Cancer
Công bố khoa học tiêu biểu
* Dữ liệu chỉ mang tính chất tham khảo
The prognosis for patients with atypical and malignant meningioma is guarded; whether the extent of resection is associated with survival‐based outcomes in this population remains poorly defined. This study investigated the association between gross total resection (GTR) and all‐cause mortality in patients with atypical and malignant meningioma.
The Surveillance, Epidemiology, and End Results program was used to identify 575 and 64 patients betweens the ages of 18 and 70 years who were diagnosed with atypical and malignant meningioma, respectively, between 2004 and 2009. Multivariate Cox proportional hazards regression was used to assess the adjusted impact of GTR versus subtotal resection on all‐cause mortality.
Baseline patient characteristics were similar for patients who did undergo GTR and patients who did not undergo GTR. The 5‐year overall survival rates were 91.3% (95% confidence interval [CI], 86.2%‐94.5%) and 78.2% (95% CI, 70.0%‐84.3%) for patients with atypical meningioma who did and did not undergo GTR, respectively, and 64.5% (95% CI, 45.9%‐78.1%) and 41.1% (95% CI, 17.9%‐63.1%) for patients with malignant meningioma who did and did not undergo GTR, respectively. After adjustments for available, pertinent confounding variables, GTR was associated with lower all‐cause mortality in patients with atypical (hazard ratio, 0.39; 95% CI, 0.23‐0.67;
The extent of resection is a powerful predictor of outcome for patients with atypical and malignant meningioma. These data highlight the hazard associated with the presence of gross tumor bulk after surgery and suggest a value for more extensive resections that should be balanced against the additional potential morbidity.
The 5‐year survival rate for intracranial glioblastoma multiforme (GBM) has remained at 4–5% for the last 30 years, in spite of multiple randomized prospective trials. The authors hypothesized, based on the literature, that even this remarkably poor survival rate is an overstatement. They investigated this hypothesis using the the Duke University Medical Center Tumor Registry.
The authors reviewed all patients with the diagnosis of intracranial GBM recorded in the Duke University Medical Center Tumor Registry from the registry's inception in 1976 through 1996. This search identified a population of patients with a minimum of 5 years of follow‐up. Each of the long‐term survivors was assigned a code number for clinical information. The pathology slides were provided to a neuropathologist in a coded fashion so that the patients could not be identified. The neuropathologist reviewed the slides to analyze the presence or absence of nine histologic factors. A match technique was used to identify a control population of patients with GBM who were not 5‐year survivors and were all deceased. The control population was compared with the study population to ascertain if there are histologic correlates associated with long‐term survivorship.
The authors identified 766 patients recorded by the tumor registry as having an intracranial GBM with a minimum of 5 years of follow up. Of the total population, 32 patients initially appeared to be 5‐year survivors (4%). Upon review of the medical records for these 32 patients, however, the authors found only 17 patients who were truly 5‐year survivors. The most common reason for miscoding was the presence of a low‐grade astrocytoma that subsequently dedifferentiated into GBM. The 17 long‐term survivors included 11 males and 6 females. Their mean age at diagnosis was 40.2 years. Therapy consisted of a macroscopic total resection in 4 patients (22%), a biopsy in 1 patient (6%), a subtotal resection in 10 patients (56%), and unknown extent of resection in 2 patients (11%). All patients received partial brain irradiation (mean dose, 62.6 Gy) and chemotherapy. Thirteen different single‐agent or combination chemotherapy programs were used. Two patients also received I‐131 monoclonal antibody therapy. Analysis of the nine histopathologic factors studied showed that intermediate fibrillary elements were more common and small anaplastic elements were less common in the long‐term survivors than in the control population.
Survival data on intracranial GBM, based on tumor registry data, should be interpreted cautiously. Reliable conclusions can only be drawn when such data are supplemented with clinical information and the histopathology is reviewed carefully. The group of long‐term survivors in the current study were younger than the typical GBM population. Conventionally treated patients with GBM, chosen from an unselected population from a tumor registry, have a smaller chance of long‐term survival than is generally believed. Cancer 2003. © 2003 American Cancer Society.
