bluuebunny/crossref_metadata_2025_split huggingface dataset:
Increasing incidence of rectal cancer in patients aged younger than 40 years
Authors: Meyer Joshua E. , Narang Tarun , Schnoll‐Sussman Felice H. , Pochapin Mark B. , Christos Paul J. , Sherr David L. 
Published: August 2010

AbstractBACKGROUND:The incidence of rectal cancer in the United States in young patients is considered to be low. Underestimating this incidence may result in a failure to diagnose younger patients with rectal cancer in a timely manner.METHODS:The authors conducted a retrospective cohort study using Surveillance, Epidemiology, and End Results (SEER) cancer registry data. A total of 7661 patients with colon, rectal, and rectosigmoid cancer who were diagnosed at age <40 years were identified between 1973 and 2005. The change in incidence over time for colon and rectal/rectosigmoid cancer was calculated and the annual percent change for anatomic subsites of colorectal cancer compared.RESULTS:SEER data demonstrated an increase in the incidence of rectal cancer without any increase in colon cancer (annual percent change of 2.6% vs −0.2%). The difference was statistically significant and extended to rectosigmoid cancer, but not cancer of the sigmoid colon or descending colon (annual percent change of 2.2% vs 0.4% and −2.8%, respectively). Joinpoint analysis of the slope of the curve of rectal and rectosigmoid cancer incidence identified the beginning of the increase to be 1984. All races and both sexes demonstrated similar statistically significant increases in the incidence of rectal and rectosigmoid cancer.CONCLUSIONS:The incidence of rectal and rectosigmoid cancer appears to be increasing in patients aged <40 years. Patients presenting with rectal bleeding or other alarming signs or symptoms should be evaluated with this finding in mind. Cancer 2010. © 2010 American Cancer Society.
Does the progression‐free interval after primary chemotherapy predict survival after salvage chemotherapy in advanced and recurrent endometrial cancer?
Authors: Moore Kathleen N. , Tian Chunqiao , McMeekin D. Scott , Thigpen J. Tate , Randall Marcus E. , Gallion Holly H. 
Published: August 2010

AbstractBACKGROUND:This study evaluated whether progression‐free interval (PFI) following primary chemotherapy (PCT) was predictive of overall survival (OS) after second‐line chemotherapy in advanced/recurrent endometrial cancer (EC).METHODS:This is a pooled analysis of patients who recurred after PCT and were treated with second‐line chemotherapy on Gynecologic Oncology Group trials. PFI‐1 measured from initiation of PCT to recurrence or treatment‐free interval (TFI) measured from completion of PCT to initiation of second‐line chemotherapy was evaluated in relation to clinical outcomes.RESULTS:A total of 586 patients treated on 5 phase 3 PCT protocols were included. Baseline factors in primary setting associated with clinical outcome after PCT were also predictive of OS after second‐line chemotherapy, including race, Gynecologic Oncology Group performance status, grade, and prior radiation therapy (P< .01). PFI‐1 was the most significant factor predictive of survival after second‐line chemotherapy, with a 30% reduction in the risk of death for PFI‐1 >6 months compared with ≤6 months (hazard ratio [HR], 0.70; 95% confidence interval [CI], 0.59‐0.84 [P< .0001]) and median OS after second‐line chemotherapy of 10 versus 5 months. A total of 275 patients treated on 9 phase 2 second‐line chemotherapy protocols were also evaluated, and TFI >3 months was associated with a 25% reduction in the risk of death (HR, 0.75; 95% CI, 0.57‐0.97 [P= .030]) and median OS after second‐line chemotherapy of 10 versus 7 months compared with TFI ≤3 months. The tumor response to second‐line chemotherapy was 9.6% versus 5.8%; the difference was not statistically significant.CONCLUSIONS:Time to recurrence after PCT is predictive of survival after recurrence in advanced/recurrent EC. However, there is no evidence that this variable can be used in selecting salvage chemotherapy. Cancer 2010. © 2010 American Cancer Society.
MicroRNA‐205–directed transcriptional activation of tumor suppressor genes in prostate cancer
Authors: Majid Shahana , Dar Altaf A. , Saini Sharanjot , Yamamura Soichiro , Hirata Hiroshi , Tanaka Yuichiro , Deng Guoren , Dahiya Rajvir 
Published: August 2010

