"id":20,"text":1065,"url":20,"identifiers":20},"Bishop J, Dewar J, Toner G, et al. Initial paclitaxel improves outcome compared with CMFP combination chemotherapy as front-line therapy in untreated metastatic breast cancer. J Clin Oncol 1999; 17: 2355–64",{"id":20,"text":1067,"url":20,"identifiers":20},"Perez EA, Vogel CL, Irwin DH, Krishner JJ, Patel R. Multicenter Phase II trial of weekly paclitaxel in women with metastatic breast cancer. J Clin Oncol 2001; 18: 4216–33",{"id":20,"text":1069,"url":20,"identifiers":20},"Burstein EL, Manola J, Younger J, et al. Docetaxel administered on a weekly basis for metastatic breast cancer. J Clin Oncol 2000; 19: 1212–9",{"id":20,"text":1071,"url":20,"identifiers":20},"Tassera J. Pienkowski T, Pluzanska A, et al. 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N Engl J Med 1996; 335: 1785–91",{"id":20,"text":1125,"url":20,"identifiers":20},"Lipton A, Theriault R, Hortobagyi G, et al. Pamidronate prevents skeletal complications and is effective palliative treatment in women with breast carcinoma and osteolytic bone metastases. Cancer 2000: 88: 1082–90",{"id":20,"text":1127,"url":20,"identifiers":20},"Theriauit R, Lipton A, Hortobagyi G, et al. Pamidronate reduces skeletal morbidity in women with advanced breast cancer and lytic bone lesions: a randomized, placebo-controlled trial-protocol 18 Aredia Breast Cancer Study Group. J Clin Oncol 1999; 17: 846–54",{"id":20,"text":1129,"url":20,"identifiers":20},"Breast Specialty Group of the British Association of Surgical Oncology. The management of metastatic bone disease in the United Kingdom. Eur J Surg Oncol 1999; 25: 3–23",{"id":20,"text":1131,"url":20,"identifiers":20},"Hillner B, Ingle J, Berenson J, et al. American Society of Clinical Oncology guideline on the role of bisphosphonates in breast cancer: American Society of Oncology Bisphosphonates Expert Panel. J Clin Oncol 2000; 18: 1378–91",{"id":20,"text":1133,"url":20,"identifiers":20},"Diel I, Marschner N, Kindler M, et al. Continual oral versus intravenous interval therapy with bisphosphonates in patients with breast cancer and bone metastases [abstract 488A]. Proc Am Soc Clin Oncol 1999; 18: 128",{"id":20,"text":1135,"url":20,"identifiers":20},"Slamon DJ, Clark GM, Wong SG, et al. Human breast cancer: correlation of relapse and survival with amplification of the HER-2\u002Fneu oncogene. Science 1987; 235(4785): 177–82",{"id":20,"text":1137,"url":20,"identifiers":20},"Baselga J, Tripathy D, Mendelsohn 3, et al. Phase II study of weekly intravenous recombinant humanized Anti-p185HER2 monoclonal antibody in patients with HER2\u002Fneu-overexpressing metastatic breast cancer. J Clin Oncol 1996; 14(3): 737–44",{"id":20,"text":1139,"url":20,"identifiers":20},"Pegram MD, Lipton A, Hayes DF, et al. Phase II study of receptor-enhanced chernosensitivity using recombinant humanized anti-p185HER2\u002Fneu monoclonal antibody plus cisplatin in patients with HER2\u002Fneu-overexpressing metastatic breast cancer refractory to chemotherapy treatment. J Clin Oncol 1998; 16(8): 2659–71",{"id":20,"text":1141,"url":20,"identifiers":20},"Cobleigh M, Vogel C, Tripathy D, et al. Multinational study of the efficacy and safety of humanized anti-HER2 monoclonal antibody in women who have HER2-overexpressiing metastatic breast cancer that has progressai after chemotherapy for metastatic disease. J Clin Oncol 1999; 17(9): 2639–48",{"id":20,"text":1143,"url":20,"identifiers":20},"Vogel C, Cobleigh M, Tripathy D, et al. Efficacy and safety of trastuzumab as a single agent in first-line treatment of HER2-overexpressing metastatic breast cancer. J Clin Oncol 2002; 20(3): 719–26",{"id":20,"text":1145,"url":20,"identifiers":20},"Slamon J, Leyland-Jones B, Shak S, et al. Use of chemotherapy plus a monoclonal antibody against HER2 for metastatic breast cancer that overexpreses HER2. N Engl J Med 2001; 344: 783–92",{"id":20,"text":1147,"url":20,"identifiers":20},"Seidman A, Hudis C, Pierri M, et al. Cardiac dysfunction in the trastuzumab clinical trials experience. J Clin Oncol 2002; 20(5): 1215–21",{"id":20,"text":1149,"url":20,"identifiers":20},"Ciardiello F, Caputo R, Bianco R, et al. Antitumor effect and potentiation of cytotoxic drugs activity in human cancer cells by ZD1839 (Iressa), an epidermal growth factor receptor-selective tyrosine kinase inhibitor. Clin Cancer Res 2000; 6: 2053–63",{"id":20,"text":1151,"url":20,"identifiers":20},"Sirotnak F, Zakowski