DOI 10.1002/cncr.11666
The purpose of this study was to identify problems related to long‐term quality of life (QOL) and sexual function in cervical cancer survivors.
The authors enrolled 860 women (median time since diagnosis, 5.86 years) with a history of cervical cancer (stage I to IVa) who had been treated at any of 6 hospitals from 1983 through 2004 and 494 control subjects selected randomly from a representative sample of Korean women. Subjects filled out a questionnaire that included the European Organization for Research and Treatment of Cancer (EORTC) QLQ‐C30, its Cervical Cancer Module, and additional sexual function items.
Cervical cancer survivors had clinically significant worse problems with social functioning, constipation, diarrhea, and difficulties with their finances than controls (
These findings can increase the awareness of healthcare providers to the potential need for counseling and other interventions among women who have been successfully treated for cervical cancer and could help them improve their impaired QOL. Cancer 2007. © 2007 American Cancer Society.
The proteasome is responsible for the degradation of intracellular proteins, including several involved in cell cycle control and the regulation of apoptosis. Preclinical studies have shown that the proteasome inhibitor bortezomib decreases proliferation, induces apoptosis, enhances the activity of chemotherapy and radiation, and reverses chemoresistance in a variety of hematologic and solid malignancy models in vitro and in vivo. Proteasome inhibition with bortezomib has specifically promoted apoptosis of tumor cells through the stabilization of p53, p21, p27, Bax, and IκBα, resulting in nuclear factor κB inhibition. Bortezomib was the first proteasome inhibitor to enter clinical trials. In two Phase II trials, SUMMIT and CREST, it was found that treatment with bortezomib, alone or in combination with dexamethasone, produced durable responses with meaningful survival benefits in patients with recurrent and/or refractory multiple myeloma. In the APEX Phase III trial, bortezomib produced significant survival benefits and improved response rates over high‐dose dexamethasone at first recurrence and beyond in patients with multiple myeloma. Clinical trials evaluating the safety and activity of bortezomib alone or in combination regimens with dexamethasone, doxorubicin, melphalan, prednisone, and/or thalidomide in the treatment of patients with newly diagnosed multiple myeloma have shown encouraging results. Preliminary studies suggest that bortezomib may serve as induction therapy before stem cell transplantation. Proteasome inhibition with bortezomib also has shown activity with manageable toxicity in mantle cell and other lymphomas, leukemias, and solid malignancies, including nonsmall cell lung carcinoma. Further studies with bortezomib as monotherapy and in combination regimens in the treatment of solid and hematologic malignancies are warranted. Cancer 2005. © 2005 American Cancer Society.
The outcome of older patients with newly diagnosed, Philadelphia chromosome (Ph)‐negative acute lymphoblastic leukemia (ALL) is poor. The combination of targeted therapy with low‐intensity chemotherapy is safe and effective. The objective of the current analysis was to compare the outcome of patients who received a combination of inotuzumab ozogamicin plus low‐intensity chemotherapy (mini–hyperfractionated cyclophosphamide, vincristine, and dexamethasone [mini‐HCVD]) with or without blinatumomab versus the outcome of those who received the standard, intensive, hyperfractionated cyclophosphamide, vincristine, doxorubicin, and dexamethasone (HCVAD) regimen.
The authors analyzed 135 older patients with newly diagnosed, Ph‐negative ALL who were treated prospectively with standard HCVAD (n = 77) or with the combination of inotuzumab ozogamicin plus mini‐HCVD with or without blinatumomab (n = 58). A propensity score analysis was conducted using 1:1 matching using the nearest neighbor matching method.
Propensity score matching identified 38 patients in each cohort. The antibody plus low‐intensity chemotherapy combination induced higher response rates (98% vs 88%), with lower rates of early death (0% vs 8%) and lower rates of death in complete remission (5% vs 17%). With propensity score matching, the 3‐year event‐free survival rates for patients who received HCVAD and those who received the combination of inotuzumab ozogamicin plus mini‐HCVD with or without blinatumomab were 34% and 64%, respectively (
The combination of inotuzumab ozogamicin plus mini‐HCVD with or without blinatumomab is safe and effective in older patients with newly diagnosed, Ph‐negative ALL and confers a better outcome compared with standard HCVAD chemotherapy.
