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Recent evidence has demonstrated that human papillomavirus (HPV) is involved in up to 25% of HNCs; particularly in the oropharyngeal carcinoma (OPC) subtype where it can account for up to 60% of such cases. HPVs are double-stranded DNA viruses that infect epithelial cells; numerous HPV subtypes, including 16, 18, 31, 33, and 35, drive epithelial cell transformation and tumourigenesis. HPV positive (HPV+) HNC represents a distinct molecular and clinical entity from HPV negative (HPV−) disease; the biological basis for which remains to be fully elucidated. HPV positivity is strongly correlated with a significantly superior outcome; indicating that such tumours should have a distinct management approach. This review focuses on the recent scientific and clinical investigation of HPV+ HNC. 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Oncol., 31, 543, 10.1200\u002FJCO.2012.44.0164",{"doi":324},"10.1200\u002FJCO.2012.44.0164",{"id":21,"text":326,"url":21,"identifiers":327},"NIAID Papillomavirus Episteme Kowledge Source: HPV16, Available online: http:\u002F\u002Fpave.niaid.nih.gov\u002F.",{},{"id":21,"text":329,"url":21,"identifiers":330},"Suzich, 1995, Systemic immunization with papillomavirus L1 protein completely prevents the development of viral mucosal papillomas, Proc. Natl. Acad. Sci. USA, 92, 11553, 10.1073\u002Fpnas.92.25.11553",{"doi":331},"10.1073\u002Fpnas.92.25.11553",{"id":21,"text":333,"url":21,"identifiers":334},"Bratman, 2016, Human papillomavirus genotype association with survival in head and neck squamous cell carcinoma, JAMA Oncol., 2, 823, 10.1001\u002Fjamaoncol.2015.6587",{"doi":335},"10.1001\u002Fjamaoncol.2015.6587",{"id":21,"text":337,"url":21,"identifiers":338},"Ndiaye, 2014, HPV DNA, E6\u002FE7 mRNA, and p16INK4a detection in head and neck cancers: A systematic review and meta-analysis, Lancet. Oncol., 15, 1319, 10.1016\u002FS1470-2045(14)70471-1",{"doi":339},"10.1016\u002FS1470-2045(14)70471-1",{"id":21,"text":341,"url":21,"identifiers":342},"Anderson, 2016, HPV prevalence and type-distribution in cervical cancer and premalignant lesions of the cervix: A population-based study from Northern Ireland, J. Med. Virol., 88, 1262, 10.1002\u002Fjmv.24447",{"doi":343},"10.1002\u002Fjmv.24447",{"id":21,"text":345,"url":21,"identifiers":346},"Goodman, 2015, Human papillomavirus genotype and oropharynx cancer survival in the United States of America, Eur. J. Cancer, 51, 2759, 10.1016\u002Fj.ejca.2015.09.005",{"doi":347},"10.1016\u002Fj.ejca.2015.09.005",{"id":21,"text":349,"url":21,"identifiers":350},"Hebner, 2006, Human papillomaviruses: Basic mechanisms of pathogenesis and oncogenicity, Rev. Med. Virol., 16, 83, 10.1002\u002Frmv.488",{"doi":351},"10.1002\u002Frmv.488",{"id":21,"text":353,"url":21,"identifiers":354},"Moody, 2010, Human papillomavirus oncoproteins: Pathways to transformation, Nat. Rev. Cancer, 10, 550, 10.1038\u002Fnrc2886",{"doi":355},"10.1038\u002Fnrc2886",{"id":21,"text":357,"url":21,"identifiers":358},"Duensing, 2000, The human papillomavirus type 16 E6 and E7 oncoproteins cooperate to induce mitotic defects and genomic instability by uncoupling centrosome duplication from the cell division cycle, Proc. Natl. Acad. Sci. USA, 97, 10002, 10.1073\u002Fpnas.170093297",{"doi":359},"10.1073\u002Fpnas.170093297",{"id":21,"text":361,"url":21,"identifiers":362},"DiMaio, 2001, Mechanisms of cell transformation by papillomavirus E5 proteins, Oncogene, 20, 7866, 10.1038\u002Fsj.onc.1204915",{"doi":363},"10.1038\u002Fsj.onc.1204915",{"id":21,"text":365,"url":21,"identifiers":366},"Scheffner, 1990, The E6 oncoprotein encoded by human papillomavirus types 16 and 18 promotes the degradation of p53, Cell, 63, 1129, 10.1016\u002F0092-8674(90)90409-8",{"doi":367},"10.1016\u002F0092-8674(90)90409-8",{"id":21,"text":369,"url":21,"identifiers":370},"Munger, 1989, Complex formation of human papillomavirus E7 proteins with the retinoblastoma tumor suppressor gene product, EMBO J., 8, 4099, 10.1002\u002Fj.1460-2075.1989.tb08594.x",{"doi":371},"10.1002\u002Fj.1460-2075.1989.tb08594.x",{"id":21,"text":373,"url":21,"identifiers":374},"Song, 2000, Human papillomavirus types 16 E6 and E7 contribute differently to carcinogenesis, Virology, 267, 141, 10.1006\u002Fviro.1999.0106",{"doi":375},"10.1006\u002Fviro.1999.0106",{"id":21,"text":377,"url":21,"identifiers":378},"DiMaio, 2013, The E5 proteins, Virology, 445, 99, 10.1016\u002Fj.virol.2013.05.006",{"doi":379},"10.1016\u002Fj.virol.2013.05.006",{"id":21,"text":381,"url":21,"identifiers":382},"Goon, P.K., Stanley, M.A., Ebmeyer, J., Steinstrasser, L., Upile, T., Jerjes, W., Bernal-Sprekelsen, M., Gorner, M., and Sudhoff, H.H. 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E 1308: A phase II trial of induction chemotherapy (IC) followed by cetuximab with low dose versus standard dose IMRT in patients with human papilloma virus (HPV)-associated resectable squamous cell carcinoma of the oropharynx (OPSCC). J. Clin. Oncol., 31, abstr 6005.",{"doi":577},"10.1200\u002Fjco.2013.31.15_suppl.6005",false,{"id":580,"createTime":581,"updateTime":581,"relativeEntities":582,"slug":583,"properties":584,"entityType":129,"verifyStatus":130,"verifyTime":581,"verifyNote":131,"syncStatus":20,"languages":600,"translateLanguages":21,"viewCount":22,"primaryUrl":601,"fullTextUrl":21,"authors":602,"publicationType":239,"publisherRelationship":641,"citationCount":673,"citationInfo":674,"publishDate":21,"publishYear":21,"citationAnalyzeStatus":20,"lastCitationAnalyze":21,"indexDatabases":21,"openAccess":21,"references":678,"isForceReanalyzing":578},"9f0b5bab-8224-40fb-98d9-aa15d99045fb","2024-09-05T23:56:28.154+00:00",[],"The-Role-of-Extracellular-HSP70-in-the-Function-of-Tumor-Associated-Immune-Cells",{"mag":585,"keywords":587,"pmc":588,"openalex":590,"abstract":592,"title":594,"pm":596,"doi":598},{"VOID":586},"3199710068",{},{"VOID":589},"8466959",{"VOID":591},"W3199710068",{"EN":593},"\u003Cjats:p>Extracellular vesicles released by tumor cells (T-EVs) are known to contain danger-associated molecular patterns (DAMPs), which are released in response to cellular stress to alert the immune system to the dangerous cell. Part of this defense mechanism is the heat shock protein 70 (HSP70), and HSP70-positive T-EVs are known to trigger anti-tumor immune responses. Moreover, extracellular HSP70 acts as an immunogen that contributes to the cross-presentation of major histocompatibility complex (MHC) class I molecules. However, the release of DAMPs, including HSP70, may also induce chronic inflammation or suppress immune cell activity, promoting tumor growth. Here, we summarize the current knowledge on soluble, membrane-bound, and EV-associated HSP70 regarding their functions in regulating tumor-associated immune cells in the tumor microenvironment. The molecular mechanisms involved in the translocation of HSP70 to the plasma membrane of tumor cells and its release via exosomes or soluble proteins are summarized. Furthermore, perspectives for immunotherapies aimed to target HSP70 and its receptors for cancer treatment are discussed and presented.