M, Miller V, et al. Efficacy of cytotoxic agents against human tumor xenografts is markedly enhanced by co-administration of ZD1839 (Iressa), an inhibtor of EGFR tyrosine kinase. Clin Cancer Res 2000; 6: 4885–92",{"id":20,"text":1153,"url":20,"identifiers":20},"Jeng M, Yue W, Eischied A, et al. Role of MAP kinase in the enhanced cell proliferation of long-term estrogen deprived human breast cancer cells. Breast Cancer Res Treat 2000; 62: 167–75",{"id":20,"text":1155,"url":20,"identifiers":20},"McClelland R, Barrow D, Madden T, et al. Enhanced epidermal growth factor receptor signaling in MCF7 breast cancer cells after long-term culture in the presence of the pure antiestrogen LCI 182,780 (Faslodex). Endocrinology 2001; 142(7): 2776–88",{"id":20,"text":1157,"url":20,"identifiers":20},"Nicholson R, Hutcheson I, Harper M, et al. Modulation of epidermal growth factor receptor in endocrine-resistant, oestrogen receptor-positive breast cancer. Endocr Relat Cancer 2001; 8: 175–82",{"id":20,"text":1159,"url":20,"identifiers":20},"Gee J, Hutcheson I, Knowlden J, et al. The EGFR-selective tyrosine kinase inhibitor ZD1839 (Iressa) is an effective inhibitor of tarnoxifen-resistant breast cancer growth. Proc Am Soc Clin Oncol 2001; 20: A282",{"id":20,"text":1161,"url":20,"identifiers":20},"Clark G, Der CJ. Aberrant function of the Ras signal transduction pathway in human breast cancer. Breast Cancer Res Treat 1995; 35: 133–44",{"id":20,"text":1163,"url":20,"identifiers":20},"Johnston S, Hickish T, Ellis P, et al. Clinical activity with the farnesyl transferase inhibitor R115777 in patients with advanced breast cancer: relationship with tumour phenotype. Breast Cancer Res Treat 2000; 32: A28",{"id":1165,"createTime":1166,"updateTime":1167,"relativeEntities":1168,"slug":1169,"properties":1170,"entityType":62,"verifyStatus":19,"verifyTime":1167,"verifyNote":1174,"syncStatus":19,"languages":20,"translateLanguages":20,"viewCount":21,"primaryUrl":1175,"fullTextUrl":20,"authors":1176,"publicationType":107,"publisherRelationship":1177,"citationCount":20,"citationInfo":20,"publishDate":898,"publishYear":511,"citationAnalyzeStatus":19,"lastCitationAnalyze":20,"indexDatabases":20,"openAccess":20,"references":20,"isForceReanalyzing":430},"e0ab3197-5f52-4074-93c6-859519d1890b","2024-02-08T09:08:21.635+00:00","2025-01-01T22:47:01.566+00:00",[],"Acknowledgment",{"title":1171,"doi":1172},{"EN":1169},{"VOID":1173},"10.2165\u002F00024669-200504060-00001","Author title is blank","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.2165\u002F00024669-200504060-00001",[],{"url":1175,"publisher":1178,"properties":1193},{"id":6,"createTime":7,"updateTime":8,"relativeEntities":1179,"slug":10,"properties":1180,"entityType":18,"verifyStatus":19,"verifyTime":20,"verifyNote":20,"syncStatus":19,"languages":20,"translateLanguages":20,"viewCount":21,"subjectFields":1184,"manageAffiliations":1185,"indexDatabases":1186,"url":20,"thumbnailPath":20,"statistic":20,"gsStatistic":20,"type":20,"analyzePriority":20},[],{"issn":1181,"title":1182,"url":1183},{"VOID":13},{"EN":15},{"VOID":17},[],[],[1187],{"id":26,"indexDatabase":1188,"url":39,"indexYears":40,"academicFieldIds":20,"indexDatabaseRanking":41},{"id":28,"createTime":29,"updateTime":30,"relativeEntities":1189,"label":1190,"description":1191,"key":36,"publicationTags":1192,"standard":20},[],{"EN":33,"VI":33},{"EN":33,"VI":35},[38],{"volume":1194,"pages":1195},{"VOID":895},{"VOID":1196},"347-348",{"id":1198,"createTime":1199,"updateTime":1200,"relativeEntities":1201,"slug":1202,"properties":1203,"entityType":62,"verifyStatus":63,"verifyTime":1200,"verifyNote":64,"syncStatus":19,"languages":20,"translateLanguages":20,"viewCount":21,"primaryUrl":1212,"fullTextUrl":20,"authors":1213,"publicationType":107,"publisherRelationship":1229,"citationCount":20,"citationInfo":20,"publishDate":510,"publishYear":511,"citationAnalyzeStatus":19,"lastCitationAnalyze":20,"indexDatabases":20,"openAccess":20,"references":20,"isForceReanalyzing":430},"0aded65c-ae73-42e9-9d44-ddefde564ea1","2024-01-24T17:27:41.875+00:00","2025-01-17T22:45:03.287+00:00",[],"The-Evolving-Role-of-Aromatase-Inhibitors-in-the-Adjuvant-Breast-Cancer-Setting",{"references":1204,"abstract":1206,"title":1208,"doi":1210},{"VOID":1205},"Mouridsen H, Gershanovich M, Sun Y, et al. Superior efficacy of letrozole versus tamoxifen as first-line therapy for postmenopausal women with advanced breast cancer: results of a