bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract B129: Use of white blood cell growth factors and risk of acute myeloid leukemia or myelodysplastic syndrome among elderly non-Hodgkin's lymphoma patients
Authors: Gruschkus Stephen K. , Lairson David R. , Dunn J. Kay , Risser Jan M.H. , Du Xianglin 
Published: May 2012

Abstract
Therapy-related myelodysplastic syndromes and acute myeloid leukemia (t-MDS/AML), defined as MDS or AML occurring after myelosuppressive chemotherapy and/or radiation therapy, are devastating long-term complications of cancer therapy. White blood cell growth factors (CSFs) are supportive care agents intended to minimize risk of febrile neutropenia in patients receiving chemotherapy. However, evidence suggests that CSFs may increase risk of t-MDS/AML, possibly due to the observation that CSFs not only stimulate the proliferation and differentiation of hematopoietic stem cells, but also interfere with apoptosis. The purpose of this study was to evaluate the association between CSF use and t-MDS/AML among a large population-based cohort of elderly non-Hodgkin's lymphoma (NHL) patients treated with chemotherapy.
We identified 13,203 NHL patients from the Surveillance, Epidemiology, and End Results (SEER)-Medicare database diagnosed from 1992 to 2002 who received chemotherapy within 12 months of diagnosis. Patients were followed from their initial chemotherapy date until t-MDS/AML development, death, or end of study period (October 31, 2006). Overall, 40% (n=5,266) of patients received CSF. A total of 272 (5.2%) of patients receiving CSF developed t-MDS/AML vs. 230 (2.9%) who did not receive CSF: there was a statistically significant higher incidence of t-MDS/AML among patients receiving CSF compared to patients not receiving CSF (log-rank p&lt;0.0001). In a multivariable Cox regression analysis adjusting for gender, histology, stage, comorbidities, chemotherapy dates, and chemotherapy agent, CSF use was independently associated with a 53% increased risk of t-MDS/AML (HR 1.53; 95% CI 1.26 – 1.84). A dose-response relationship was observed, with t-MDS/AML risk increasing by quartile of CSF claims. In an evaluation of plausible biologic interactions, we found that patients who received both CSF and antimetabolite chemotherapy had a 2.5 fold increased risk of t-MDS/AML (HR 2.49; 95% CI 1.91 – 3.26) vs. patients who received neither agent (p-interaction=0.04). This observation has added clinical significance considering that approximately 10% of the overall population received this therapeutic combination.
To our knowledge, this is the first large population-based study to evaluate the association between CSF use and t-MDS/AML risk among NHL patients. Findings support our hypothesis that the administration of CSF among elderly NHL patients receiving chemotherapy may increase the risk of t-MDS/AML, even though the absolute risk is low in these populations. Future studies are necessary to verify these results and to determine the potential clinical implications of the observed interaction between CSF use and antimetabolite chemotherapy.
Citation Information: Cancer Prev Res 2010;3(1 Suppl):B129.
Abstract B134: Tubal ligation and ovarian cancer: A meta-analysis
Authors: Rice Megan , Hankinson Sue , Tworoger Shelley 
Published: May 2012

Abstract
Background: While several studies have reported varying associations between tubal ligation and ovarian cancer, no recent meta-analysis has been conducted. In addition, past meta-analyses have not examined whether study factors, such as study design, or individual factors, such as age at procedure, modify the relationship between ovarian cancer and tubal ligation.
Methods: We sought to identify all English-language articles in the PubMed database with quantitative data on the effect of tubal ligation and ovarian cancer using the keywords “ovarian cancer” and “tubal ligation” or “tubal sterilization”. We identified 21 articles which provided estimates of the risk of ovarian cancer in relation to tubal ligation and six articles which reported stratum-specific estimates of ovarian cancer risk by age at and years since tubal ligation. The summary relative risk (RR) estimate and the 95% confidence interval (CI) for the summary estimate were calculated using a random-effects model. Tests for homogeneity were used to evaluate the consistency of findings among studies, and Begg's and Egger's tests were used to assess publication bias.
Results: The RRs for ovarian cancer comparing women who had a tubal ligation to those who did not ranged from 0.20 to 2.40 across the studies. The summary RR was 0.68 (95% CI: 0.62–0.75), demonstrating a statistically significant protective effect of tubal ligation on ovarian cancer. We found no evidence of heterogeneity by study design (e.g., cohort versus case-control) or residence of participants (United States vs. non-United States) as well as no evidence of publication bias. In secondary analyses based on four studies, we did not detect a difference in the risk of ovarian cancer between women who had a tubal ligation less than 20 years ago versus 20 or more years ago (p for heterogeneity = 0.65). Similarly, we did not detect effect modification by age (&lt;35 years of age, &gt;35 years of age) at tubal ligation (p for heterogeneity = 0.92). Though data were insufficient to calculate summary RRs by histologic subtype, a qualitative examination of study results demonstrated a stronger protective effect of tubal ligation for endometroid tumors.
Conclusions: Observational epidemiologic evidence strongly suggests that there is a decreased risk of ovarian cancer among women who have had a tubal ligation. We found a 30 percent reduction in ovarian cancer among women who had ever had a tubal ligation compared to women who have never had a tubal ligation. This estimate did not vary by study design or residence of participants. In addition, we did not detect any effect modification by age at tubal ligation or years since tubal ligation. While there is some evidence that the effect of tubal ligation varies by histologic subtype, further research is needed in this area.
Citation Information: Cancer Prev Res 2010;3(1 Suppl):B134.
Abstract B140: Exposure and the risk of pancreatic cancer: Results of the Netherlands Cohort Study
Authors: Heinen Mirjam M. , Verhage Bas A.J. , Goldbohm R. Alexandra , van den Brandt Piet A. 
Published: May 2012