\u003C\u002Fjats:p>",{"EN":595},"The Role of Extracellular HSP70 in the Function of Tumor-Associated Immune Cells",{"VOID":597},"34572948",{"VOID":599},"10.3390\u002Fcancers13184721",[133],"https:\u002F\u002Fwww.mdpi.com\u002F2072-6694\u002F13\u002F18\u002F4721",[603,624],{"id":604,"sortIndex":22,"researcher":21,"roles":605,"affiliations":606,"properties":617},"8ce6b8dd-7a3b-45fa-a110-f25a42f43dc7",[],[607],{"id":608,"sortIndex":22,"affiliation":609,"properties":21},"aa612110-69cc-4273-bfd4-cdef3df49c24",{"id":610,"createTime":611,"updateTime":611,"relativeEntities":612,"slug":613,"properties":614,"entityType":50,"verifyStatus":20,"verifyTime":21,"verifyNote":21,"syncStatus":20,"languages":21,"translateLanguages":21,"viewCount":22},"f7b67060-acf9-4950-a778-d41db8d52986","2024-09-05T23:56:28.183+00:00",[],"Institute-for-Tumor-Immunology-Clinic-for-Hematology-Immunology-and-Oncology-Philipps-University-of-Marburg-Hans-Meerwein-Strasse-3-35043-Marburg-Germany",{"title":615},{"EN":616},"Institute for Tumor Immunology, Clinic for Hematology, Immunology, and Oncology, Philipps University of Marburg, Hans-Meerwein-Strasse 3, 35043 Marburg, Germany",{"openalex":618,"orcid":620,"title":622},{"VOID":619},"A5076554970",{"VOID":621},"https:\u002F\u002Forcid.org\u002F0000-0003-4614-7000",{"EN":623},"Manuel Linder",{"id":625,"sortIndex":138,"researcher":21,"roles":626,"affiliations":627,"properties":634},"edbc08f6-d4f3-4f0a-908e-69cb6d45df14",[],[628],{"id":629,"sortIndex":22,"affiliation":630,"properties":21},"9c47c058-58fe-419e-bdb8-7ecdbe814b18",{"id":610,"createTime":611,"updateTime":611,"relativeEntities":631,"slug":613,"properties":632,"entityType":50,"verifyStatus":20,"verifyTime":21,"verifyNote":21,"syncStatus":20,"languages":21,"translateLanguages":21,"viewCount":22},[],{"title":633},{"EN":616},{"openalex":635,"orcid":637,"title":639},{"VOID":636},"A5052001856",{"VOID":638},"https:\u002F\u002Forcid.org\u002F0000-0003-4785-9165",{"EN":640},"Elke Pogge von Strandmann",{"url":21,"publisher":642,"properties":666},{"id":6,"createTime":7,"updateTime":8,"relativeEntities":643,"slug":10,"properties":644,"entityType":19,"verifyStatus":20,"verifyTime":21,"verifyNote":21,"syncStatus":20,"languages":21,"translateLanguages":21,"viewCount":22,"subjectFields":649,"manageAffiliations":650,"indexDatabases":651,"url":103,"thumbnailPath":21,"statistic":21,"gsStatistic":21,"type":21,"analyzePriority":21},[],{"country":645,"issn":646,"introduce":647,"title":648},{"VOID":13},{"VOID":15},{"EN":17},{"EN":10},[],[],[652,659],{"id":65,"indexDatabase":653,"url":80,"indexYears":21,"academicFieldIds":658,"indexDatabaseRanking":21},{"id":67,"createTime":68,"updateTime":69,"relativeEntities":654,"label":655,"description":656,"key":76,"publicationTags":657,"standard":21},[],{"EN":72,"VI":72},{"VI":74,"EN":75},[78,79],[82],{"id":84,"indexDatabase":660,"url":97,"indexYears":98,"academicFieldIds":665,"indexDatabaseRanking":102},{"id":86,"createTime":87,"updateTime":88,"relativeEntities":661,"label":662,"description":663,"key":94,"publicationTags":664,"standard":21},[],{"EN":91,"VI":91},{"EN":91,"VI":93},[96],[100,101],{"volume":667,"pages":669,"issue":671},{"VOID":668},"13",{"VOID":670},"4721",{"VOID":672},"18",34,{"total":673,"publishYear":21,"statisticByYear":675},{"2022":276,"2023":676,"2024":677},20,5,[679,683,687,691,695,699,703,707,711,715,719,723,727,731,735,739,743,747,751,755,759,763,767,771,775,779,782,786,790,794,798,802,806,810,814,818,822,826,830,834,838,842,846,850,854,858,862,866,869,873,877,881,885,889,893,897,900,904,908,912,916,920,924,928,932,936,940,944,948,952,956,960,964,968,972,976,980,984,988,992,996,1000,1004,1008,1012,1016,1020,1023,1027,1031,1035,1039,1043,1047,1051,1055,1058,1061,1065,1069,1073,1077,1081,1085,1088,1092,1096,1100,1104,1108,1112,1116,1120,1124,1128,1132,1136,1140,1144,1148,1152,1156,1160,1164,1168,1172,1176,1180,1184,1188,1192,1196,1200,1204,1208,1211,1215,1219,1223,1227,1231,1235,1239,1243,1247,1251,1255,1258,1262],{"id":21,"text":680,"url":21,"identifiers":681},"Rosenzweig, 2019, The Hsp70 Chaperone Network, Nat. 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Cancer Res., 15, 361, 10.1158\u002F1078-0432.CCR-08-1725",{"doi":1265},"10.1158\u002F1078-0432.CCR-08-1725",{"id":1267,"createTime":1268,"updateTime":1268,"relativeEntities":1269,"slug":1270,"properties":1271,"entityType":129,"verifyStatus":130,"verifyTime":1287,"verifyNote":131,"syncStatus":20,"languages":1288,"translateLanguages":21,"viewCount":22,"primaryUrl":1289,"fullTextUrl":21,"authors":1290,"publicationType":239,"publisherRelationship":1380,"citationCount":1412,"citationInfo":1413,"publishDate":21,"publishYear":21,"citationAnalyzeStatus":20,"lastCitationAnalyze":21,"indexDatabases":21,"openAccess":21,"references":1417,"isForceReanalyzing":578},"8160d1ac-d254-4e05-afe8-04ccc8453b9b","2024-10-09T23:56:03.699+00:00",[],"Glucose-Metabolism-and-Oxidative-Stress-in-Hepatocellular-Carcinoma-Role-and-Possible-Implications-in-Novel-Therapeutic-Strategies",{"mag":1272,"keywords":1274,"pmc":1275,"openalex":1277,"abstract":1279,"title":1281,"pm":1283,"doi":1285},{"VOID":1273},"3036796178",{},{"VOID":1276},"7352479",{"VOID":1278},"W3036796178",{"EN":1280},"\u003Cjats:p>Hepatocellular carcinoma (HCC) metabolism is redirected to glycolysis to enhance the production of metabolic compounds employed by cancer cells to produce proteins, lipids, and nucleotides in order to maintain a high proliferative rate. This mechanism drives towards uncontrolled growth and causes a further increase in reactive oxygen species (ROS), which could lead to cell death. HCC overcomes the problem generated by ROS increase by increasing the antioxidant machinery, in which key mechanisms involve glutathione, nuclear factor erythroid 2-related factor 2 (Nrf2), and hypoxia-inducible transcription factor (HIF-1α). These mechanisms could represent optimal targets for innovative therapies. The tumor microenvironment (TME) exerts a key role in HCC pathogenesis and progression. Various metabolic machineries modulate the activity of immune cells in the TME. The deregulated metabolic activity of tumor cells could impair antitumor response. Lactic acid–lactate, derived from the anaerobic glycolytic rate of tumor cells, as well as adenosine, derived from the catabolism of ATP, have an immunosuppressive activity. Metabolic reprogramming of the TME via targeted therapies could enhance the treatment efficacy of anti-cancer immunotherapy. This review describes the metabolic pathways mainly involved in the HCC pathogenesis and progression. 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Oncol., 9.",{"doi":2309},"10.3389\u002Ffonc.2019.01143",{"id":2311,"createTime":2312,"updateTime":2312,"relativeEntities":2313,"slug":2314,"properties":2315,"entityType":129,"verifyStatus":130,"verifyTime":2312,"verifyNote":131,"syncStatus":20,"languages":2331,"translateLanguages":21,"viewCount":22,"primaryUrl":2332,"fullTextUrl":21,"authors":2333,"publicationType":239,"publisherRelationship":2389,"citationCount":2421,"citationInfo":2422,"publishDate":21,"publishYear":21,"citationAnalyzeStatus":20,"lastCitationAnalyze":21,"indexDatabases":21,"openAccess":21,"references":2427,"isForceReanalyzing":578},"a9ada030-5dfa-4528-bfbf-cc7205ea9e97","2024-10-09T23:49:55.456+00:00",[],"Mucins-and-Pancreatic-Cancer",{"mag":2316,"keywords":2318,"pmc":2319,"openalex":2321,"abstract":2323,"title":2325,"pm":2327,"doi":2329},{"VOID":2317},"2160178444",{},{"VOID":2320},"3840449",{"VOID":2322},"W2160178444",{"EN":2324},"\u003Cjats:p>Pancreatic cancer is characterized by an often dramatic outcome (five year survival < 5%) related to a late diagnosis and a lack of efficient therapy. Therefore, clinicians desperately need new biomarkers and new therapeutic tools to develop new efficient therapies. Mucins belong to an ever increasing family of O-glycoproteins. Secreted mucins are the main component of mucus protecting the epithelia whereas membrane-bound mucins are thought to play important biological roles in cell-cell and cell-matrix interactions, in cell signaling and in modulating biological properties of cancer cells. In this review, we will focus on the altered expression pattern of mucins in pancreatic cancer, from the early neoplastic lesion Pancreatic Intraepithelial Neoplasia (PanIN) to invasive pancreatic carcinomas, and the molecular mechanisms (including genetic and epigenetic regulation) and signaling pathways known to control their expression. Moreover, we will discuss the recent advances about the biology of both secreted and membrane-bound mucins and their key roles in pancreatic carcinogenesis and resistance to therapy. Finally, we will discuss exciting opportunities that mucins offer as potential therapeutic targets in pancreatic cancer.