Nodular, lymphocyte‐predominant Hodgkin lymphoma (NLPHL) represents a rare entity.
A clinical registry was launched from 1973 to 2003 in France. To determine the histologic transformation (HT) rate to diffuse large B‐cell lymphoma (DLBCL) and long‐term outcomes, 164 patients were selected after histologic review.
The median follow‐up was 9.5 years. The high biopsy rate (85%) at each recurrence enabled the analysis of HT. The median patient age was 30 years (range, 6‐69 years), 80% of patients were men, 83% had Ann Arbor stage I/II disease, 65% had supradiaphragmatic‐disease; 27% received radiotherapy, 9% received chemotherapy, 29% received combined‐modality therapy, and 35% were followed with a watch‐and‐wait strategy. All 106 treated patients achieved complete remission and 66 patients developed disease recurrence at a median of 3.3 years (range, 0.4‐18.3 years after diagnosis). The majority of recurrences were NLPHL, but 19 patients progressed to DLBCL at a median of 4.7 years (range, 0.4‐18 years after diagnosis). The 10‐year cumulative HT rate was 12% and was found to be associated significantly with a poor prognosis. The 10‐year overall survival rate was 91%. Fourteen patients died (7 died of progressive disease, 3 died of secondary cancers, and 4 died from other causes). HT was diagnosed at a median of 4.7 years (range, 0.4‐18 years after diagnosis). The 19 patients who had HT were treated with curative intent: Nine patients received high‐dose therapy with subsequent autologous stem cell transplantation (ASCT), and 10 patients received different chemotherapy regimens. The overall survival rate after HT did not differ between patients who underwent ASCT and the others.
This long‐term follow‐up study confirmed that NLPHL is a separate entity that has a favorable clinical presentation and outcome despite frequent recurrences. The current findings also emphasize the importance of biopsies at the time patients develop recurrent disease to evaluate HT. Cancer 2010. © 2009 American Cancer Society.
The optimal administration of radiotherapy for patients with high‐risk neuroblastoma (NB) currently is undefined in the context of modern therapy using myeloablative chemotherapy with autologous stem cell rescue (hematopoietic stem cell transplantation [HSCT]).
The authors conducted a retrospective review of the records of 21 consecutive patients with high‐risk NB to assess local control and toxicity of external beam radiotherapy (XRT). Therapy included multiagent induction chemotherapy and delayed surgical resection, consolidation of HSCT and local XRT, and 13‐
Four of 21 patients did not receive XRT due to toxic death (
Post‐HSCT, fractionated XRT to 2100 cGy was a tolerable and effective treatment for patients with high‐risk NB, and minimal recurrences were observed at designated XRT sites. Cancer 2004. © 2004 American Cancer Society.
Bovine leukemia virus (BLV) and human papillomavirus (HPV) were previously identified in human breast tissue and have been associated with breast cancer in independent studies. The objective of the current study was to test for the presence of BLV and HPV in the same breast tissue specimens to determine whether the viruses were associated with breast cancer either singly or together.
Archival formalin‐fixed paraffin‐embedded breast tissue sections from 216 women were received from The University of Texas MD Anderson Cancer Center along with patient diagnosis. In situ polymerase chain reaction and/or DNA hybridization methods were used to detect targeted DNA segments of BLV and HPV. Standard statistical methods were used to calculate age‐adjusted odds ratios, attributable risk, and
Women diagnosed with breast cancer were significantly more likely to have BLV DNA in their breast tissue compared with women with benign diagnoses and no history of breast cancer. Women with breast pathology classified as premalignant and no history of breast cancer also were found to have an elevated risk of harboring BLV DNA in their breast tissue. HPV status was not associated with malignancy, premalignant breast disease, or the presence of BLV in the breast tissues.