phase III study of the International Letrozole Breast Cancer Group. J Clin Oncol 2001; 19(10): 2596–606\nNabholtz JM, Buzdar A, Pollak M, et al. Anastrozole is superior to tamoxifen as first-line therapy for advanced breast cancer in postmenopausal women: results of a North American multicenter randomized trial. Arimidex Study Group. J Clin Oncol 2000; 18(22): 3758–67\nBonneterre J, Thurlimann B, Robertson IF, et al. Anastrozole versus tamoxifen as first-line therapy for advanced breast cancer in 668 postmenopausal women: results of the tamoxifen or Arimidex randomized group efficacy and tolerability study. J Clin Oncol 2000; 18(22): 3748–57\nDirix L, Piccant MJ, Lohrisch G, et al. Efficacy of and tolerance to exemestane (E) versus tamoxifen (T) in 1st line hormone therapy (HT) of postmenopausal metastatic breast cancer (MBC) patients (pts): a European Organisation for the Research and Treatment of Cancer (EORTC Breast Group) phase II trial with Pharmacia and Upjohn [abstract 114]. Proc Am Soc Clin Oncol 2001; 20: 29a\nParidaens R, Dirix LY, Beex L, et al. Exemestane (Aromasin) is active and well tolerated as first-line hormonal therapy (HT) of metastatic breast cancer (MBc) patients (pts): results of a randomized phase II trial [abstract 316]. Proc Am Soc Clin Oncol 2000; 19: 83A\nEarly Breast Cancer Trialists’ Collaborative Group. Tamoxifen for early breast cancer: an overview of the randomised trials. Lancet 1998; 351(9114): 1451–67\nRoss D, Whitehead M. Hormonal manipulation and gynaecological cancer: the tamoxifen dilemma. Curr Opin Obstet Gynecol 1995; 7: 63–8\nJones AL, Powles TJ, Treleaven JG, et al. Haemostatic changes and thromboembolic risk during tamoxifen therapy in normal women. Br J Cancer 1992; 66(4): 744–7\nBergman L, Beelen ML, Gallee MP, et al. Risk and prognosis of endometrial cancer after tamoxifen for breast cancer. Comprehensive Cancer Centres’ ALERT Group: assessment of liver and endometrial cancer risk following tamoxifen. Lancet 2000; 356(9233): 881–7\nResch A, Biber E, Seifert M, et al. Evidence that tamoxifen preserves bone density in late postmenopausal women with breast cancer. Acta Oncol 1998; 37: 661–4\nThangaraju M, Kumar K, Gandhirajan R. Effect of tamoxifen on plasma lipid and lipoproteins in postmenopausal women with breast cancer. Cancer 1994; 73: 659–63\nBrodie AM, Schwarzel WC, Shaikh AA, et al. The effect of an aromatase inhibitor, 4-hydroxy-4-androstene-3,17-dione, on estrogen-dependent processes in reproduction and breast cancer. Endocrinology 1977; 100(6): 1684–95\nBonneterre J, Buzdar A, Nabholtz JM, et al. Anastrozole is superior to tamoxifen as first-line therapy in hormone receptor positive advanced breast carcinoma. Cancer 2001; 92(9): 2247–58\nMouridsen H, Gershanovich M, Sun Y, et al. Phase III study of letrozole versus tamoxifen as first-line therapy of advanced breast cancer in postmenopausal women: analysis of survival and update of efficacy from the International Letrozole Breast Cancer Group. J Clin Oncol 2003; 21(11): 2101–9\nArimidex statistical review. Available from URL: http:\u002F\u002Fwww.fda.gov\u002Fcder\u002Ffoi\u002Fnda\u002F2000\u002F20-541S006_Arimidex_statr.pdf\nElisaf MS, Bairaktari ET, Nicolaides C, et al. Effect of letrozole on the lipid profile in postmenopausal women with breast cancer. Eur J Cancer 2001; 37(12): 1510–3\nWojtacki J, Kruszewski W, Sliwinska M, et al. Effect of non-steroidal aromatase inhibitors (AI) on serum lipid profile in patients with breast cancer: preliminary report [abstract 146]. Eur J Cancer 2000; 36Suppl. 5: S71\nHeshmati HM, Khosla S, Robins SP, et al. Role of low levels of endogenous estrogen in regulation of bone resorption in late postmenopausal women. J Bone Miner Res 2002; 17(1): 172–8\nCalle E, Miracle-McMahill HL, Thun MJ, et al. Estrogen replacement therapy and risk of fatal colon cancer in a prospective cohort of postmenopausal women. J Natl Cancer Inst 1995; 87: 517–23\nATAC Trialists’ Group. Anastrozole alone or in combination with tamoxifen versus tamoxifen alone for adjuvant treatment of postmenopausal women with early breast cancer: first results of the ATAC randomised trial. Lancet 2002; 359(9324): 2131–9\nBrodie AH, Jelovac D, Long B. Treatment strategies using letrozole and tamoxifen in a xenograft model for breast cancer: combined treatment versus alternating or sequential treatment. Am J Cancer 2003; 2Suppl. 