\u003C\u002Fjats:p>",{"EN":2326},"Mucins and Pancreatic Cancer",{"VOID":2328},"24281201",{"VOID":2330},"10.3390\u002Fcancers2041794",[133],"https:\u002F\u002Fwww.mdpi.com\u002F2072-6694\u002F2\u002F4\u002F1794",[2334,2355,2372],{"id":2335,"sortIndex":138,"researcher":21,"roles":2336,"affiliations":2337,"properties":2348},"cdd30bf6-fd11-444f-bff9-70c5a3cc0719",[],[2338],{"id":2339,"sortIndex":22,"affiliation":2340,"properties":21},"b08c36ab-8c35-49e0-8592-3ce054e42a78",{"id":2341,"createTime":2342,"updateTime":2342,"relativeEntities":2343,"slug":2344,"properties":2345,"entityType":50,"verifyStatus":20,"verifyTime":21,"verifyNote":21,"syncStatus":20,"languages":21,"translateLanguages":21,"viewCount":22},"7dfb91b7-5ff3-4e05-a190-5020492eea51","2024-10-09T23:49:55.472+00:00",[],"INSERM-U837-Jean-Pierre-Aubert-Research-Center-Team-5-Mucins-epithelial-differentiation-and-carcinogenesis-Lille-France",{"title":2346},{"EN":2347},"INSERM, U837, Jean-Pierre Aubert Research Center, Team 5 \"Mucins, epithelial differentiation and carcinogenesis\", Lille, France",{"openalex":2349,"orcid":2351,"title":2353},{"VOID":2350},"A5082334504",{"VOID":2352},"https:\u002F\u002Forcid.org\u002F0000-0002-9648-8033",{"EN":2354},"Nicolas Skrypek",{"id":2356,"sortIndex":22,"researcher":21,"roles":2357,"affiliations":2358,"properties":2365},"0d750126-245a-43a3-ad64-ee876ef33d2f",[],[2359],{"id":2360,"sortIndex":22,"affiliation":2361,"properties":21},"b251c5d9-4362-4fd2-90d4-e546f4a32542",{"id":2341,"createTime":2342,"updateTime":2342,"relativeEntities":2362,"slug":2344,"properties":2363,"entityType":50,"verifyStatus":20,"verifyTime":21,"verifyNote":21,"syncStatus":20,"languages":21,"translateLanguages":21,"viewCount":22},[],{"title":2364},{"EN":2347},{"openalex":2366,"orcid":2368,"title":2370},{"VOID":2367},"A5028455629",{"VOID":2369},"https:\u002F\u002Forcid.org\u002F0000-0002-0496-0661",{"EN":2371},"Nicolas Jonckheere",{"id":2373,"sortIndex":61,"researcher":21,"roles":2374,"affiliations":2375,"properties":2382},"7f9415cf-125f-4575-966f-9b8b343cfb3c",[],[2376],{"id":2377,"sortIndex":22,"affiliation":2378,"properties":21},"d10a48ca-2629-46b7-b118-3000064af578",{"id":2341,"createTime":2342,"updateTime":2342,"relativeEntities":2379,"slug":2344,"properties":2380,"entityType":50,"verifyStatus":20,"verifyTime":21,"verifyNote":21,"syncStatus":20,"languages":21,"translateLanguages":21,"viewCount":22},[],{"title":2381},{"EN":2347},{"openalex":2383,"orcid":2385,"title":2387},{"VOID":2384},"A5010941913",{"VOID":2386},"https:\u002F\u002Forcid.org\u002F0000-0002-3131-2694",{"EN":2388},"Isabelle Van Seuningen",{"url":21,"publisher":2390,"properties":2414},{"id":6,"createTime":7,"updateTime":8,"relativeEntities":2391,"slug":10,"properties":2392,"entityType":19,"verifyStatus":20,"verifyTime":21,"verifyNote":21,"syncStatus":20,"languages":21,"translateLanguages":21,"viewCount":22,"subjectFields":2397,"manageAffiliations":2398,"indexDatabases":2399,"url":103,"thumbnailPath":21,"statistic":21,"gsStatistic":21,"type":21,"analyzePriority":21},[],{"country":2393,"issn":2394,"introduce":2395,"title":2396},{"VOID":13},{"VOID":15},{"EN":17},{"EN":10},[],[],[2400,2407],{"id":65,"indexDatabase":2401,"url":80,"indexYears":21,"academicFieldIds":2406,"indexDatabaseRanking":21},{"id":67,"createTime":68,"updateTime":69,"relativeEntities":2402,"label":2403,"description":2404,"key":76,"publicationTags":2405,"standard":21},[],{"EN":72,"VI":72},{"VI":74,"EN":75},[78,79],[82],{"id":84,"indexDatabase":2408,"url":97,"indexYears":98,"academicFieldIds":2413,"indexDatabaseRanking":102},{"id":86,"createTime":87,"updateTime":88,"relativeEntities":2409,"label":2410,"description":2411,"key":94,"publicationTags":2412,"standard":21},[],{"EN":91,"VI":91},{"EN":91,"VI":93},[96],[100,101],{"volume":2415,"pages":2417,"issue":2419},{"VOID":2416},"2",{"VOID":2418},"1794-1812",{"VOID":2420},"4",83,{"total":2421,"publishYear":21,"statisticByYear":2423},{"2012":51,"2013":677,"2014":2424,"2015":2424,"2016":276,"2017":2424,"2018":274,"2019":274,"2020":274,"2021":2425,"2022":2426,"2023":2424,"2024":61},6,10,8,[2428,2432,2436,2440,2443,2447,2451,2455,2459,2462,2466,2468,2472,2476,2480,2484,2488,2492,2496,2500,2504,2508,2512,2516,2520,2524,2528,2532,2536,2540,2544,2548,2552,2556,2558,2562,2566,2569,2573,2577,2581,2585,2589,2593,2597,2601,2605,2609,2613,2617,2620,2624,2628,2632,2636,2640,2643,2647,2651,2655,2659,2663,2667,2670,2673,2675,2679,2683,2687,2691,2695,2698,2702,2706,2710,2714,2717,2721,2725,2729,2733,2737,2741,2745,2749,2753,2756,2759,2763,2767,2771,2775,2779,2783,2787,2791,2795,2799,2803,2807],{"id":21,"text":2429,"url":21,"identifiers":2430},"Bardeesy, 2002, Pancreatic cancer biology and genetics, Nat. 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Chem., 266, 15420, 10.1016\u002FS0021-9258(18)98632-1",{"doi":2786},"10.1016\u002FS0021-9258(18)98632-1",{"id":21,"text":2788,"url":21,"identifiers":2789},"Aguirre, 2003, Activated Kras and Ink4a\u002FArf deficiency cooperate to produce metastatic pancreatic ductal adenocarcinoma, Genes Dev., 17, 3112, 10.1101\u002Fgad.1158703",{"doi":2790},"10.1101\u002Fgad.1158703",{"id":21,"text":2792,"url":21,"identifiers":2793},"Hingorani, 2003, Preinvasive and invasive ductal pancreatic cancer and its early detection in the mouse, Cancer Cell, 4, 437, 10.1016\u002FS1535-6108(03)00309-X",{"doi":2794},"10.1016\u002FS1535-6108(03)00309-X",{"id":21,"text":2796,"url":21,"identifiers":2797},"Hingorani, 2005, Trp53R172H and KrasG12D cooperate to promote chromosomal instability and widely metastatic pancreatic ductal adenocarcinoma in mice, Cancer Cell, 7, 469, 10.1016\u002Fj.ccr.2005.04.023",{"doi":2798},"10.1016\u002Fj.ccr.2005.04.023",{"id":21,"text":2800,"url":21,"identifiers":2801},"Izeradjene, 2007, Kras(G12D) and Smad4\u002FDpc4 haploinsufficiency cooperate to induce mucinous cystic neoplasms and invasive adenocarcinoma of the pancreas, Cancer Cell, 11, 229, 10.1016\u002Fj.ccr.2007.01.017",{"doi":2802},"10.1016\u002Fj.ccr.2007.01.017",{"id":21,"text":2804,"url":21,"identifiers":2805},"Velcich, 2002, Colorectal cancer in mice genetically deficient in the mucin Muc2, Science, 295, 1726, 10.1126\u002Fscience.1069094",{"doi":2806},"10.1126\u002Fscience.1069094",{"id":21,"text":2808,"url":21,"identifiers":2809},"Cheon, 2009, CA125\u002FMUC16 is dispensable for mouse development and reproduction, PLoS One, 4, e4675, 10.1371\u002Fjournal.pone.0004675",{"doi":2810},"10.1371\u002Fjournal.pone.0004675",{"id":2812,"createTime":2813,"updateTime":2813,"relativeEntities":2814,"slug":2815,"properties":2816,"entityType":129,"verifyStatus":130,"verifyTime":2813,"verifyNote":131,"syncStatus":20,"languages":2832,"translateLanguages":21,"viewCount":22,"primaryUrl":2833,"fullTextUrl":21,"authors":2834,"publicationType":239,"publisherRelationship":2968,"citationCount":2999,"citationInfo":3000,"publishDate":21,"publishYear":21,"citationAnalyzeStatus":20,"lastCitationAnalyze":21,"indexDatabases":21,"openAccess":21,"references":3002,"isForceReanalyzing":578},"560d7e99-411a-493b-84ab-f548da1e3261","2024-09-18T23:35:48.439+00:00",[],"Atypical-Histiocytoid-Cells-and-Multinucleated-Giant-Cells-in-Fine-Needle-Aspiration-Cytology-of-the-Thyroid-Predict-Lymph-Node-Metastasis-of-Papillary-Thyroid-Carcinoma",{"mag":2817,"keywords":2819,"pmc":2820,"openalex":2822,"abstract":2824,"title":2826,"pm":2828,"doi":2830},{"VOID":2818},"2951499934",{},{"VOID":2821},"6627749",{"VOID":2823},"W2951499934",{"EN":2825},"\u003Cjats:p>Preoperative detection of cervical lymph node metastasis in papillary thyroid carcinoma (PTC) is crucial for determining the surgical strategy to prevent locoregional recurrence of the disease. We identified the cytological predictors of lymph node metastasis in 222 consecutive patients with PTC using fine-needle aspiration cytology (FNAC) of the thyroid. Cervical lymph node metastases occurred in 99 (44.6%) of 222 PTC patients. Lymph node metastasis was significantly associated with tumor multifocality (p = 0.003), and high cellularity (p = 0.021), atypical histiocytoid cells (p < 0.001), and multinucleated giant cells (p < 0.001) in thyroid FNAC. The BRAF V600E mutation was marginally associated with lymph node metastasis (p = 0.054). Multivariate analysis revealed that atypical histiocytoid cells (odds ratio = 2.717; p = 0.001) and multinucleated giant cells (odds ratio = 3.070; p = 0.031) were independent predictors of lymph node metastasis in patients with PTC. In a subgroup analysis of 164 patients with microcarcinomas, atypical histiocytoid cells (odds ratio = 2.761; p = 0.005) was an independent predictor of lymph node metastasis. Cytological detection of atypical histiocytoid cells and multinucleated giant cells on thyroid FNAC can be used to preoperatively predict cervical lymph node metastasis in patients with PTC.