bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract 875: Ovarian and uterine carcinosarcoma: A comparative analysis of prognostic variables and survival outcomes
Authors: Garg Gunjal , Shah Jay P. , Bryant Christopher , Kumar Sanjeev , Morris Robert T. 
Published: February 2011

Abstract
Objective: Carcinosarcomas (malignant mixed mullerian tumor) of the female genital tract are rare tumors associated with poor outcome. Previous studies have demonstrated that even tumors of similar histology originating in organs that are in proximity may be biologically distinct entities by virtue of their occurrence through different molecular pathways. The objective of this study was to identify site specific differences in the clinical behavior and survival outcome of carcinosarcomas originating in female genital tract by comparing carcinosarcomas arising in the uterus and ovaries. Methods: Data on patients with uterine carcinosarcoma and ovarian carcinosarcoma were extracted from the Surveillance, Epidemiology, and End Results database between 1988 and 2005. Kaplan-Meier log rank and Cox proportional hazards models were used for survival analysis and to identify possible predictors for survival. Results: The identified cohort included 3,683 women, with 2,759 (75%) uterine carcinosarcomas and 924 (25%) ovarian carcinosarcomas. Uterine carcinosarcoma patients were older than patients with ovarian carcinosarcoma (median age 67.61 vs. 65.83 years, p&lt;0.001). Women with uterine carcinosarcomas compared with ovarian carcinosarcoma were more often African American (17.3% versus 6%; P&lt;0.001) and presented more often with early stage disease (Stage I/II 56.6% compared with 24.6%; P &lt;0.001). Uterine compared to ovarian carcinosarcomas differed significantly with regards to the performance of salpingo-oopherectomy (96 % versus 99.4 %; P = 0.001), lymphadenectomy (62.6% versus 41.2%; P &lt;0.001), and administration of radiotherapy (38.2% versus 4.8%; P &lt;0.001). No difference was found in survival between patients with uterine and ovarian carcinosarcoma on stage- stratified Kaplan- Meier survival analysis or multivariate analysis using Cox model. Although, age (p&lt;0.001), race (p&lt;0.001), marital status (p&lt;0.001), stage (p&lt;0.001), lymphadenectomy (p&lt;0.001), and radiation (p=0.005) were all significant prognostic factors in uterine carcinosarcoma, only age (p=0.001), stage (p&lt;0.001), and lymphadenectomy(p&lt;0.001) reached statistical significance in ovarian carcinosarcoma on multivariate analysis. Conclusion: Ovarian carcinosarcomas present at a more advanced stage and have a comparable prognosis at each stage with uterine carcinosarcomas. Improved survival observed in lymphadenectomy group argues in favor of routinely performing lymph node dissection in patients with uterine and ovarian carcinosarcoma.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 875.
Abstract 879: Mitochondrial DNA content and its association with lung cancer risk and clinical outcomes
Authors: Pu Xia , Lippman Scott M. , Gu Jian , Xing Jingliang , Chang Joe , Chang David , Spitz Margaret R. , Wu Xifeng 
Published: February 2011

Abstract
Mitochondrion is an essential cellular organelle generating energy, and also plays a key role in the initiation and regulation of apoptosis. Impaired mitochondria function may inhibit apoptosis; enhance reactive oxygen species and generate cancer related proteins. The difference in mitochondrial DNA (mtDNA) content (also termed mtDNA copy number) may contribute to cancer predisposition as well as variations in clinical outcomes. To test this hypothesis, we conducted a large-scale case-control study to investigate the role of mtDNA content in lung cancer etiology and clinical outcomes. MtDNA content in 2,442 newly diagnosed lung cancer patients and 2,417 matched controls were measured by quantitative real-time polymerase chain reaction. Clinical outcome data were collected for non-small cell lung cancer (NSCLC) patients (2,020 subjects). We analyzed the association of MtDNA copy number with the risk of developing lung cancer and also the clinical outcomes in NSCLC patients. MtDNA content was significantly lower in patients than controls (mean=1.17 vs. 1.23, P=4.28×10−4). Compared to higher mtDNA content (above the median value in the controls), lower mtDNA content was associated with a significantly increased risk for lung cancer (OR=1.25, 95%CI=1.11-1.41, P=1.52×10−4). In the trend analysis, we detected a significant dose-response relationship between mtDNA content and risk, as lower mtDNA content was associated with a progressively increased risk for lung cancer (P-trend=1.40×10−4). In the analysis of clinical outcomes, a significant difference in mtDNA content was observed between death and survival groups (mean=1.12 vs. 1.27, P=6.62×10−4) in early stage (stage I and II) NSCLC patients. Compared to those who have higher mtDNA content, patients who have lower mtDNA content had a 45% higher risk for death (HR=1.34, 95%CI=1.05-1.71, P=0.019), and a dramatically shorter survival time (58 months vs. 96 months, log-rank P=5.68×10−4). A dose-response effect of increased risk for death was found with decreased mtDNA content (P-trend=0.048) in this group of patients. No significant results were found in advance stage (stage III and IV) patients. To our knowledge, this is the first study to evaluate the association of MtDNA copy number with lung cancer risk and clinical outcomes. Our results suggested that lower mtDNA content is associated with increased lung cancer risk and poor prognosis in early stage NSCLC patients.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 879.
Abstract 884: Enhancing cultural communication to reduce cancer disparities
Authors: Quinn Gwendolyn P. , Chavez Julio Jimenez , Simmons Vani N. , Castro Eida , Gwede Clement K. , Vadaparampil Susan T. , Antonia Teresita M. , Meade Cathy , Brandon Thomas 
Published: February 2011