1: 1–6\nWolmark N, Dunn B. The role of tamoxifen in breast cancer prevention: issues sparked by the NSABP Breast Cancer Prevention Trial (P1). Ann N Y Acad Sci 2001; 949: 99–108\nMasamura S, Santner SJ, Heitjan DF, et al. Estrogen deprivation causes estradiol hypersensitivity in human breast cancer cells. J Clin Endocrinol Metab 1995; 80(10): 2918–25\nKirma N, Gill K, Mandava U, et al. Overexpression of aromatase leads to hyperplasia and changes in the expression of genes involved in apoptosis, cell cycle, growth, and tumor suppressor function in the mammary glands of transgenic mice. Cancer Res 2001; 61: 1910–8\nDowsett M, Jones A, Johnston SR, et al. In vivo measurement of aromatase inhibition by letrozole (CGS 20267) in postmenopausal patients with breast cancer. Clin Cancer Res 1995; 1(12): 1511–5\nGeisler J, Haynes B, Anker G, et al. Influence of letrozole and anastrozole on total body aromatization and plasma estrogen levels in postmenopausal breast cancer patients evaluated in a randomized, cross-over study. J Clin Oncol 2002; 20(3): 751–7\nLønning PE. Pharmacology of new aromatase inhibitors. Breast 1996; 5: 202–8\nGeisler J, King N, Anker G. In vivo inhibition of aromatization by exemestane, a novel irreversible aromatase inhibitor, in postmenopausal breast cancer patients. Clin Cancer Res 1998; 4: 2089–93\nGeisler J, Dowsett M, Lønning P. Letrozole is more effective than anastrozole in suppressing total body aromatization and plasma estrogen levels in postmenopausal breast cancer patients. Am J Oncol Rev 2002; 1: 99–102",{"EN":1207},"Third-generation aromatase inhibitors (AIs) have shown at least equivalent or superior efficacy to tamoxifen in the first-line treatment of women with hormone-dependent metastatic breast cancer. Similar results have been obtained in the neoadjuvant setting. These studies suggested that AIs may also have significant efficacy in the adjuvant setting, and evaluation against tamoxifen is ongoing. Unlike tamoxifen, which interferes with estrogen receptor-dependent gene expression, AIs prevent the formation of estrogen. Therefore, they do not have the mixed agonistic\u002Fantagonistic properties inherent in tamoxifen that cause the adverse events (thromboembolism, endometrial cancer) associated with this agent. In contrast, estrogen depletion may adversely affect bone density and lipid profile. The evaluation of AIs in the adjuvant setting is ongoing in eight major clinical trials. Many of these trials also have subprotocols designed to assess the safety of these agents. Although it will take many years to assess the full impact of adjuvant therapy with AIs, early results from the ATAC (Arimidex and Tamoxifen Alone or in Combination) trial with anastrozole have been reported, and a significant advantage in disease-free survival and the occurrence of contralateral breast cancer noted with the AI compared with tamoxifen. Early results with letrozole from the (J)MA-17 and BIG 1–98 trial (the International Breast Cancer Study Group trial) are expected to follow shortly. It is expected that the ongoing adjuvant trials will provide valuable information concerning efficacy, adverse-effect profile of long-term therapy, resistance to endocrine therapy and the usefulness of sequential treatment with multiple agents. A number of important questions will remain to be answered, however, including the length of time an AI should be administered after surgery and whether any one of the AIs would show superiority over the others in head-to-head comparison.",{"EN":1209},"The Evolving Role of Aromatase Inhibitors in the Adjuvant Breast Cancer Setting",{"VOID":1211},"10.2165\u002F00024669-200302001-00003","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.2165\u002F00024669-200302001-00003",[1214],{"id":1215,"sortIndex":21,"researcher":20,"roles":1216,"affiliations":1217,"properties":1226},"87e26568-3c59-4321-a0b2-746fc7b90b80",[635],[1218],{"id":20,"sortIndex":21,"affiliation":1219,"properties":20},{"id":1220,"createTime":1221,"updateTime":1221,"relativeEntities":1222,"slug":20,"properties":1223,"entityType":84,"verifyStatus":19,"verifyTime":20,"verifyNote":20,"syncStatus":19,"languages":20,"translateLanguages":20,"viewCount":21},"4467f1dc-be01-46a9-831e-a03cef1387e5","2024-01-25T02:47:25.454+00:00",[],{"title":1224},{"VI":1225},"Department of Medical Oncology and Hematology, Princess Margaret Hospital, University Health Network, Toronto, Canada",{"title":1227},{"VI":1228},"Paul E. 