AbstractBACKGROUND:MicroRNAs (miRNAs) are small noncoding RNAs that regulate the expression of approximately 60% of all human genes. They play important roles in numerous cellular processes, including development, proliferation, and apoptosis. Currently, it is believed that miRNAs elicit their effect by silencing the expression of target genes. In this study, the authors demonstrated that miRNA‐205 (miR‐205) induced the expression the interleukin (IL) tumor suppressor genes IL24 and IL32 by targeting specific sites in their promoters.METHODS:The methods used in this study included transfection of small RNAs; quantitative real‐time polymerase chain reaction; in situ hybridization; fluorescence‐labeled in situ hybridization; cell cycle, apoptosis, cell viability, migratory, clonability, and invasion assays; immunoblotting; and luciferase reporter, nuclear run‐on, and chromatin immunoprecipitation assays.RESULTS:The results revealed that miR‐205 was silenced in prostate cancer. Its re‐expression induced apoptosis and cell cycle arrest. It also impaired cell growth, migration, clonability, and invasiveness of prostate cancer cells. Micro‐RNA‐205 induced the expression of tumor suppressor genes IL24 and IL32 at both the messenger RNA and protein levels. The induction of in vitro transcription and enrichment of markers for transcriptionally active promoters in the IL24 and IL32 genes was observed in response to miR‐205.CONCLUSIONS:In this study, a new function for miR‐205 was identified that specifically activated tumor suppressor genes by targeting specific sites in their promoters. These results corroborate a newly identified function that miRNAs have in regulating gene expression at the transcriptional level. The specific activation of tumor suppressor genes (eg, IL24, IL32) or other dysregulated genes by miRNA may contribute to a novel therapeutic approach for the treatment of prostate cancer. Cancer 2010. © 2010 American Cancer Society.
Screening for major depression in cancer outpatients
Authors: Thekkumpurath Parvez , Walker Jane , Butcher Isabella , Hodges Laura , Kleiboer Annet , O'Connor Mark , Wall Lucy , Murray Gordon , Kroenke Kurt , Sharpe Michael 
Published: August 2010

AbstractBACKGROUND:Systematic screening for depression has been recommended for patients who have medical conditions like cancer. The 9‐item Patient Health Questionnaire (PHQ‐9) is becoming widely used, but its diagnostic accuracy has not yet been tested in a cancer patient population. In this article, the authors report on the performance of the PHQ‐9 as a screening instrument for major depressive disorder (MDD) in patients with cancer.METHODS:Data obtained from a depression screening service for patients who were attending clinics of a Regional Cancer Centre in Edinburgh, United Kingdom were used. Patients had completed both the PHQ‐9 and a 2‐stage procedure to identify cases of MDD. Performance of the PHQ‐9 in identifying cases of MDD was determined using receiver operating characteristic (ROC) analysis.RESULTS:Data were available on 4264 patients. When scored as a continuous measure, the PHQ‐9 performed well with an area under the ROC curve of 0.94 (95% confidence interval [CI], 0.93‐0.95). A cutoff score of ≥8 provided a sensitivity of 93% (95% CI, 89%‐95%), a specificity of 81% (95% CI, 80%‐82%), a positive predictive value (PPV) of 25%, and a negative predictive value (NPV) of 99% and could be considered optimum in a screening context. The PHQ‐9 did not perform as well when it was scored using an algorithm with a sensitivity of 56% (95% CI, 55%‐57%), a specificity of 96% (95% CI, 95%‐97%), a PPV of 52%, and an NPV of 97%.CONCLUSIONS:The PHQ‐9 scored as a continuous measure with a cutoff score of ≥8 performed well in identifying MDD in cancer patients and should be considered as a screening instrument in this population. Cancer 2011. © 2010 American Cancer Society.
How does initial treatment choice affect short‐term and long‐term costs for clinically localized prostate cancer?
Authors: Snyder Claire F. , Frick Kevin D. , Blackford Amanda L. , Herbert Robert J. , Neville Bridget A. , Carducci Michael A. , Earle Craig C. 
Published: August 2010