Abstract
An alliance between a patient's cultural identity and a physician's cultural competency can improve patient physician communication and ultimately reduce health disparities[1]. However, communication barriers in the patient-physician relationship contribute to health disparities in the cancer care setting.[2] Providers are often unaware of their skill level and perceptions and may believe they do not need improvement. 2 This study sought to develop and evaluate a brief intervention for oncology care providers to improve cultural communication related to Hispanic patients and families. Oncologists at a major cancer center were surveyed to identify which of the nine AHRQ cultural competency techniques they desired to receive more training (n= 72). 66% selected, “I am interested in receiving information on how to communicate difficult issues such as terminal illness and controversial diagnosis, in a way that is respectful to Hispanic culture.” A workshop was held for 55 staff containing a didactic lecture from an Hispanic provider addressing culture, terminal illness, and communication strategies. A panel of interpreters, translators, and bi-lingual providers answered questions from the audience and a group discussion was held. A seven item pre-test was administered prior to the workshop, followed by a three item post-test. 62% agreed the panel discussion was helpful in developing techniques for communicating bad news to Spanish speaking patients. At baseline 20% of participants felt very comfortable with their cultural communication skills, however, only 3% felt very comfortable after attending the intervention. At pre-test 25% reported having very little knowledge about the cultural context of breaking bad news to Hispanic patients, yet at post-test 0% reported having very little knowledge. These data suggest the training was successful overall, as well as aiding in identifying providers who previously had a high level of comfort based on misperceptions of good cultural communication and through the workshop realized they needed improvement.
[1] Brach, Cindy, Fraser, Irene
Can Cultural Competency Reduce Racial And Ethnic Health Disparities? A Review And Conceptual Model
Med Care Res Rev 2000 57: 181-217
[2] Saha, Somnath, Arbelaez, Jose J., Cooper, Lisa A.
Patient-Physician Relationships and Racial Disparities in the Quality of Health Care
Am J Public Health 2003 93: 1713-1719
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 884.
Abstract 885: GSTM1 CNV and promoter SNPs are associated with REC/SPT and survival after Retinoid Acid treatment for head and neck cancer
Authors: Zhang Xuemei , Huang Maosheng , Wu Xifeng , Kadlubar Susan , Yu Xinfeng , Caldwell David , Lin Jie , Ning Baitang , Kadlubar Fred F. 
Published: February 2011

Abstract
Purpose: This study sought to determine if copy number variant (CNV) combined with other genetic variants in the glutatione S-transferase Mu class1 (GSTM1) promoter have an important impact on recurrence and overall survival in head and neck cancer patients after retinoid acid treatment. Experimental Method: This study included 441 head and neck patients treated with retinoid acid. Among these cases, 133 experienced recurrence of disease and/or a second primary tumor, while 308 have single primary disease. TaqMan real-time PCR and direct sequencing were used to determine genetic variants in GSTM1. Recurrence and secondary primary tumor (REC/SPT) were evaluated by logistic regression modeling and overall survival was estimated by Kaplan-Meier analysis using STATA. Results: Regression analysis revealed significantly decreased REC/SPT and increased overall survival in subjects with at least 2 copies of GSTM1 (OR=0.57; 95%CI=0.35-0.95) but not in those with 1 copy of the gene. Kaplan-Meier survival analysis also revealed longer overall survival in patients with at least 2 copies of GSTM1. Allele frequency analysis showed −498 C&gt;G, −426 A&gt;G, −339 C&gt;T polymorphisms were significantly associated with REC/SPT in head and neck cancer patients a(OR 0.12 (0.02-0.87), 0.30 (0.11-0.80) and 1.87 (1.00-3.51), respectively. Further survival analysis demonstrated that the −498G, −426G and −339C alleles significantly increased the overall survival in head and neck cancer subjects. Conclusion: These results suggest the GSTM1 CNV combined with single nucleotide polymorphisms is a better predictor of REC/SPT and overall survival of head and neck cancer after retinoic acid treatment than just measuring the presence/absence of GSTM1.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 885.
Abstract 892: Recurrence prediction model for early gastric cancer
Authors: Hoon Kim Joo , Kim Hyo Song , Chung Hyun Cheol , Noh Sung Hoon , Rha Sun Young 
Published: February 2011