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Docetaxel: an update of its use in advanced breast cancer. Drags 2000; 59(3): 621–51\nAventis Pharma SA. Taxotere summary of product characteristics [online]. Available from URL: http:\u002F\u002Fwww.emea.eu.int\u002Fhumandocs\u002FHumans\u002FEPAR\u002FTaxotere\u002FTaxotere.htm [Accessed 2004 Jul 20]\nAventis Pharmaceuticals Inc. Taxotere (docetaxel): US prescribing information [online]. Available from URL: http:\u002F\u002Fwww.fda.gov\u002Fcder\u002Ffoi\u002Flabel\u002F2004\u002F020449s0291bl.pdf [Accessed 2004 Aug 23]\nNabholtz J-M, Tonkin K, Smylie M, et al. Review of docetaxel and doxorubicin-based combinations in the management of breast cancer: from metastatic to adjuvant setting. Semin Oncol 1999 Feb; 26(1 Suppl. 3): 10–6\nPiccart M. The role of taxanes in the adjuvant treatment of early stage breast cancer. Breast Cancer Res Treat 2003; 79Suppl. 1: S25–34\nEarly Breast Cancer Trialists’ Collaborative Group. Polychemotherapy for early breast cancer: an overview of the randomised trials. Lancet 1998; 352: 930–42\nBlum JL, Jones SE, Fay JW, et al. Guidelines for systemic therapy of early stage breast cancer. Breast Cancer Res Treat 1997 May; 43(3): 259–76\nGoldhirsch A, Wood WC, Gelber RD, et al. Meeting highlights: updated international expert consensus on the primary therapy of early breast cancer. J Clin Oncol 2003 Sep 1; 21(17): 3357–65\nFulton B, Spencer CM. Docetaxel: a review of its pharmacodynamic and pharmacokinetic properties and therapeutic efficacy in the management of metastatic breast cancer. Drags 1996; 51(6): 1075–92\nMartin M, Pienkowski T, Mackey J, et al. TAC improves disease free survival and overall survival over FAC in node positive breast cancer patients, BCIRG 001: 55 months follow-up [abstract no. 43]. Breast Cancer Res Treat 2004 May; 85(2): 173–195. Plus oral presentation available at http:\u002F\u002Fwww.bcirg.org\u002FInternet\u002FStudies\u002FBCIRG+001.htm\nMartin M, Pienkowski T, Mackey J, et al. Docetaxel-based regimen (TAC) improves DFS and OS over FAC in node positive early breast cancer patients: efficacy, safety and quality of life at 55 month follow-up [abstract no. 50]. Eur J Cancer 2004; 2(3 Suppl.): 70\nVogel CL, Mackey JR, Martin M, on behalf of the BCIRG 001 Investigators. The role of growth factor support following neutropenic events in early stage breast cancer (BC) patients treated with adjuvant docetaxel, doxorubicin, and cyclophosphamide (TAC): a subanalysis of BCIRG 001 [abstract no. 677]. J Clin Oncol 2004; 22(14 Suppl.): 46s. Plus poster presented at the 40th Annual Meeting of the American Society of Clinical Oncology, 2004 June 5–8; New Orleans\nJones SE, Savin MA, Asmar L, et al. Three year results of a prospective randomized trial of adjuvant chemotherapy for patients (pts) with stage I–III operable, invasive breast cancer comparing 4 courses of doxorabicin\u002Fcyclophosphamide (AC) to 4 courses of docetaxel\u002Fcyclophosphamide (TC) [abstract 59]. Proc Am Soc Clin Oncol 2003; 22: 15. Plus oral presentation given at the 39th Annual Meeting of the American Society of Clinical Oncology, 2003 May 31–June 3; Chicago\nSmith IC, Heys SD, Hutcheon AW, et al. Neoadjuvant chemotherapy in breast cancer: significantly enhanced response with docetaxel. J Clin Oncol 2002 Mar 15; 20: 1456–66\nBear HD, Anderson S, Brown A, et al. The effect on tumor response of adding sequential preoperative docetaxel to preoperative doxorubicin and cyclophosphamide: preliminary results from National Surgical Adjuvant Breast and Bowel Project protocol B-27. J Clin Oncol 2003; 21(22): 4165–74\nJackisch C, von Minckwitz G, Eidtmann H, et al. Dose-dense biweekly doxorubicin\u002Fdocetaxel versus sequential neoadjuvant chemotherapy with doxorubicin\u002Fcyclophosphamide\u002Fdocetaxel in operable breast cancer: second interim analysis. Clin Breast Cancer 2002; 3(4): 276–80\nHutcheon AW, Heys SD, Sarkar TK, et al. Docetaxel primary chemotherapy in breast cancer: a five year update of the Aberdeen trial [abstract no. 11]. 