AbstractBACKGROUND.Data regarding costs of prostate cancer treatment are scarce. This study investigates how initial treatment choice affects short‐term and long‐term costs.METHODS.This retrospective, longitudinal cohort study followed prostate‐cancer cases diagnosed in 2000 for 5 years using the Surveillance, Epidemiology, and End Results (SEER)‐Medicare database. Men age ≥66 years, in Medicare fee for service, diagnosed with clinically localized prostate cancer in 2000 while residing in a SEER region, were matched to noncancer controls using age, sex, race, region, comorbidity, and survival. On the basis of treatment received during the first 9 months postdiagnosis, patients were assigned to watchful waiting, radiation, hormonal therapy, hormonal + radiation, and surgery (may have received other treatments). Incremental costs for prostate cancer were the difference in costs for prostate cancer cases versus matched controls. Costs were divided into initial treatment (months −1 to 12), long‐term (each 12 months thereafter), and total (months −1 to 60). Sensitivity analyses excluded the last 12 months of life.RESULTS.A total of 13,769 prostate‐cancer cases were matched to 13,769 noncancer controls. Watchful waiting had the lowest initial treatment ($4270) and 5‐year total costs ($9130). Initial treatment costs were highest for hormonal + radiation ($17,474) and surgery ($15,197). At $26,896, 5‐year total costs were highest for hormonal therapy only followed by hormonal + radiation ($25,097) and surgery ($19,214). After excluding the last 12 months of life, total costs were highest for hormonal + radiation ($23,488) and hormonal therapy ($23,199).CONCLUSIONS.Patterns of costs vary widely based on initial treatment. These data can inform patients and clinicians considering treatment options and policy makers interested in patterns of costs. Cancer 2010. © 2010 American Cancer Society.
Putative tumor suppressor miR‐145 inhibits colon cancer cell growth by targeting oncogene friend leukemia virus integration 1 gene
Authors: Zhang Jianjun , Guo Haiyan , Zhang He , Wang Haibo , Qian Guanxiang , Fan Xianqun , Hoffman Andrew R. , Hu Ji‐Fan , Ge Shengfang 
Published: August 2010

AbstractBACKGROUND:Tumor suppressor microRNA miR‐145 is commonly down‐regulated in colon carcinoma tissues, but its specific role in tumors remains unknown.METHODS:In this study, the authors identified the Friend leukemia virus integration 1 gene (FLI1) as a novel target of miR‐145. FLI1 is involved in t(11;22)(q24:q12) reciprocal chromosomal translocation in Ewing sarcoma, and its expression appears to be associated with biologically more aggressive tumors.RESULTS:The authors demonstrated that miR‐145 targets a putative microRNA regulatory element in the 3′‐untranslated region (UTR) of FLI1, and its abundance is reversely associated with FLI1 expression in colon cancer tissues and cell lines. By using a luciferase/FLI1 3′‐UTR reporter system, they found that miR‐145 down‐regulated the reporter activity, and this down‐regulation was reversed by anti–miR‐145. Mutation of the miR‐145 microRNA regulatory element sequence in the FLI1 3′‐UTR abolished the activity of miR‐145. miR‐145 decreased FLI1 protein but not FLI1 mRNA, suggesting a mechanism of translational regulation. Furthermore, the authors demonstrated that miR‐145 inhibited cell proliferation and sensitized LS174T cells to 5‐fluorouracil–induced apoptosis.CONCLUSIONS:Taken together, these results suggest that miR‐145 functions as a tumor suppressor by down‐regulating oncogenic FLI1 in colon cancer. Cancer 2011. © 2010 American Cancer Society.
Common arm comparative outcomes analysis of phase 3 trials of cisplatin + irinotecan versus cisplatin + etoposide in extensive stage small cell lung cancer1
Authors: Lara Primo N. , Chansky Kari , Shibata Taro , Fukuda Haruhiko , Tamura Tomohide , Crowley John , Redman Mary W. , Natale Ronald , Saijo Nagahiro , Gandara David R 
Published: August 2010

AbstractBACKGROUND:Southwest Oncology Group 0124 was a large North American phase 3 trial that failed to confirm a survival benefit for cisplatin/irinotecan over cisplatin/etoposide in patients with extensive stage small cell lung cancer (SCLC). These results were contrary to Japan Clinical Oncology Group 9511, a phase 3 trial exclusively in Japanese patients. Because 0124 and 9511 used identical treatment regimens and similar eligibility criteria, patient‐level data were pooled from both trials, and a common arm analysis was performed to explore potential reasons for the divergent results.METHODS:Patients with documented extensive stage SCLC and adequate end‐organ function were randomized to intravenously receive either cisplatin 60 mg/m2 Day 1 + irinotecan 60 mg/m2 Days 1, 8, and 15 every 4 weeks or cisplatin 80 mg/m2 Day 1 + etoposide 100 mg/m2 Days 1‐3 every 3 weeks. Demographic and outcome data were compared among 805 patients enrolled in 9511 and 0124 receiving identical treatment using a logistic model adjusted for age, sex, and performance status (PS).RESULTS:Of 671 patients in 0124, 651 eligible patients were included, as were all 154 patients from 9511. Significant differences in sex and PS distribution as well as toxicity were seen between trials. There were also significant differences in response rates (87% vs 60%, P<.001) and median overall survival (12.8 vs 9.8 months, P<.001) when the cisplatin/irinotecan arms from both trials were compared.CONCLUSIONS:Significant differences in patient demographics, toxicity, and efficacy were identified in the 9511 and 0124 populations. These results, relevant in the current era of clinical trials globalization, warrant: 1) consideration of differential patient characteristics and outcomes among populations receiving identical therapy; 2) utilization of the common arm model in prospective trials; and 3) inclusion of pharmacogenomic correlates in cancer trials where ethnic/racial differences in drug disposition are expected. Cancer 2010. © 2010 American Cancer Society.
Influence of abdominal adiposity, waist circumference, and body mass index on clinical and pathologic findings in patients treated with radiotherapy for localized prostate cancer
Authors: Zilli Thomas , Chagnon Miguel , Van Nguyen Thu , Bahary Jean‐Paul , Guay Jean‐Pierre , Dufresne Alix , Taussky Daniel 
Published: August 2010