Abstract
Recurrence Prediction Model for Early Gastric Cancer
Joo Hoon Kim, Hyo Song Kim, Kiyeol Kim, MD, 5 Ji Fu Lai, MD, Hyun Cheol Chung, MD, 2,3,4 Sung Hoon Noh, MD 1,2,3 Sun Young Rha, MD, 2,3,4
1Cancer Metastasis Research Center, 2National Biochip Research Center, 3Brain Korea 21 Project for Medical Science, 4Yonsei Cancer Center, Yonsei Cancer Research Institute, 5Department of Internal Medicine, 1 Department of Surgery, Yonsei University College of Medicine
5 Oral cancer research institute,
Purpose: Recurrence in early gastric cancer (EGC) after curative resection is rare, and in which type of EGC would recur is not well studied. We tried to make a predicting system for recurrence in EGC after curative resection.
Methods: From January 1987 to April 2005, 2923 patients with EGC underwent R0 curative resection in at Severance Hospital, Yonsei University were enrolled. Logistic regression was performed to identify independent risk factors for recurrence in EGC. Nomogram was developed on the basis of the Cox regression. The concordance index (c-index) was used for accuracy measure, with bootstrapping to correct for optimistic bias. Calibration plots were constructed.
Results: Out of enrolled 2923 patients, 79 patients were recurred (2.7%). The median time to recurrence was 20.5 months, and among them early recurrence developed within 2 years after surgery were 60.7%. In logistic results, lymph node metastasis and elevated gross type were independent risk factors for overall recurrence; whereas overall recurrence rate was higher in patients with both identified risk factors (17.5%). Meanwhile, male gender, elevated gross type and lymph node metastasis were significantly associated with early recurrence, and in patients with all identified risk factors above, the early recurrence rate was 12.2%. Nomogram for predicting the disease-free survival after curative surgery was constructed. Its c-index was 0.79 and the calibration appeared to be accurate as internal validation.
Conclusion: Recurrence in EGC after R0 resection is predictable by using common clinical characteristics. Analyzing the combination of independent risk factors, patients in high risk of early and overall recurrence could be identified. An internally validated nomogram is established to predict disease-free survival accurately and individually.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 892.
Abstract 90: Mining for cancer causing mutations in whole genome sequence data
Authors: Menzies Andrew , Stephens Philip J. , Beare David , Butler Adam , Forbes Simon , Jia Mingming , Jones David , Leroy Catherine , Marshall John , Raine Keiran , Stebbings Lucy A. , Teague Jon W. , Futreal P Andrew , Stratton Michael R. , Campbell Peter J. 
Published: February 2011

Abstract
The Cancer Genome Project at the Wellcome Trust Sanger Institute, UK is using massively parallel sequencing technologies to systematically screen exome and genome sequence for diverse categories of mutations. The rapid developments in new sequencing technologies have allowed many new approaches for the detection and characterisation of a wide range of mutation types. We employ a variety of automated and semi-automated techniques to identify and classify copy number variation, chromosomal rearrangements, small insertion/deletion and substitution mutations in both cell lines and primary tumours.
Large scale, genome wide changes are detected by mapping read-pairs to a reference genome. Copy number is assessed by taking correctly mapping read-pairs, applying a circular binary segmentation algorithm and correcting for regional mapping bias throughout the genome. Using the high quality read mappings where the paired reads are an unexpected distance apart, putative rearrangements can be identified and confirmed either by local de novo sequence assembly where high sequencing coverage is available or by capillary sequencing for low coverage data.
Smaller scale mutations are detected using local read coverage to provide detailed information on the genotype and allelic content of samples. The detection techniques can be used on both whole genome and exome pull-down sequence data. Substitutions are detected using a novel algorithm based on expectation maximisation (Calculate Variants with Expectation Maximisation using New sequencing technology, or CaVEMaN) written in-house and confirmed using capillary sequencing.
Putative mutations of all types are compared to external resources (eg Ensembl, dbSNP) to infer genomic context and possible deleterious consequences. In-house tools have been developed to help automate the curation and annotation of mutations and once confirmed they are submitted to COSMIC as gene associated mutations, small scale intragenic mutations, chromosomal rearrangements or fusion gene products.
Reference URL's
Wellcome Trust Sanger Institute - http://www.sanger.ac.uk
COSMIC - http://www.sanger.ac.uk/genetics/CGP/cosmic
CGP - http://www.sanger.ac.uk/genetics/CGP/
Ensembl - http://www.ensembl.org
dbSNP - http://www.ncbi.nlm.nih.gov/projects/SNP
Note: This abstract was not presented at the AACR 101st Annual Meeting 2010 because the presenter was unable to attend.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 90.
Abstract 900: Associations between orotate phosphoribosyl transferase polymorphism and survival in patients with colorectal cancer treated with 5-FU-based adjuvant chemotherapy: A thirteen year follow-up study
Authors: Lai Ching-Yu , Chang Shih-Ni , Sung Fung-Chang , Hsieh Ling-Ling , Tang Reiping , Yeh Chih-Ching 
Published: February 2011