26th Annual San Antonio Breast Cancer Symposium; 2003 Dec 3–6; San Antonio\nvon Minckwitz G, Raab G, Schuette M, et al. Dose-dense versus sequential adriamycin\u002Fdocetaxel combination as preoperative chemotherapy (pCHT) in operable breast cancer (T2-3, NO-2, M0): primary endpoint analysis of the GEPAR-DUO study [abstract no. 168]. Proc Am Soc Clin Oncol 2002; 21 Pt 1: 43a. Plus poster presented at the 38th Annual Meeting of the American Society of Clinical Oncology; 2002 May 18–21; Orlando\nJones SE, Savin M, Holmes FA, et al. Preliminary results of a prospective randomized trial of adjuvant chemotherapy for patients (pts) with stage I–III operable, invasive breast cancer comparing 4 courses of adriamycin\u002Fcyclophosphamide (AC) to 4 courses of Taxotere\u002Fcyclophosphamide (TC) [abstract no. 128]. Proc Am Soc Clin Oncol 2001; 20 Pt 1: 33a\nMartin M, Lluch A, Seguí MA, et al. Prophylactic growth factor (GF) support with adjuvant docetaxel, doxorubicin, and cyclophosphamide (TAC) for node-negative breast cancer (BC): an interim safety analysis of the GEICAM 9805 study [abstract no. 620]. J Clin Oncol 2004; 22(14 Suppl.): 32s. Plus poster presented at the 40th Annual Meeting of the American Society of Clinical Oncology; 2004 June 5–8; New Orleans\nBrain EGC, Bachelot T, Serin D, et al. Phase III trial comparing doxorubicin docetaxel (AT) with doxorubicin cyclophosphamide (AC) in the adjuvant treatment of high-risk node negative (pN0) and limited node positive (pN+≤3) breast cancer (BC) patients (pts): first analysis of toxicity [abstract no. 617]. J Clin Oncol 2004; 22(14 Suppl.): 31s\nGoldstein LJ, O’Neill A, Sparano JA, et al. LVEF assessment of adjuvant doxorubicin\u002Fcyclophosphamide (AC) vs. doxorabicin\u002Fdocetaxel (AT) in early stage breast cancer: cardiac safety results of ECOG 2197 [abstract no. 73]. Proc Am Soc Clin Oncol 2003; 22: 19\nRoche H, Spielmann M, Fumoleau P, et al. Safety analysis of the PACS 01 adjuvant trial comparing 6 cycles of FEC 100 to 3 cycles of FEC 100 followed by 3 cycles of docetaxel (Taxotere®) or node positive breast cancer [abstract no. 144]. 26th Annual San Antonio Breast Cancer Symposium; 2003 Dec 3—6; San Antonio\nAventis Pharmaceuticals Inc. FDA approves Taxotere® for the treatment of women with early stage breast cancer [media release]. 2004 Aug 19\nDe Laurentiis M. Sequential epirubicin-docetaxel-CMF regimen as adjuvant therapy of early breast cancer: preliminary results of the Taxit-216 multicenter phase III trial [abstract no. 115]. Proc Am Soc Clin Oncol 2003; 22: 29\nBreast International Group. B.I.G.-aisbl Newsletter 2004; 6 (2) [online]. Available from URL: http:\u002F\u002Fwww.breastinternationalgroup.org [Accessed 2004 Jul 19]\nBreast Cancer International Research Group. Study: BCIRG 005 (GMA TAX301) [online]. Available from URL: http:\u002F\u002Fwww.bcirg.org [Accessed 2004 Jul 19]\nBreast Cancer International Research Group. BCIRG 006 (GMA TAX302) [online]. Available from URL: http:\u002F\u002Fwww.bcirg.org [Accessed 2004 Jul 19]\nParticipating Institutions of Goim 9902 Trial, Italian Cooperative Group. Epirubicin and cyclophosphamide (EC) vs docetaxel (D) followed by EC in adjuvant (ADJ) treatment of node positive (pN1) breast cancer (BC): a multi-center randomized phase III study [abstract no. 1836]. Proc Am Soc Clin Oncol 2001; 20 Pt 2: 22b\nRack B, Janni W, Harbeck N, et al. Phase III study evaluating the role of docetaxel in the adjuvant therapy of breast cancer patients with extensive lymph node involvement (4 nodes +): ADEBAR study [abstract no. P78]. Breast 2003 Feb; 12Suppl. 1: S37\nPhase III randomized study of adjuvant doxorubicin and cyclophosphamide followed by docetaxel versus doxorubicin and docetaxel versus doxorubicin, docetaxel, and cyclophosphamide in women with breast cancer and positive axillary lymph nodes (NSABP-B-30) [online]. Available from URL: http:\u002F\u002Fwww.cancer.gov [Accessed 2004 Jul 19]\nPhase III randomized study of doxorubicin and cyclophosphamide followed by paclitaxel or docetaxel in women with node-positive or high-risk node-negative stage II or IIIA breast cancer (E-1199) [online]. Available from URL: http:\u002F\u002Fwww.cancer.gov URL [Accessed 2004 Jul 19]\nPhase III study of adjuvant epirubicin with or without docetaxel and concurrent or sequential tamoxifen in postmenopausal women with node-positive breast cancer (ICCG-C\u002F14\u002F96) [online]. Available from URL: http:\u002F\u002Fwww.cancer.gov [Accessed 2004 Jul 19]\nPhase III randomized study of adjuvant docetaxel and epirubicin versus adjuvant cyclophosphamide, epirubicin, and fluorouracil with or without trastuzumab (herceptin) in women with nonmetastatic adenocarcinoma of the breast with lymph node invasion (PACS-004) [online]. Available from URL: http:\u002F\u002Fwww.cancer.gov [Accessed 2004 Jul 19]\nPhase