\u003C\u002Fjats:p>",{"EN":2827},"Atypical Histiocytoid Cells and Multinucleated Giant Cells in Fine-Needle Aspiration Cytology of the Thyroid Predict Lymph Node Metastasis of Papillary Thyroid 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of Endocrinology and Metabolism, Department of Internal Medicine, College of Medicine, The Catholic University of Korea, Seoul 06591, Korea",{"openalex":2908,"orcid":2910,"title":2912},{"VOID":2909},"A5049204705",{"VOID":2911},"https:\u002F\u002Forcid.org\u002F0000-0003-0995-6482",{"EN":2913},"Dong‐Jun 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of Pathology, Design Hospital, Jeonju-si, Jeollabuk-do 54910, Korea",{"openalex":2935,"orcid":2937,"title":2939},{"VOID":2936},"A5006122589",{"VOID":2938},"https:\u002F\u002Forcid.org\u002F0000-0001-9132-2029",{"EN":2940},"Ji Eun Choi",{"id":2942,"sortIndex":138,"researcher":21,"roles":2943,"affiliations":2944,"properties":2961},"12b33582-eddf-46b9-a588-18635d5971de",[],[2945,2955],{"id":2946,"sortIndex":138,"affiliation":2947,"properties":21},"6f7b24e6-64b5-486a-a437-03068125f356",{"id":2948,"createTime":2949,"updateTime":2949,"relativeEntities":2950,"slug":2951,"properties":2952,"entityType":50,"verifyStatus":20,"verifyTime":21,"verifyNote":21,"syncStatus":20,"languages":21,"translateLanguages":21,"viewCount":22},"48a83fdc-9bba-4464-8a47-92257e17b1f9","2024-09-18T23:35:48.486+00:00",[],"Department-of-Surgery-College-of-Medicine-The-Catholic-University-of-Korea-Seoul-06591-Korea",{"title":2953},{"EN":2954},"Department of Surgery, College of Medicine, The Catholic University of Korea, Seoul 06591, Korea",{"id":2956,"sortIndex":22,"affiliation":2957,"properties":21},"38130cdd-a558-4a4d-b4dd-a7a7e942c5bf",{"id":2842,"createTime":2843,"updateTime":2843,"relativeEntities":2958,"slug":2845,"properties":2959,"entityType":50,"verifyStatus":20,"verifyTime":21,"verifyNote":21,"syncStatus":20,"languages":21,"translateLanguages":21,"viewCount":22},[],{"title":2960},{"EN":2848},{"openalex":2962,"orcid":2964,"title":2966},{"VOID":2963},"A5017460777",{"VOID":2965},"https:\u002F\u002Forcid.org\u002F0000-0002-6271-2105",{"EN":2967},"Ja Seong 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2016, 2015 American Thyroid Association Management Guidelines for Adult Patients with Thyroid Nodules and Differentiated Thyroid Cancer: The American Thyroid Association Guidelines Task Force on Thyroid Nodules and Differentiated Thyroid Cancer, Thyroid, 26, 1, 10.1089\u002Fthy.2015.0020",{"doi":3006},"10.1089\u002Fthy.2015.0020",{"id":21,"text":3008,"url":21,"identifiers":3009},"Liu, 2015, Postoperative recurrence of papillary thyroid carcinoma with lymph node metastasis, J. Surg. Oncol., 112, 149, 10.1002\u002Fjso.23967",{"doi":3010},"10.1002\u002Fjso.23967",{"id":21,"text":3012,"url":21,"identifiers":3013},"Mazzaferri, 2001, Clinical review 128: Current approaches to primary therapy for papillary and follicular thyroid cancer, J. Clin. Endocrinol. Metab., 86, 1447, 10.1210\u002Fjcem.86.4.7407",{"doi":3014},"10.1210\u002Fjcem.86.4.7407",{"id":21,"text":3016,"url":21,"identifiers":3017},"Pyo, 2018, Prognostic Role of Metastatic Lymph Node Ratio in Papillary Thyroid Carcinoma, J. Pathol. Trans. Med., 52, 331, 10.4132\u002Fjptm.2018.08.07",{"doi":3018},"10.4132\u002Fjptm.2018.08.07",{"id":21,"text":3020,"url":21,"identifiers":3021},"Das, 2009, Psammoma body: A product of dystrophic calcification or of a biologically active process that aims at limiting the growth and spread of tumor?, Diagn. Cytopathol., 37, 534, 10.1002\u002Fdc.21081",{"doi":3022},"10.1002\u002Fdc.21081",{"id":21,"text":3024,"url":21,"identifiers":3025},"Hwang, 2011, Efficacy of preoperative neck ultrasound in the detection of cervical lymph node metastasis from thyroid cancer, Laryngoscope, 121, 487, 10.1002\u002Flary.21227",{"doi":3026},"10.1002\u002Flary.21227",{"id":21,"text":3028,"url":21,"identifiers":3029},"Lee, 2013, Roles of ultrasonography and computed tomography in the surgical management of cervical lymph node metastases in papillary thyroid carcinoma, Eur. J. Surg. Oncol., 39, 191, 10.1016\u002Fj.ejso.2012.07.119",{"doi":3030},"10.1016\u002Fj.ejso.2012.07.119",{"id":21,"text":3032,"url":21,"identifiers":3033},"Lee, 2015, Pre-operative ultrasound diagnosis of nodal metastasis in papillary thyroid carcinoma patients according to nodal compartment, Ultrasound Med. Biol., 41, 1294, 10.1016\u002Fj.ultrasmedbio.2015.01.003",{"doi":3034},"10.1016\u002Fj.ultrasmedbio.2015.01.003",{"id":21,"text":3036,"url":21,"identifiers":3037},"Cai, 2015, The Clinical Relevance of Psammoma Body and Hashimoto Thyroiditis in Papillary Thyroid Carcinoma: A Large Case-control Study, Medicine (Baltimore), 94, e1881, 10.1097\u002FMD.0000000000001881",{"doi":3038},"10.1097\u002FMD.0000000000001881",{"id":21,"text":3040,"url":21,"identifiers":3041},"Kim, Y., Kim, M.H., Jeon, S., Kim, J., Kim, C., Bae, J.S., and Jung, C.K. (2017). Prognostic implication of histological features associated with EHD2 expression in papillary thyroid carcinoma. PLoS ONE, 12.",{"doi":3042},"10.1371\u002Fjournal.pone.0174737",{"id":21,"text":3044,"url":21,"identifiers":3045},"Bai, 2008, Subclassification of non-solid-type papillary thyroid carcinoma identification of high-risk group in common type, Cancer Sci., 99, 1908, 10.1111\u002Fj.1349-7006.2008.00908.x",{"doi":3046},"10.1111\u002Fj.1349-7006.2008.00908.x",{"id":21,"text":3048,"url":21,"identifiers":3049},"Das, 2004, Psammoma body and its precursors in papillary thyroid carcinoma: A study by fine-needle aspiration cytology, Diagn. Cytopathol., 31, 380, 10.1002\u002Fdc.20124",{"doi":3050},"10.1002\u002Fdc.20124",{"id":21,"text":3052,"url":21,"identifiers":3053},"Ali, S.Z., and Cibas, E.S. (2018). Papillary Thyroid Carcinoma, Variants, and Related Tumors. The Bethesda System for Reporting Thyroid Cytopathology: Definitions, Criteria, and Explanatory Notes, Springer International Publishing.",{},{"id":21,"text":3055,"url":21,"identifiers":3056},"Lee, 2014, Liquid-based cytology improves preoperative diagnostic accuracy of the tall cell variant of papillary thyroid carcinoma, Diagn. Cytopathol., 42, 11, 10.1002\u002Fdc.23007",{"doi":3057},"10.1002\u002Fdc.23007",{"id":21,"text":3059,"url":21,"identifiers":3060},"Renshaw, 2002, “Histiocytoid” cells in fine-needle aspirations of papillary carcinoma of the thyroid: Frequency and significance of an under-recognized cytologic pattern, Cancer, 96, 240, 10.1002\u002Fcncr.10715",{"doi":3061},"10.1002\u002Fcncr.10715",{"id":21,"text":3063,"url":21,"identifiers":3064},"Harshan, 2009, Papillary thyroid carcinoma with atypical histiocytoid cells on fine-needle aspiration, Diagn. Cytopathol., 37, 244, 10.1002\u002Fdc.20990",{"doi":3065},"10.1002\u002Fdc.20990",{"id":21,"text":3067,"url":21,"identifiers":3068},"Canepa, 2017, Atypical Histiocytoid Cells in Metastatic Papillary Thyroid Carcinoma: An Underrecognized Cytologic Pattern, Am. J. Clin. Pathol., 148, 58, 10.1093\u002Fajcp\u002Faqx049",{"doi":3069},"10.1093\u002Fajcp\u002Faqx049",{"id":21,"text":3071,"url":21,"identifiers":3072},"Brooks, 2009, Multinucleated giant cells’ incidence, immune markers, and significance: A study of 172 cases of papillary thyroid carcinoma, Head Neck Pathol., 3, 95, 10.1007\u002Fs12105-009-0110-9",{"doi":3073},"10.1007\u002Fs12105-009-0110-9",{"id":21,"text":3075,"url":21,"identifiers":3076},"Lundgren, 2003, Incidence and survival of Swedish patients with differentiated thyroid cancer, Int. J. Cancer, 106, 569, 10.1002\u002Fijc.11275",{"doi":3077},"10.1002\u002Fijc.11275",{"id":21,"text":3079,"url":21,"identifiers":3080},"Lundgren, 2006, Clinically significant prognostic factors for differentiated thyroid carcinoma: A population-based, nested case-control study, Cancer, 106, 524, 10.1002\u002Fcncr.21653",{"doi":3081},"10.1002\u002Fcncr.21653",{"id":21,"text":3083,"url":21,"identifiers":3084},"Eun, 