The data from the current study supported previous findings of a significant association between BLV DNA in breast tissue and a diagnosis of breast cancer, but did not demonstrate oncogenic strains of HPV associated with breast cancer or the presence of BLV DNA in breast tissue. The authors believe the findings of the current study contribute to overall knowledge regarding a possible causal role for viruses in human breast cancer.
Randomized trials report equivalent efficacy among various combinations of platinum‐based regimens in advanced non–small cell lung cancer (NSCLC). Their relative effectiveness and comparability based on squamous versus nonsquamous histology is uncertain.
The authors used the Surveillance, Epidemiology, and End Results (SEER)‐Medicare linked data to identify first‐line chemotherapy agents administered to Medicare beneficiaries with stage IIIB or IV NSCLC diagnosed from 2000 to 2007. Overall survival was compared between patients who received the 3 most common regimens: carboplatin‐paclitaxel, carboplatin‐gemcitabine, and carboplatin‐docetaxel. Stratified analyses distinguished between the outcomes of patients with squamous versus nonsquamous cell histology. Multivariable Cox proportional hazards models and propensity score analyses facilitated adjustment for imbalance in measurable patient characteristics.
Of the 15,318 patients who received first‐line chemotherapy, 43.1% received carboplatin‐paclitaxel, 14.3% received carboplatin‐gemcitabine, 8.5% received carboplatin‐docetaxel, and 34.1% received other regimens. The median survival was 8.0 months (interquartile range [IQR], 3.5‐17.4 months) for carboplatin‐paclitaxel, 7.3 months (IQR, 3.4‐15.2 months) for carboplatin‐gemcitabine, and 7.5 months (IQR, 3.2‐16.0 months) for carboplatin‐docetaxel. Both multivariable and propensity score‐adjusted Cox models demonstrated a slight inferiority associated with carboplatin‐gemcitabine or carboplatin‐docetaxel versus carboplatin‐paclitaxel, with a hazard ratio of 1.10 (95% confidence interval, 1.04‐1.15) and 1.09 (95% confidence interval, 1.02‐1.16), respectively, in propensity score‐stratified models. Among the subgroup of 2063 patients with squamous carcinoma, propensity score‐stratified analyses had a higher risk of death (hazard ratio, 1.20; 95% confidence interval, 1.07‐1.35) associated with carboplatin‐gemcitabine versus carboplatin‐paclitaxel.
Carboplatin‐paclitaxel was associated with slightly better survival compared with carboplatin‐gemcitabine or carboplatin‐docetaxel within the Medicare population with advanced NSCLC, and this was most pronounced for patients who had squamous cell histology. Cancer 2013;119:2048–2060. © 2013 American Cancer Society.
Chordomas are rare bone tumors arising from remnants of the embryonic notochord.
Data for this study were obtained from the Surveillance, Epidemiology, and End Results (SEER) Program of the National Cancer Institute (1973‐2009) to calculate the incidence, relative survival (RS), and standardized mortality ratio (SMR) of patients diagnosed with intracranial and extracranial chordomas and to assess the effects of age and sex on this disease.
The overall incidence of extracranial and intracranial chordomas was 8.4 per 10 million population. The median overall survival of patients with chordoma patients was 7.7 years. The median survival was 7.7 years for male patients and 7.8 years for female patients. Younger patients (aged <40 years) survived longer compared with older patients (10‐year RS, 68% vs 43%). The estimated age‐standardized 5‐year, 10‐year, and 20‐year RS rates was 72%, 48%, and 31%, respectively. The SMR in the overall cohort was 4.6 (95% confidence interval, 4.22‐5.0) or 21.0 (95% confidence interval, 16.6‐27.2) in young adult patients and 3.0 (95% confidence interval, 2.6‐3.4) in elderly patients.
The elderly had a more aggressive form of this disease; and, other than the incidence, sex did not influence outcome in this disease. The study of chordomas presents a good case for the contribution that the SMR can have on measuring the impact of a disease on a population of patients. Although the younger population has better survival rates, the impact (SMR) in the younger age groups is much higher than in older populations. Cancer 2013;119:2029–2037. © 2013 American Cancer Society.
- 1
- 2
- 3
- 4
- 5
- 6
- 10