Abstract
Introduction: 5-Fluorouracil (5-FU) is one of the first line anti-cancer drugs used in the chemotherapy for colorectal cancer (CRC) in older to raise survival rate. Orotate phosphoribosyl transferase (OPRT) plays an important role to regulate the 5-FU activity. This study examined the association between OPRT polymorphism and overall survival of CRC patients treated with 5-FU-based chemotherapy.
Method: A total of 532 patients diagnosed with CRC and received 5-FU-based chemotherapy after surgery between 1995 January and 2001 December was included in the present study. We genotyped the OPRT G638C (Gly213Ala) polymorphism using the polymerase chain reaction combined with the restriction fragment length polymorphism analysis (PCR-RFLP). Survival analyses on OPRT polymorphism were displayed with Kaplan-Meier curves and performed with log-rank test. The association between OPRT genotypes and survival was analyzed using Cox proportional hazard models.
Results: There were no significantly genetic effects on overall survival, even the adjustment for age, gender, or tumor stage in the Cox proportional hazard models. However, the Kaplan-Meier curves showed that stage II and III CRC patients with OPRT G/G genotype had a significantly poor survival (log-rank p = 0.02). Compared to the OPRT G/G genotype, the OPRT G/C + C/C genotype was significantly associated with better overall survival (Hazard ratio (HR) = 0.64, 95% CI = 0.43 − 0.96).
Conclusion: Our findings suggest that the OPRT polymorphism may modify drugs activity to serve a prognostic predictor for CRC patients who receive 5-FU-based chemotherapy.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 900.
Abstract 907: Subtypes, race and long-term survival in the Carolina Breast Cancer Study
Authors: O'Brien Katie M. , Millikan Robert C. , Cole Stephen R. 
Published: February 2011

Abstract
Previous analyses from the Carolina Breast Cancer Study identified significant differences in breast cancer (BC) specific mortality across the four ‘intrinsic’ BC subtypes: luminal A, luminal B, basal-like, and human epidermal growth factor receptor 2 positive / estrogen receptor negative (HER2+/ER-). Here, we expand the assessment by including additional cases and longer follow-up time, and present analyses stratified by race and menopausal status. We used immunohistochemical markers to subtype 1149 invasive BC cases (518 Black, 631 Non-black) in this population-based epidemiologic study of women diagnosed with BC in North Carolina between 1993 and 2001. Vital status was determined through 2006 using the National Death Index, with median follow-up of 9.1 years. Hazard ratios (HRs) were estimated using Cox proportional hazards models for BC-specific mortality. Compared to Luminal A, women with HER2+/ER- BC had the highest mortality (HR=2.3, 95% CI: 1.5, 3.6, adjusting for age at diagnosis, race, and year of diagnosis), followed by basal-like BC (HR=1.7, 95% CI: 1.2, 2.4). Differences in mortality by subtype remained, albeit attenuated, after further adjustment for stage at diagnosis. Race-stratified HRs were similar for HER2+/ER- BC (HR=2.4, 95% CI: 1.2, 4.7 and HR=2.3, 95% CI: 1.3, 4.0 for non-Blacks and Blacks, respectively), but appeared to differ for basal-like BC (HR=2.0, 95% CI: 1.2, 3.4 for non-Blacks and HR=1.5, 95% CI: 1.0, 2.4 for Blacks). For basal-like BC, mortality was slightly higher among premenopausal, non-Black women (HR=1.8, 95% CI: 1.0, 3.4) compared to premenopausal Black women (HR=1.3, 95% CI: 0.8, 2.3). HRs for basal-like versus Luminal A BC were highest among postmenopausal women (HR=3.9, 95% CI: 1.5, 10.0 for non-Blacks; HR=1.9, 95% CI: 0.9, 3.8 for Blacks). Stage, tumor size and lymph node status were associated with mortality in all subtypes. We also used flexible models to permit departures from the proportional hazards assumption and therefore allow HRs for BC to vary over time since diagnosis. In summary, these results confirmed previous analyses that during a time interval prior to the introduction of Herceptin®, HER2+/ER- cases exhibited the highest mortality of the four subtypes. Possible racial differences in mortality were observed according to BC subtype. Additional analyses are needed in populations with known treatment profiles to more fully understand the role of intrinsic subtypes and race in BC survival.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 907.