2018, Comparison of the diagnostic performances of ultrasonography, CT and fine needle aspiration cytology for the prediction of lymph node metastasis in patients with lymph node dissection of papillary thyroid carcinoma: A retrospective cohort study, Int. J. Surg., 51, 145, 10.1016\u002Fj.ijsu.2017.12.036",{"doi":3085},"10.1016\u002Fj.ijsu.2017.12.036",{"id":21,"text":3087,"url":21,"identifiers":3088},"Cooper, 2009, Revised American Thyroid Association management guidelines for patients with thyroid nodules and differentiated thyroid cancer, Thyroid, 19, 1167, 10.1089\u002Fthy.2009.0110",{"doi":3089},"10.1089\u002Fthy.2009.0110",{"id":21,"text":3091,"url":21,"identifiers":3092},"Tsou, 2002, Multinucleated giant cells in fine needle aspirates. Can they help differentiate papillary thyroid cancer from benign nodular goiter?, Acta Cytol., 46, 823, 10.1159\u002F000327054",{"doi":3093},"10.1159\u002F000327054",{"id":21,"text":3095,"url":21,"identifiers":3096},"Legesse, 2019, Distinguishing non-invasive follicular thyroid neoplasm with papillary-like nuclear features (NIFTP) from classic and invasive follicular-variant papillary thyroid carcinomas based on cytologic features, J. Am. Soc. Cytopathol., 8, 11, 10.1016\u002Fj.jasc.2018.07.004",{"doi":3097},"10.1016\u002Fj.jasc.2018.07.004",{"id":21,"text":3099,"url":21,"identifiers":3100},"Fadda, 2011, Liquid-Based Cytology in Fine-Needle Aspiration Biopsies of the Thyroid Gland, Acta Cytol., 55, 389, 10.1159\u002F000329029",{"doi":3101},"10.1159\u002F000329029",{"id":21,"text":3103,"url":21,"identifiers":3104},"Baum, 2019, Cytological diagnosis of papillary thyroid carcinoma with tall cells on ThinPrep liquid-based cytology, Diagn. Cytopathol., 47, 541, 10.1002\u002Fdc.24146",{"doi":3105},"10.1002\u002Fdc.24146",{"id":21,"text":3107,"url":21,"identifiers":3108},"Chong, 2017, Can liquid-based preparation substitute for conventional smear in thyroid fine-needle aspiration? A systematic review based on meta-analysis, Endocr. Connect., 6, 817, 10.1530\u002FEC-17-0165",{"doi":3109},"10.1530\u002FEC-17-0165",{"id":21,"text":3111,"url":21,"identifiers":3112},"Cooper, 2006, Management guidelines for patients with thyroid nodules and differentiated thyroid cancer, Thyroid, 16, 109, 10.1089\u002Fthy.2006.16.109",{"doi":3113},"10.1089\u002Fthy.2006.16.109",{"id":21,"text":3115,"url":21,"identifiers":3116},"Lorente, 2015, Therapy of Endocrine Disease: Central neck dissection: A step forward in the treatment of papillary thyroid cancer, Eur. J. Endocrinol., 173, R199, 10.1530\u002FEJE-15-0481",{"doi":3117},"10.1530\u002FEJE-15-0481",{"id":21,"text":3119,"url":21,"identifiers":3120},"Zhao, 2019, Meta-analysis of ultrasound for cervical lymph nodes in papillary thyroid cancer: Diagnosis of central and lateral compartment nodal metastases, Eur. J. Radiol., 112, 14, 10.1016\u002Fj.ejrad.2019.01.006",{"doi":3121},"10.1016\u002Fj.ejrad.2019.01.006",{"id":21,"text":3123,"url":21,"identifiers":3124},"Cho, 2014, Clinicopathological features of rare BRAF mutations in Korean thyroid cancer patients, J. Korean Med. Sci., 29, 1054, 10.3346\u002Fjkms.2014.29.8.1054",{"doi":3125},"10.3346\u002Fjkms.2014.29.8.1054",{"id":21,"text":3127,"url":21,"identifiers":3128},"Yu, 2019, Precise Detection of Gene Mutations in Fine-Needle Aspiration Specimens of the Papillary Thyroid Microcarcinoma Using Next-Generation Sequencing, Int. J. Endocrinol., 2019, 4723958, 10.1155\u002F2019\u002F4723958",{"doi":3129},"10.1155\u002F2019\u002F4723958",{"id":21,"text":3131,"url":21,"identifiers":3132},"Yang, 2018, Mutation Status and Immunohistochemical Correlation of KRAS, NRAS, and BRAF in 260 Chinese Colorectal and Gastric Cancers, Front. Oncol., 8, 487, 10.3389\u002Ffonc.2018.00487",{"doi":3133},"10.3389\u002Ffonc.2018.00487",{"id":21,"text":3135,"url":21,"identifiers":3136},"Jennings, 2017, Guidelines for Validation of Next-Generation Sequencing-Based Oncology Panels: A Joint Consensus Recommendation of the Association for Molecular Pathology and College of American Pathologists, J. Mol. Diagn., 19, 341, 10.1016\u002Fj.jmoldx.2017.01.011",{"doi":3137},"10.1016\u002Fj.jmoldx.2017.01.011",{"id":21,"text":3139,"url":21,"identifiers":3140},"Jeon, S., Kim, Y., Jeong, Y.M., Bae, J.S., and Jung, C.K. (2018). CCND1 Splice Variant as A Novel Diagnostic and Predictive Biomarker for Thyroid Cancer. Cancers (Basel), 10.",{"doi":3141},"10.3390\u002Fcancers10110437",{"id":21,"text":3143,"url":21,"identifiers":3144},"Jung, 2018, Clinical utility of EZH1 mutations in the diagnosis of follicular-patterned thyroid tumors, Hum. Pathol., 81, 9, 10.1016\u002Fj.humpath.2018.04.018",{"doi":3145},"10.1016\u002Fj.humpath.2018.04.018",{"id":3147,"createTime":3148,"updateTime":3148,"relativeEntities":3149,"slug":3150,"properties":3151,"entityType":129,"verifyStatus":130,"verifyTime":3148,"verifyNote":131,"syncStatus":20,"languages":3167,"translateLanguages":21,"viewCount":22,"primaryUrl":3168,"fullTextUrl":21,"authors":3169,"publicationType":239,"publisherRelationship":3395,"citationCount":3425,"citationInfo":3426,"publishDate":21,"publishYear":21,"citationAnalyzeStatus":20,"lastCitationAnalyze":21,"indexDatabases":21,"openAccess":21,"references":3428,"isForceReanalyzing":578},"a625b4e6-28fb-4b55-ad39-5bfcdbf426d1","2024-09-01T23:26:07.983+00:00",[],"Molecular-Classification-to-Prognosticate-Response-in-Medically-Managed-Endometrial-Cancers-and-Endometrial-Intraepithelial-Neoplasia",{"mag":3152,"keywords":3154,"pmc":3155,"openalex":3157,"abstract":3159,"title":3161,"pm":3163,"doi":3165},{"VOID":3153},"3166290435",{},{"VOID":3156},"8201008",{"VOID":3158},"W3166290435",{"EN":3160},"\u003Cjats:p>Background: The aim of this study was to evaluate whether molecular classification prognosticates treatment response in women with endometrial cancers and endometrial intraepithelial neoplasia (EIN) treated with levonorgestrel intrauterine system (LNG-IUS). Methods: Patients treated with LNG-IUS for endometrial cancer or EIN from 2013 to 2018 were evaluated. Using immunohistochemistry and single gene sequencing of POLE, patients were classified into four groups as per the Proactive Molecular Risk Classifier for Endometrial cancer (ProMisE): POLE-mutated, mismatch repair-deficient (MMRd), p53 wild type (p53wt), and p53-abnormal (p53abn). Groups were assessed relative to the primary outcome of progression or receipt of definitive treatment. Results: Fifty-eight subjects with endometrioid endometrial cancer or EIN treated with LNG-IUS were included. Of these, 22 subjects (37.9%) had endometrial cancer and 36 subjects (62.1%) had EIN. Per the ProMisE algorithm, 44 patients (75.9%) were classified as p53wt, 6 (10.3%) as MMRd, 4 (6.9%) as p53abn, and 4 (6.9%) as POLE-mutated. Of the 58 patients, 11 (19.0%) progressed or opted for definitive therapy. Median time to progression or definitive therapy was 7.5 months, with p53abn tumors having the shortest time to progression or definitive therapy. Conclusions: Molecular classification of endometrial cancer and EIN prior to management with LNG-IUS is feasible and may predict patients at risk of progression.\u003C\u002Fjats:p>",{"EN":3162},"Molecular Classification to Prognosticate Response in Medically Managed Endometrial Cancers and Endometrial Intraepithelial Neoplasia",{"VOID":3164},"34200374",{"VOID":3166},"10.3390\u002Fcancers13112847",[133],"https:\u002F\u002Fwww.mdpi.com\u002F2072-6694\u002F13\u002F11\u002F2847",[3170,3191,3212,3231,3246,3267,3284,3301,3318,3337,3352,3374],{"id":3171,"sortIndex":276,"researcher":21,"roles":3172,"affiliations":3173,"properties":3184},"7817e4d4-2139-4765-b0be-cf7bbe789f9a",[],[3174],{"id":3175,"sortIndex":22,"affiliation":3176,"properties":21},"6b2db77b-37ce-40fa-b42f-5788aab2f7ff",{"id":3177,"createTime":3178,"updateTime":3178,"relativeEntities":3179,"slug":3180,"properties":3181,"entityType":50,"verifyStatus":20,"verifyTime":21,"verifyNote":21,"syncStatus":20,"languages":21,"translateLanguages":21,"viewCount":22},"c45812a1-3700-4024-9c01-40fe8358518f","2024-09-01T23:26:08.468+00:00",[],"Duke-Center-for-Genomics-and-Computational-Biology-Durham-NC-27710-USA-",{"title":3182},{"EN":3183},"Duke Center for Genomics and Computational Biology, Durham, NC 27710, USA;",{"openalex":3185,"orcid":3187,"title":3189},{"VOID":3186},"A5058546269",{"VOID":3188},"https:\u002F\u002Forcid.org\u002F0000-0001-7460-9247",{"EN":3190},"David L. 