III randomized adjuvant study of fluorouracil, epirubicin, and cyclophosphamide (FEC) or epirubicin followed by cyclophosphamide, methotrexate, and fluorouracil (EPI-CMF versus FEC followed by sequential docetaxel in women with resected stage I or II breast cancer (ICR-TACT) [online]. Available from URL: http:\u002F\u002Fwww.cancer.gov [Accessed 2004 Jul 19]\nScottish Cancer Therapy Network. Recruitment update: Anglo Celtic II — primary medical therapy; Scottish Cancer Therapy Network newsletter No.30 Spring 2001 [online]. Available from URL: http:\u002F\u002Fwww.show.scot.nhs.uk\u002Fisdonline\u002Fcancer\u002Fresearch\u002FSCTN30.pdf [Accessed 2004 Jul 19]\nvon Minckwitz G, Raab G, Blohmer JU, et al. In vivo chemosensitivity-adapted neoadjuvant chemotherapy (docetaxel-doxorubicin-cyclophosphamide followed by vinorelbine-capecitabine salvage therapy) in patients with primary breast cancer: results of the GEPAR-TRIO randomized pilot study [abstract no. 236]. 26th Annual San Antonio Breast Cancer Symposium; 2003 Dec 3–6; San Antonio\nCosta S, von Minckwitz G, Jackisch C, et al. TAC as neoadjuvant chemotherapy in patients with primary breast cancer: interim progress report on 907 cases of the randomized prospective Gepartrio-trial [abstract no. 825]. Proc Am Soc Clin Oncol 2004; 23: 82",{"EN":1257},"▴ Docetaxel is an antimicrotubule agent established as a first- and\u002For second-line intravenous therapy in a variety of cancers, including locally advanced or metastatic breast cancer. It also is approved in the US as adjuvant therapy in early breast cancer, and continues to be investigated in this setting in combination with other agents and in various dosing schedules. ▴ The efficacy of docetaxel-containing adjuvant therapy has been evaluated in two large (n >1000 per trial), randomized clinical trials. One trial compared intravenous docetaxel plus doxorubicin and cyclophosphamide (TAC) every 3 weeks with standard fluorouracil plus doxorubicin and cyclophosphamide (FAC) chemotherapy. Another trial compared intravenous docetaxel plus cyclophosphamide (TC) every 3 weeks with doxorubicin plus cyclophosphamide (AC). ▴ Treatment with TAC improved disease-free survival (75% vs 68%; p = 0.001) and overall survival (87% vs 81%; p = 0.008) at 55 months to a greater extent than FAC. ▴ There were no significant differences in disease-free survival and overall survival between TC and AC. Nevertheless, a nonsignificant trend in disease-free survival favors TC and follow-up data were for a period of only 43 months. ▴ Tolerability in docetaxel-containing adjuvant chemotherapy regimens was manageable. The most frequently reported severe adverse events with TAC were predominantly hematologic, including neutropenia, febrile neutropenia, and neutropenic infection.",{"EN":1259},"Docetaxel",{"VOID":1261},"10.2165\u002F00024669-200403050-00006","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.2165\u002F00024669-200403050-00006",[1264,1276],{"id":1265,"sortIndex":21,"researcher":20,"roles":1266,"affiliations":1267,"properties":1273},"23f1f41c-204a-4181-afde-59a7289f2bb2",[635],[1268],{"id":20,"sortIndex":21,"affiliation":1269,"properties":20},{"id":856,"createTime":857,"updateTime":857,"relativeEntities":1270,"slug":20,"properties":1271,"entityType":84,"verifyStatus":19,"verifyTime":20,"verifyNote":20,"syncStatus":19,"languages":20,"translateLanguages":20,"viewCount":21},[],{"title":1272},{"VI":861},{"title":1274},{"VI":1275},"Susan J. 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Scott",{"url":1262,"publisher":1289,"properties":1304},{"id":6,"createTime":7,"updateTime":8,"relativeEntities":1290,"slug":10,"properties":1291,"entityType":18,"verifyStatus":19,"verifyTime":20,"verifyNote":20,"syncStatus":19,"languages":20,"translateLanguages":20,"viewCount":21,"subjectFields":1295,"manageAffiliations":1296,"indexDatabases":1297,"url":20,"thumbnailPath":20,"statistic":20,"gsStatistic":20,"type":20,"analyzePriority":20},[],{"issn":1292,"title":1293,"url":1294},{"VOID":13},{"EN":15},{"VOID":17},[],[],[1298],{"id":26,"indexDatabase":1299,"url":39,"indexYears":40,"academicFieldIds":20,"indexDatabaseRanking":41},{"id":28,"createTime":29,"updateTime":30,"relativeEntities":1300,"label":1301,"description":1302,"key":36,"publicationTags":1303,"standard":20},[],{"EN":33,"VI":33},{"EN":33,"VI":35},[38],{"volume":1305,"pages":1306},{"VOID":830},{"VOID":1307},"325-332",{"id":1309,"createTime":1310,"