AbstractBACKGROUND:Increased body mass index (BMI) has been associated with more aggressive prostate cancer (PC). The relation among abdominal visceral adipose tissue (VAT), subcutaneous adipose tissue (SAT), waist circumference (WC), and BMI was compared with clinical and pathologic findings in patients treated with radiotherapy for localized PC.METHODS:VAT, SAT, WC (all measured by planning abdominopelvic computed tomography scan) and BMI were compared with clinical and pathologic factors using univariate analyses. Cox regression analyses were performed to evaluate whether obesity measures significantly predicted risk for secondary malignancies.RESULTS:Of 276 analyzed patients, 80 (29%) were obese (BMI ≥ 30 kg/m2). Median BMI at baseline was 27.6 kg/m2 (interquartile range [IQR], 25.1‐30.5 kg/m2). Increased SAT and VAT were associated with a higher National Comprehensive Cancer Network (NCCN) PC risk group (P = .0001 and .008, respectively). Greater SAT was associated with a higher Gleason score (GS) (P = .030). Younger age at diagnosis was significantly correlated with higher SAT and BMI, whereas increased prostate size was found in patients with higher BMI, WC, SAT, and VAT. At a median follow‐up of 42.3 months (IQR, 32.3‐59.9 months), 15 secondary malignancies were observed. On multivariate analysis, VAT was a significant predictor for secondary cancers (adjusted hazards ratio, 1.014; P = .0001).CONCLUSIONS:Measurements of greater abdominal adiposity were strongly associated with adverse pathologic features in patients with localized PC, including higher GS and NCCN PC risk groups. Moreover, VAT was found to be a strong risk factor for secondary malignancies. Cancer 2010. © 2010 American Cancer Society.
Incidence of atypical teratoid/rhabdoid tumors in children
Authors: Woehrer Adelheid , Slavc Irene , Waldhoer Thomas , Heinzl Harald , Zielonke Nadine , Czech Thomas , Benesch Martin , Hainfellner Johannes A. , Haberler Christine 
Published: August 2010

AbstractBACKGROUND:Atypical teratoid/rhabdoid tumors are highly malignant embryonal central nervous system (CNS) tumors that were defined as an entity in 1996. As compared with other malignant CNS tumors, their biological behavior is particularly aggressive, but patients may benefit from an intensified treatment. Atypical teratoid/rhabdoid tumors display a complex histomorphology, which renders them prone to misdiagnosis. They occur predominantly in young children, with an estimated prevalence of 1% to 2% among all pediatric CNS tumors. However, population‐based data on the incidence of these tumors are not yet available.METHODS:A nation‐wide survey of malignant high‐grade CNS tumors (World Health Organization grade III/IV), diagnosed in children (aged birth to 14 years) from 1996 to 2006 was conducted by the Austrian Brain Tumor Registry. A central histopathology review was performed including the assessment of SMARCB1 (INI1) protein status.RESULTS:A total of 311 newly diagnosed, malignant CNS tumors were included. Atypical teratoid/rhabdoid tumors constituted the sixth most common entity (6.1%), referring to an age‐standardized incidence rate of 1.38 per 1,000,000 person‐years in children. Peak incidence was found in the birth to 2 years age group, where they were as common as CNS primitive neuroectodermal tumors and medulloblastomas. A total of 47.4% of atypical teratoid/rhabdoid tumors were initially diagnosed, whereas 52.6% were retrospectively detected by the central review. The 5‐year survival of atypical teratoid/rhabdoid tumor patients was 39.5%, with 66.7% in the correctly diagnosed group versus 15.0% in the not recognized group (P = .0469).CONCLUSIONS:Clinicians and pathologists should be aware of the high incidence of atypical teratoid/rhabdoid tumors in young children to optimize diagnostic and therapeutic management of patients with these tumors. Cancer 2010. © 2010 American Cancer Society.
Evaluation of the Seventh American Joint Committee on Cancer/International Union Against Cancer Classification of gastric adenocarcinoma in comparison with the sixth classification
Authors: Ahn Hye Seong , Lee Hyuk‐Joon , Hahn Seokyung , Kim Woo‐Ho , Lee Kuhn Uk , Sano Takeshi , Edge Stephen B , Yang Han‐Kwang 
Published: August 2010