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Young Adult Oncol., 10, 193, 10.1089\u002Fjayao.2020.0100",{"doi":3482},"10.1089\u002Fjayao.2020.0100",{"id":21,"text":3484,"url":21,"identifiers":3485},"Koskas, 2014, Prognostic factors of oncologic and reproductive outcomes in fertility-sparing management of endometrial atypical hyperplasia and adenocarcinoma: Systematic review and meta-analysis, Fertil. Steril., 101, 785, 10.1016\u002Fj.fertnstert.2013.11.028",{"doi":3486},"10.1016\u002Fj.fertnstert.2013.11.028",{"id":21,"text":3488,"url":21,"identifiers":3489},"Raffone, A., Travaglino, A., Zullo, F.M., Gencarelli, A., Micheli, M., Miranda, S., De Franciscis, P., Insabato, L., Sardo, A.D.S., and Zullo, F. (2020). Predictive Accuracy of Progesterone Receptor B in Young Women with Atypical Endometrial Hyperplasia and Early Endometrial Cancer Treated with Hysteroscopic Resection plus LNG-IUD Insertion. J. Minim. 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2018, Global cancer statistics 2018: GLOBOCAN estimates of incidence and mortality worldwide for 36 cancers in 185 countries, CA Cancer J. 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KRAS: The Critical Driver and Therapeutic Target for Pancreatic Cancer. Cold Spring Harb. Perspect. Med., 8.",{"doi":3934},"10.1101\u002Fcshperspect.a031435",{"id":21,"text":3936,"url":21,"identifiers":3937},"Baek, 2015, Diagnostic accuracy of endoscopic ultrasound-guided fine needle aspiration cytology of pancreatic lesions, J. Pathol. Transl. Med., 49, 52, 10.4132\u002Fjptm.2014.10.26",{"doi":3938},"10.4132\u002Fjptm.2014.10.26",{"id":21,"text":3940,"url":21,"identifiers":3941},"Luchini, C., Veronese, N., Nottegar, A., Cappelletti, V., Daidone, M.G., Smith, L., Parris, C., Brosens, L.A.A., Caruso, M.G., and Cheng, L. (2019). Liquid Biopsy as Surrogate for Tissue for Molecular Profiling in Pancreatic Cancer: A Meta-Analysis Towards Precision Medicine. Cancers, 11.",{"doi":3942},"10.3390\u002Fcancers11081152",{"id":21,"text":3944,"url":21,"identifiers":3945},"Tjensvoll, 2016, Clinical relevance of circulating KRAS mutated DNA in plasma from patients with advanced pancreatic cancer, Mol. Oncol., 10, 635, 10.1016\u002Fj.molonc.2015.11.012",{"doi":3946},"10.1016\u002Fj.molonc.2015.11.012",{"id":21,"text":3948,"url":21,"identifiers":3949},"Mouliere, 2016, Circulating DNA as a Strong Multimarker Prognostic Tool for Metastatic Colorectal Cancer Patient Management Care, Clin. Cancer Res., 22, 3067, 10.1158\u002F1078-0432.CCR-15-0297",{"doi":3950},"10.1158\u002F1078-0432.CCR-15-0297",{"id":21,"text":3952,"url":21,"identifiers":3953},"Tabernero, 2015, Analysis of circulating DNA and protein biomarkers to predict the clinical activity of regorafenib and assess prognosis in patients with metastatic colorectal cancer: A retrospective, exploratory analysis of the CORRECT trial, Lancet Oncol., 16, 937, 10.1016\u002FS1470-2045(15)00138-2",{"doi":3954},"10.1016\u002FS1470-2045(15)00138-2",{"id":21,"text":3956,"url":21,"identifiers":3957},"Kinugasa, 2015, Detection of K-ras gene mutation by liquid biopsy in patients with pancreatic cancer, Cancer, 121, 2271, 10.1002\u002Fcncr.29364",{"doi":3958},"10.1002\u002Fcncr.29364",{"id":21,"text":3960,"url":21,"identifiers":3961},"Park, 2018, Utility of targeted deep sequencing for detecting circulating tumor DNA in pancreatic cancer patients, Sci. Rep., 8, 11631, 10.1038\u002Fs41598-018-30100-w",{"doi":3962},"10.1038\u002Fs41598-018-30100-w",{"id":21,"text":3964,"url":21,"identifiers":3965},"Wang, 2019, KRAS Mutant Allele Fraction in Circulating Cell-Free DNA Correlates With Clinical Stage in Pancreatic Cancer Patients, Front. Oncol., 9, 1295, 10.3389\u002Ffonc.2019.01295",{"doi":3966},"10.3389\u002Ffonc.2019.01295",{"id":21,"text":3968,"url":21,"identifiers":3969},"Chen, 2017, Ultrasensitive plasma ctDNA KRAS assay for detection, prognosis, and assessment of therapeutic response in patients with unresectable pancreatic ductal adenocarcinoma, Oncotarget, 8, 97769, 10.18632\u002Foncotarget.22080",{"doi":3970},"10.18632\u002Foncotarget.22080",{"id":21,"text":3972,"url":21,"identifiers":3973},"Perets, 2018, Mutant KRAS Circulating Tumor DNA Is an Accurate Tool for Pancreatic Cancer Monitoring, Oncologist, 23, 566, 10.1634\u002Ftheoncologist.2017-0467",{"doi":3974},"10.1634\u002Ftheoncologist.2017-0467",{"id":21,"text":3976,"url":21,"identifiers":3977},"Hadano, 2016, Prognostic value of circulating tumour DNA in patients undergoing curative resection for pancreatic cancer, Br. J. Cancer, 115, 59, 10.1038\u002Fbjc.2016.175",{"doi":3978},"10.1038\u002Fbjc.2016.175",{"id":21,"text":3980,"url":21,"identifiers":3981},"Gall, 2019, Circulating Tumor Cells and Cell-Free DNA in Pancreatic Ductal Adenocarcinoma, Am. J. Pathol., 189, 71, 10.1016\u002Fj.ajpath.2018.03.020",{"doi":3982},"10.1016\u002Fj.ajpath.2018.03.020",{"id":21,"text":3984,"url":21,"identifiers":3985},"Lennerz, 2015, Allelic ratio of KRAS mutations in pancreatic cancer, Oncologist, 20, e8, 10.1634\u002Ftheoncologist.2014-0408",{"doi":3986},"10.1634\u002Ftheoncologist.2014-0408",{"id":21,"text":3988,"url":21,"identifiers":3989},"Bernard, 2019, Circulating Nucleic Acids Are Associated With Outcomes of Patients With Pancreatic Cancer, Gastroenterology, 156, 108, 10.1053\u002Fj.gastro.2018.09.022",{"doi":3990},"10.1053\u002Fj.gastro.2018.09.022",{"id":21,"text":3992,"url":21,"identifiers":3993},"Mueller, 2018, Evolutionary routes and KRAS dosage define pancreatic cancer phenotypes, Nature, 554, 62, 10.1038\u002Fnature25459",{"doi":3994},"10.1038\u002Fnature25459",{"id":21,"text":3996,"url":21,"identifiers":3997},"Birnbaum, D.J., Bertucci, F., Finetti, P., Birnbaum, D., and Mamessier, E. (2019). Head and Body\u002FTail Pancreatic Carcinomas Are Not the Same Tumors. Cancers, 11.",{"doi":3998},"10.3390\u002Fcancers11040497",{"id":21,"text":4000,"url":21,"identifiers":4001},"Dreyer, S.B., Jamieson, N.B., Upstill-Goddard, R., Bailey, P.J., McKay, C.J., Biankin, A.V., and Chang, D.K. (2018). Defining the molecular pathology of pancreatic body and tail adenocarcinoma. Br. J. Surg.",{},{"id":21,"text":4003,"url":21,"identifiers":4004},"Mackay, 2018, Association of the location of pancreatic ductal adenocarcinoma (head, body, tail) with tumor stage, treatment, and survival: A population-based analysis, Acta Oncol., 57, 1655, 10.1080\u002F0284186X.2018.1518593",{"doi":4005},"10.1080\u002F0284186X.2018.1518593",{"id":21,"text":4007,"url":21,"identifiers":4008},"Tomasello, 2019, Outcome of head compared to body and tail pancreatic cancer: A systematic review and meta-analysis of 93 studies, J. Gastrointest. Oncol., 10, 259, 10.21037\u002Fjgo.2018.12.08",{"doi":4009},"10.21037\u002Fjgo.2018.12.08",{"id":21,"text":4011,"url":21,"identifiers":4012},"Artinyan, 2008, The anatomic location of pancreatic cancer is a prognostic factor for survival, HPB, 10, 371, 10.1080\u002F13651820802291233",{"doi":4013},"10.1080\u002F13651820802291233",{"id":21,"text":4015,"url":21,"identifiers":4016},"Valpione, 2018, Plasma total cell-free DNA (cfDNA) is a surrogate biomarker for tumour burden and a prognostic biomarker for survival in metastatic melanoma patients, Eur. J. Cancer, 88, 1, 10.1016\u002Fj.ejca.2017.10.029",{"doi":4017},"10.1016\u002Fj.ejca.2017.10.029",{"id":21,"text":4019,"url":21,"identifiers":4020},"Lapin, 2018, Fragment size and level of cell-free DNA provide prognostic information in patients with advanced pancreatic cancer, J. Transl. Med., 16, 300, 10.1186\u002Fs12967-018-1677-2",{"doi":4021},"10.1186\u002Fs12967-018-1677-2",{"id":21,"text":4023,"url":21,"identifiers":4024},"Heitzer, 2020, Cell-Free DNA and Apoptosis: How Dead Cells Inform About the Living, Trends Mol. Med., 26, 519, 10.1016\u002Fj.molmed.2020.01.012",{"doi":4025},"10.1016\u002Fj.molmed.2020.01.012",{"id":21,"text":4027,"url":21,"identifiers":4028},"Zvereva, M., Roberti, G., Durand, G., Voegele, C., Nguyen, M.D., Delhomme, T.M., Chopard, P., Fabianova, E., Adamcakova, Z., and