updateTime":1311,"relativeEntities":1312,"slug":1313,"properties":1314,"entityType":62,"verifyStatus":63,"verifyTime":1311,"verifyNote":64,"syncStatus":19,"languages":20,"translateLanguages":20,"viewCount":21,"primaryUrl":1323,"fullTextUrl":20,"authors":1324,"publicationType":107,"publisherRelationship":1355,"citationCount":20,"citationInfo":20,"publishDate":898,"publishYear":511,"citationAnalyzeStatus":19,"lastCitationAnalyze":20,"indexDatabases":20,"openAccess":20,"references":20,"isForceReanalyzing":430},"3d707803-1ca0-423c-acbc-fa094066e25c","2023-12-07T00:24:17.290+00:00","2025-02-12T22:31:27.921+00:00",[],"Oral-Chemotherapy-for-the-Older-Patient-with-Cancer",{"references":1315,"abstract":1317,"title":1319,"doi":1321},{"VOID":1316},"Balducci L, Extermann M. 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Curr Oncol Rep 2001; 3: 141–6",{"EN":1318},"Oral chemotherapy presents a number of theoretical advantages in older cancer patients, including convenience of administration and dosage flexibility. Of the oral fluorinated pyrimidines, capecitabine is the most promising, because it minimizes the exposure of normal tissue to the active drug and substantially reduces the risk of mucositis, that is particularly common and severe in the aged. Despite promising initial results, oral etoposide does not offer any special advantage over the intravenous formulation for older patients, while oral temozolomide may have a role in the palliation of malignant melanoma and primary and secondary brain tumors. Of the experimental agents, oral platinum (satraplatin) and oral taxane formulations appear to be the most promising for minimization of the toxicity of the corresponding intravenous drug. Of special interest are tumor-specific agents, including inhibitors of tyrosine phosphokinase (e.g. imatinib mesylate) and angiogenesis. In conclusion, oral chemotherapy of cancer appears to be a very promising option for older patients.",{"EN":1320},"Oral Chemotherapy for the Older Patient with Cancer",{"VOID":1322},"10.2165\u002F00024669-200201020-00003","http:\u002F\u002Flink.springer.com\u002F10.2165\u002F00024669-200201020-00003",[1325,1340],{"id":1326,"sortIndex":21,"researcher":20,"roles":1327,"affiliations":1328,"properties":1337},"29205267-dd72-4e3e-9033-4803b8b0cb5a",[635],[1329],{"id":20,"sortIndex":21,"affiliation":1330,"properties":20},{"id":1331,"createTime":1332,"updateTime":1332,"relativeEntities":1333,"slug":20,"properties":1334,"entityType":84,"verifyStatus":19,"verifyTime":20,"verifyNote":20,"syncStatus":19,"languages":20,"translateLanguages":20,"viewCount":21},"b48f2c82-ea16-41c8-b865-aa7dcad9ba2e","2023-12-07T00:24:17.301+00:00",[],{"title":1335},{"VI":1336},"Department of Oncology, University of Palermo School of Medicine, Palermo, Italy",{"title":1338},{"VI":1339},"Ignazio Carreca",{"id":1341,"sortIndex":71,"researcher":20,"roles":1342,"affiliations":1343,"properties":1352},"ad92cc3f-37dc-4826-aaa1-3ced3af51385",[635],[1344],{"id":20,"sortIndex":21,"affiliation":1345,"properties":20},{"id":1346,"createTime":1347,"updateTime":1347,"relativeEntities":1348,"slug":20,"properties":1349,"entityType":84,"verifyStatus":19,"verifyTime":20,"verifyNote":20,"syncStatus":19,"languages":20,"translateLanguages":20,"viewCount":21},"924e7f5a-16bd-45af-8c30-eb1663101051","2023-12-07T00:24:17.309+00:00",[],{"title":1350},{"VI":1351},"Senior Adult Oncology Program, University of South Florida College of Medicine, H. Lee Moffitt Cancer Center & Research Institute, Tampa, USA",{"title":1353},{"VI":1354},"Lodovico Balducci",{"url":1323,"publisher":1356,"properties":1371},{"id":6,"createTime":7,"updateTime":8,"relativeEntities":1357,"slug":10,"properties":1358,"entityType":18,"verifyStatus":19,"verifyTime":20,"verifyNote":20,"syncStatus":19,"languages":20,"translateLanguages":20,"viewCount":21,"subjectFields":1362,"manageAffiliations":1363,"indexDatabases":1364,"url":20,"thumbnailPath":20,"statistic":20,"gsStatistic":20,"type":20,"analyzePriority":20},[],{"issn":1359,"title":1360,"url":1361},{"VOID":13},{"EN":15},{"VOID":17},[],[],[1365],{"id":26,"indexDatabase":1366,"url":39,"indexYears":40,"academicFieldIds":20,"indexDatabaseRanking":41},{"id":28,"createTime":29,"updateTime":30,"relativeEntities":1367,"label":1368,"description":1369,"key":36,"publicationTags":1370,"standard":20},[],{"EN":33,"VI":33},{"EN":33,"VI":35},[38],{"volume":1372,"pages":1374},{"VOID":1373},"1",{"VOID":1375},"101-108"]