AbstractBACKGROUND:The seventh TNM staging system for gastric cancer of the American Joint Committee on Cancer/International Union Against Cancer (AJCC/UICC) had a more detailed classification than the sixth TNM staging system for both the tumor (T) and lymph nodes (N). The authors compared survival rates assessed by the seventh staging system with those by the sixth system.METHODS:The authors analyzed the prospectively collected database on patients with gastric cancer who underwent surgery at Seoul National University Hospital between 1986 and 2006, and calculated the survival rates of 9998 cases with primary cancer, R0 resection, and >14 retrieved lymph nodes.RESULTS:The 5‐year cumulative survival rates (5YSR) according to the seventh edition T or N classifications were significantly different. The 5YSR according to seventh edition of the TNM staging system were 95.1% (stage IA), 88.4% (stage IB), 84.0% (stage IIA), 71.7% (stage IIB), 58.4% (stage IIIA), 41.3% (stage IIIB), and 26.1% (stage IIIC), which were significantly different from each other. The 5YSR of the seventh edition T2 and T3 classifications had significant differences in patients with every N classification, and the 5YSR of seventh edition N1 and N2 classifications had significant differences in T2 patients, T3 patients, and T4 patients. Each stage in the sixth edition was divided into the seventh edition stage with different survival rates. In addition, the number of homogenous groupings in seventh edition TNM stages was increased from 1 to 2.CONCLUSIONS:The seventh system provided a more detailed classification of prognosis than the sixth system, especially between T2 and T3 tumors and N1 and N2 tumors, although further studies were found to be needed for the N3a and N3b classification. Cancer 2010. © 2010 American Cancer Society.
Prognostic impact of Notch ligands and receptors in nonsmall cell lung cancer
Authors: Donnem Tom , Andersen Sigve , Al‐Shibli Khalid , Al‐Saad Samer , Busund Lill‐Tove , Bremnes Roy M. 
Published: August 2010

AbstractBACKGROUND:Notch signaling plays a key role in embryonic vascular development and angiogenesis. The authors aimed to study the prognostic role of the angiogenesis‐related Notch ligands and receptors and investigate the prognostic impact of the coexpression of vascular endothelial growth factor‐A (VEGF‐A) and Notch signaling.METHODS:Tumor tissue samples from 335 resected patients with stage I to IIIA nonsmall cell lung cancer (NSCLC) were obtained, and tissue microarrays were constructed from duplicate cores of tumor cells and tumor‐related stroma from each specimen. Immunohistochemistry was used to evaluate the expression of the molecular markers Notch‐1, Notch‐4, Delta‐like ligand 4 (DLL4), and Jagged‐1.RESULTS:There were 191 squamous cell carcinomas (SCCs), 113 adenocarcinomas (ACs), and 31 large cell carcinomas. In AC, low tumor cell Delta‐like ligand 4 expression was an independent negative prognostic factor (hazard ratio [HR], 2.9; 95% confidence interval [CI], 1.4‐6.3 [P = .006]), whereas high tumor cell Notch‐1 expression was an independent negative prognostic factor (HR, 2.2; 95% CI, 1.2‐4.1 [P<.001]). In SCC, low stromal Delta‐like ligand 4 expression was an independent indicator of poor prognosis (HR, 3.3; 95% CI, 1.8‐6.1 [P<.001]). The coexpression of Notch‐1 and VEGF‐A had a significant prognostic impact (P<.001). For Notch‐1 and VEGF‐A, low/low (n = 142) versus high/high (n = 35) expression resulted in 5‐year survival rates of 69% and 32%, respectively.CONCLUSIONS:Delta‐like ligand 4 and Notch‐1 are independent prognostic factors in NSCLC, but have diverse impacts in SCC and AC. The coexpression of tumor cell Notch‐1/VEGF‐A has a major impact on survival. Cancer 2010. © 2010 American Cancer Society.