Holcatova, I. (2020). Circulating tumour-derived KRAS mutations in pancreatic cancer cases are predominantly carried by very short fragments of cell-free DNA. EBioMedicine, 102462.",{"doi":4029},"10.1016\u002Fj.ebiom.2019.09.042",{"id":21,"text":4031,"url":21,"identifiers":4032},"Saad, 2002, Pretreatment CA 19-9 level as a prognostic factor in patients with advanced pancreatic cancer treated with gemcitabine, Int. J. Gastrointest. Cancer, 32, 35, 10.1385\u002FIJGC:32:1:35",{"doi":4033},"10.1385\u002FIJGC:32:1:35",{"id":21,"text":4035,"url":21,"identifiers":4036},"Maisey, 2005, CA19-9 as a prognostic factor in inoperable pancreatic cancer: The implication for clinical trials, Br. J. Cancer, 93, 740, 10.1038\u002Fsj.bjc.6602760",{"doi":4037},"10.1038\u002Fsj.bjc.6602760",{"id":21,"text":4039,"url":21,"identifiers":4040},"Scara, 2015, CA 19-9: Biochemical and Clinical Aspects, Adv. Exp. Med. Biol., 867, 247, 10.1007\u002F978-94-017-7215-0_15",{"doi":4041},"10.1007\u002F978-94-017-7215-0_15",{"id":21,"text":4043,"url":21,"identifiers":4044},"Bauer, 2013, Carbohydrate antigen 19-9 is a prognostic and predictive biomarker in patients with advanced pancreatic cancer who receive gemcitabine-containing chemotherapy: A pooled analysis of 6 prospective trials, Cancer, 119, 285, 10.1002\u002Fcncr.27734",{"doi":4045},"10.1002\u002Fcncr.27734",{"id":21,"text":4047,"url":21,"identifiers":4048},"van der Sijde, F., Vietsch, E.E., Mustafa, D.A.M., Besselink, M.G., Groot Koerkamp, B., and van Eijck, C.H.J. (2019). Circulating Biomarkers for Prediction of Objective Response to Chemotherapy in Pancreatic Cancer Patients. Cancers, 11.",{"doi":4049},"10.3390\u002Fcancers11010093",{"id":21,"text":4051,"url":21,"identifiers":4052},"Vivancos, 2019, Comparison of the Clinical Sensitivity of the Idylla Platform and the OncoBEAM RAS CRC Assay for KRAS Mutation Detection in Liquid Biopsy Samples, Sci. Rep., 9, 8976, 10.1038\u002Fs41598-019-45616-y",{"doi":4053},"10.1038\u002Fs41598-019-45616-y",{"id":4055,"createTime":4056,"updateTime":4056,"relativeEntities":4057,"slug":4058,"properties":4059,"entityType":129,"verifyStatus":130,"verifyTime":4056,"verifyNote":131,"syncStatus":20,"languages":4075,"translateLanguages":21,"viewCount":22,"primaryUrl":4076,"fullTextUrl":21,"authors":4077,"publicationType":239,"publisherRelationship":4254,"citationCount":2999,"citationInfo":4285,"publishDate":21,"publishYear":21,"citationAnalyzeStatus":20,"lastCitationAnalyze":21,"indexDatabases":21,"openAccess":21,"references":4287,"isForceReanalyzing":578},"d28f3380-1c52-4da6-a0cc-a15972efa7e3","2024-10-13T23:22:11.738+00:00",[],"Long-Term-Outcome-and-Comparison-of-Treatment-Modalities-of-Temporal-Bone-Paragangliomas",{"mag":4060,"keywords":4062,"pmc":4063,"openalex":4065,"abstract":4067,"title":4069,"pm":4071,"doi":4073},{"VOID":4061},"3205544970",{},{"VOID":4064},"8534247",{"VOID":4066},"W3205544970",{"EN":4068},"\u003Cjats:p>Introduction: Temporal bone paragangliomas are rare tumors with high vascularization and usually benign entity. A variety of modalities, including gross total resection, subtotal resection, conventional or stereotactic radiotherapy including gamma-knife, embolization, and wait-and-scan strategy can be considered. The aim of this study was to compare long-term outcomes of different primary treatment modalities in temporal bone paragangliomas. Materials and Methods: Patients with temporal bone paragangliomas treated between 1976 and 2018 at a tertiary referral center were retrospectively analyzed in this study. Collected patient data of 42 years were analyzed and long-term results including interdisciplinary management were assessed. Patient outcomes were compared within the different therapy modalities according to tumor control rate and complications. Clinical characteristics, radiological imaging, tumor extent and location (according to Fisch classification), symptoms, and follow-up were evaluated and a descriptive analysis for each treatment modality was performed. Tumor recurrence or growth progression and respective cranial nerve function before and after therapy were described. Results: A total of 59 patients were treated with a single or combined treatment modality and clinical follow-up was 7 (13) years (median, interquartile range). Of the included patients 45 (76%) were female and 14 (24%) male (ratio 3:1) with a patient age range from 18 to 83 years. Total resection was performed on 31 patients, while 14 patients underwent subtotal resection. Eleven patients were treated with conventional primary radiotherapy or gamma-knife radiosurgery. Pulsatile tinnitus (n = 17, 29%) and hearing impairment (n = 16, 27%) were the most common symptoms in our patient group. Permanent lower cranial nerve deficits were observed only in patients with large tumors (Fisch C and D, n = 14, 24%). Among the 45 patients who were treated surgically, 88% of patients with Fisch A and B paragangliomas had no recurrent disease, while no tumor growth was perceived in 83% of patients with Fisch C and D paragangliomas. Conclusion: In conclusion, we propose surgery as a treatment option for patients with small tumors, due to a high control rate and less cranial nerve deficits compared to larger tumors. Although patients with Fisch C and D temporal bone paraganglioma can be treated surgically, only subtotal resections are possible in many cases. Additionally, frequent occurrence of cranial nerve deficits in those patients and tumor growth progression in long-term follow-up examinations make a combination of the therapy modalities or a primary radiotherapy more suitable in larger tumors.\u003C\u002Fjats:p>",{"EN":4070},"Long-Term Outcome and Comparison of Treatment Modalities of Temporal Bone Paragangliomas",{"VOID":4072},"34680232",{"VOID":4074},"10.3390\u002Fcancers13205083",[133],"https:\u002F\u002Fwww.mdpi.com\u002F2072-6694\u002F13\u002F20\u002F5083",[4078,4097,4114,4135,4152,4169,4184,4205,4222,4237],{"id":4079,"sortIndex":2426,"researcher":21,"roles":4080,"affiliations":4081,"properties":4092},"b9840dbd-64d4-4964-bdc9-11cec2443aa5",[],[4082],{"id":4083,"sortIndex":22,"affiliation":4084,"properties":21},"be1dc6ca-c5e4-4ba5-9b84-a187542a31e9",{"id":4085,"createTime":4086,"updateTime":4086,"relativeEntities":4087,"slug":4088,"properties":4089,"entityType":50,"verifyStatus":20,"verifyTime":21,"verifyNote":21,"syncStatus":20,"languages":21,"translateLanguages":21,"viewCount":22},"e1a38cf4-9da2-4ab5-98cd-aeed7b2885f9","2024-10-13T23:22:11.784+00:00",[],"Department-of-Neurosurgery-Medical-University-of-Vienna-1090-Vienna-Austria",{"title":4090},{"EN":4091},"Department of Neurosurgery, Medical University of Vienna, 1090 Vienna, Austria",{"openalex":4093,"title":4095},{"VOID":4094},"A5058974915",{"EN":4096},"Christian Matula",{"id":4098,"sortIndex":51,"researcher":21,"roles":4099,"affiliations":4100,"properties":4107},"6d6573a1-b770-4081-869f-a26e9f0ff55c",[],[4101],{"id":4102,"sortIndex":22,"affiliation":4103,"properties":21},"a4786466-d108-4816-94d1-9994d02c108d",{"id":4085,"createTime":4086,"updateTime":4086,"relativeEntities":4104,"slug":4088,"properties":4105,"entityType":50,"verifyStatus":20,"verifyTime":21,"verifyNote":21,"syncStatus":20,"languages":21,"translateLanguages":21,"viewCount":22},[],{"title":4106},{"EN":4091},{"openalex":4108,"orcid":4110,"title":4112},{"VOID":4109},"A5006848706",{"VOID":4111},"https:\u002F\u002Forcid.org\u002F0000-0002-9249-8082",{"EN":4113},"Karl 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Otolaryngol., 43, 1566, 10.1111\u002Fcoa.13216",{"doi":4382},"10.1111\u002Fcoa.13216",{"id":4384,"createTime":4385,"updateTime":4385,"relativeEntities":4386,"slug":4387,"properties":4388,"entityType":129,"verifyStatus":130,"verifyTime":4385,"verifyNote":131,"syncStatus":20,"languages":4404,"translateLanguages":21,"viewCount":22,"primaryUrl":4405,"fullTextUrl":21,"authors":4406,"publicationType":239,"publisherRelationship":4428,"citationCount":4459,"citationInfo":4460,"publishDate":21,"publishYear":21,"citationAnalyzeStatus":20,"lastCitationAnalyze":21,"indexDatabases":21,"openAccess":21,"references":4462,"isForceReanalyzing":578},"5cc240bc-a7a6-45c1-8eff-7ecbc1b8bc08","2024-10-14T23:21:13.993+00:00",[],"Lysophospholipid-Signaling-in-the-Epithelial-Ovarian-Cancer-Tumor-Microenvironment",{"mag":4389,"keywords":4391,"pmc":4392,"openalex":4394,"abstract":4396,"title":4398,"pm":4400,"doi":4402},{"VOID":4390},"2846183811",{},{"VOID":4393},"6071084",{"VOID":4395},"W2846183811",{"EN":4397},"\u003Cjats:p>As one of the important cancer hallmarks, metabolism reprogramming, including lipid metabolism alterations, occurs in tumor cells and the tumor microenvironment (TME). 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Rev., 23, 113, 10.1016\u002FS0305-7372(97)90024-4",{"doi":4466},"10.1016\u002FS0305-7372(97)90024-4",{"id":21,"text":4468,"url":21,"identifiers":4469},"Amsterdam, 2010, Novel role of growth factors in ovary function, Harefuah, 149, 789",{},{"id":21,"text":4471,"url":21,"identifiers":4472},"Thibault, 2014, Ovarian cancer microenvironment: Implications for cancer dissemination and chemoresistance acquisition, Cancer Metastasis Rev., 33, 17, 10.1007\u002Fs10555-013-9456-2",{"doi":4473},"10.1007\u002Fs10555-013-9456-2",{"id":21,"text":4475,"url":21,"identifiers":4476},"Luo, 2016, Tumor microenvironment: The culprit for ovarian cancer metastasis?, Cancer Lett., 377, 174, 10.1016\u002Fj.canlet.2016.04.038",{"doi":4477},"10.1016\u002Fj.canlet.2016.04.038",{"id":21,"text":4479,"url":21,"identifiers":4480},"Hodeib, 2015, A review of HER2-targeted therapy in breast and ovarian cancer: Lessons from antiquity—Cleopatra and Penelope, Future Oncol., 11, 3113, 10.2217\u002Ffon.15.266",{"doi":4481},"10.2217\u002Ffon.15.266",{"id":21,"text":4483,"url":21,"identifiers":4484},"Fotopoulos, 2016, The emerging role of tyrosine kinase inhibitors in ovarian cancer treatment: A systematic review, Cancer Investig., 34, 313, 10.1080\u002F07357907.2016.1206117",{"doi":4485},"10.1080\u002F07357907.2016.1206117",{"id":21,"text":4487,"url":21,"identifiers":4488},"Cai, H., Chiorean, E.G., Chiorean, M.V., Rex, D.K., Robb, B.W., Hahn, N.M., Liu, Z., Loehrer, P.J., Harrison, M.L., and Xu, Y. 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Sin., 27, 1359, 10.1111\u002Fj.1745-7254.2006.00426.x",{"doi":5164},"10.1111\u002Fj.1745-7254.2006.00426.x",{"id":21,"text":5166,"url":21,"identifiers":5167},"Ceballos, 2007, Sphingosylphosphorylcholine activates dendritic cells, stimulating the production of interleukin-12, Immunology, 121, 328, 10.1111\u002Fj.1365-2567.2007.02578.x",{"doi":5168},"10.1111\u002Fj.1365-2567.2007.02578.x",{"id":5170,"createTime":5171,"updateTime":5171,"relativeEntities":5172,"slug":5173,"properties":5174,"entityType":129,"verifyStatus":130,"verifyTime":5171,"verifyNote":131,"syncStatus":20,"languages":5190,"translateLanguages":21,"viewCount":22,"primaryUrl":5191,"fullTextUrl":21,"authors":5192,"publicationType":239,"publisherRelationship":5214,"citationCount":5245,"citationInfo":5246,"publishDate":21,"publishYear":21,"citationAnalyzeStatus":20,"lastCitationAnalyze":21,"indexDatabases":21,"openAccess":21,"references":5250,"isForceReanalyzing":578},"72be464c-c576-4815-b3a9-aa55c1cf15df","2024-09-28T23:08:43.363+00:00",[],"Roles-of-StearoylCoA-Desaturase-1-in-the-Regulation-of-Cancer-Cell-Growth-Survival-and-Tumorigenesis",{"mag":5175,"keywords":5177,"pmc":5178,"openalex":5180,"abstract":5182,"title":5184,"pm":5186,"doi":5188},{"VOID":5176},"1987586561",{},{"VOID":5179},"3757427",{"VOID":5181},"W1987586561",{"EN":5183},"\u003Cjats:p>The development and maintenance of defining features of cancer, such as unremitting cell proliferation, evasion of programmed cell death, and the capacity for colonizing local tissues and distant organs, demand a massive production of structural, signaling and energy-storing lipid biomolecules of appropriate fatty acid composition. Due to constitutive activation of fatty acid biosynthesis, cancer cell lipids are enriched with saturated (SFA) and, in particular, monounsaturated fatty acids (MUFA), which are generated by StearoylCoA desaturase-1, the main enzyme that transforms SFA into MUFA. An increasing number of experimental and epidemiological studies suggest that high levels of SCD1 activity is a major factor in establishing the biochemical and metabolic perturbations that favors the oncogenic process. This review examines evidence that suggests the critical implication of SCD1 in the modulation of multiple biological mechanisms, specifically lipid biosynthesis and proliferation and survival signaling pathways that contribute to the development and progression of cancer.\u003C\u002Fjats:p>",{"EN":5185},"Roles of StearoylCoA Desaturase-1 in the Regulation of Cancer Cell Growth, Survival and Tumorigenesis",{"VOID":5187},"24212819",{"VOID":5189},"10.3390\u002Fcancers3022462",[133],"https:\u002F\u002Fwww.mdpi.com\u002F2072-6694\u002F3\u002F2\u002F2462",[5193],{"id":5194,"sortIndex":22,"researcher":21,"roles":5195,"affiliations":5196,"properties":5207},"8b78c582-a13b-4921-aabf-c3f81a24c225",[],[5197],{"id":5198,"sortIndex":22,"affiliation":5199,"properties":21},"f2420a42-853a-4538-b88b-21a95397412a",{"id":5200,"createTime":5201,"updateTime":5201,"relativeEntities":5202,"slug":5203,"properties":5204,"entityType":50,"verifyStatus":20,"verifyTime":21,"verifyNote":21,"syncStatus":20,"languages":21,"translateLanguages":21,"viewCount":22},"bf366c65-bb85-4f8f-af68-feae8f8fe42f","2024-09-28T23:08:43.400+00:00",[],"Department-of-Nutritional-Sciences-and-Rutgers-Center-for-Lipid-Research-Rutgers-the-State-University-of-New-Jersey-96-Lipman-Drive-New-Brunswick-NJ-08901-USA-igal-aesop-rutgers-edu-",{"title":5205},{"EN":5206},"Department of Nutritional Sciences and Rutgers Center for Lipid Research, Rutgers, the State University of New Jersey, 96 Lipman Drive, New Brunswick, NJ 08901, USA. igal@aesop.rutgers.edu.",{"openalex":5208,"orcid":5210,"title":5212},{"VOID":5209},"A5054812638",{"VOID":5211},"https:\u002F\u002Forcid.org\u002F0000-0003-0766-4574",{"EN":5213},"R. Ariel Igal",{"url":21,"publisher":5215,"properties":5239},{"id":6,"createTime":7,"updateTime":8,"relativeEntities":5216,"slug":10,"properties":5217,"entityType":19,"verifyStatus":20,"verifyTime":21,"verifyNote":21,"syncStatus":20,"languages":21,"translateLanguages":21,"viewCount":22,"subjectFields":5222,"manageAffiliations":5223,"indexDatabases":5224,"url":103,"thumbnailPath":21,"statistic":21,"gsStatistic":21,"type":21,"analyzePriority":21},[],{"country":5218,"issn":5219,"introduce":5220,"title":5221},{"VOID":13},{"VOID":15},{"EN":17},{"EN":10},[],[],[5225,5232],{"id":65,"indexDatabase":5226,"url":80,"indexYears":21,"academicFieldIds":5231,"indexDatabaseRanking":21},{"id":67,"createTime":68,"updateTime":69,"relativeEntities":5227,"label":5228,"description":5229,"key":76,"publicationTags":5230,"standard":21},[],{"EN":72,"VI":72},{"VI":74,"EN":75},[78,79],[82],{"id":84,"indexDatabase":5233,"url":97,"indexYears":98,"academicFieldIds":5238,"indexDatabaseRanking":102},{"id":86,"createTime":87,"updateTime":88,"relativeEntities":5234,"label":5235,"description":5236,"key":94,"publicationTags":5237,"standard":21},[],{"EN":91,"VI":91},{"EN":91,"VI":93},[96],[100,101],{"volume":5240,"pages":5242,"issue":5244},{"VOID":5241},"3",{"VOID":5243},"2462-2477",{"VOID":2416},97,{"total":5245,"publishYear":21,"statisticByYear":5247},{"2012":61,"2013":51,"2014":51,"2015":2426,"2016":276,"2017":677,"2018":2426,"2019":2426,"2020":5248,"2021":5249,"2022":276,"2023":274,"2024":274},14,13,[5251,5255,5259,5263,5267,5271,5275,5279,5283,5287,5291,5295,5298,5302,5306,5309,5313,5317,5321,5325,5329,5333,5336,5340,5344,5348,5352,5356,5360,5363,5367,5371,5375,5379,5383,5387,5391,5395,5399,5403,5407,5411,5415,5419,5423,5427,5431,5435,5439,5443,5447,5451,5455,5459,5463,5467,5471,5475,5479,5483,5487,5491,5495,5499,5503,5507,5511,5515,5519,5523,5527,5531,5535,5539,5543,5547,5551,5555,5559,5562,5566,5570,5574,5577,5581],{"id":21,"text":5252,"url":21,"identifiers":5253},"Menendez, 2007, Fatty acid synthase and the lipogenic phenotype in cancer pathogenesis, Nat. 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