Abstract
Objective: We examined the role of active cigarette smoking, smoking cessation, and environmental tobacco smoking (ETS) as determinants for pancreatic cancer in a large prospective cohort study.
Methods: The Netherlands Cohort Study consisted of 120,852 men and women who completed a baseline questionnaire in 1986. After 16.3 years of follow-up, 520 pancreatic cancer cases were available for analysis.
Results: Compared to never cigarette smokers, both former and current cigarette smokers had an increased pancreatic cancer risk (multivariable-adjusted hazard rate ratio (HR) = 1.34; 95% confidence interval (CI) = 1.02–1.75 and HR = 1.82; 95% CI = 1.40–2.38, respectively). We observed an increased pancreatic cancer risk of 38% (95% CI = 1.01–1.87) with smoking ≥20 cigarettes per day compared to never cigarette smoking. The trend test was significant (P = 0.03), but no clear dose-response relation was present. For duration of smoking, we observed an increased pancreatic cancer risk per increment of 10 years (multivariable-adjusted HR = 1.15; 95% CI = 1.08–1.22), with a clear dose response effect observing a 2-fold increased cancer risk comparing ≥40 years of smoking to never cigarette smoking. Quitting smoking gradually reduced the risk of pancreatic cancer (HR = 1.83, 1.41, and 1.42 for currents smokers, ex-smokers quitted 0.1–&lt;10 yrs, and quitted 10–&lt;20 yrs, respectively) and reached unity after ≥20 years of quitting smoking (multivariable-adjusted HR = 1.17; 95% CI=0.80–1.70). Based on the current study, hypothetically 27% (95% CI = 15–37) of pancreatic cancer cases could be prevented if people would not smoke. We investigated which smoking aspect was most important in pancreatic cancer etiology by including smoking variables simultaneously in the model. Only duration remained significantly associated with pancreatic cancer risk (≥40 years of smoking vs. never cigarette smokers, multivariable-adjusted HR = 1.87; 95% CI = 1.24–2.80); the risk estimates of other smoking variables attenuated and became non-significant. When we investigated the interaction between ethanol intake and cigarette smoking, no significant interaction was found (P = 0.97). However, current smokers who consumed ≥30 g of ethanol daily experienced a significantly increased risk compared to abstainers who never smoked (multivariable-adjusted HR = 2.40; 95% CI = 1.06–5.41). No association was observed for ETS and pancreatic cancer risk in women.
Conclusion: Overall, our findings confirmed that cigarette smoking is an important risk factor for pancreatic cancer, while quitting smoking reduced risk. Therefore from a public health perspective, quitting smoking would benefit the burden on pancreatic cancer incidence and mortality. No association was observed between ETS and pancreatic cancer.
Citation Information: Cancer Prev Res 2010;3(1 Suppl):B140.
Abstract B29: African American men never or rarely screened for prostate cancer
Authors: Williams-Brown Shanita D. , Ross Louie E. , Hinton Lisa 
Published: May 2012

Abstract
Introduction: Prostate cancer is the leading cancer and the second leading cause of cancer deaths among men in the United States. African American (AA) men are at greater risk than Caucasian American (CA) and other men in both incidence and mortality related to prostate cancer. Incidence among AA men is about 60 percent greater and mortality about 240 percent greater than in CA men. AA men also have a greater likelihood of presenting at higher stage and grade with poorer health and other outcomes. Little is known about factors related to AA men who never or are rarely screened for prostate cancer using the DRE and PSA tests. The purpose of this study was to explore prostate cancer screening practices of AA men and to examine demographic characteristics that are associated with AA men who never or are rarely screened.
Methods: AA men age 40 or older were asked questions about their knowledge, awareness, and attitudes regarding prostate cancer and prostate cancer screening using DRE and PSA. The study used a convenience sample of 448 AA men 40 years and older residing in the Southeastern U.S. Data were self-reported survey responses and analyzed using SAS.
Results: The majority of study participants were married (52%), had some college or technical training (78%), and employed (59%). Over 90% of the AA men had prior knowledge of DRE and 77% were aware of the PSA test. The percentage of AA men who had not had prostate cancer screening in over 5 years or not at all (never or rarely screened) was 33% for DRE and 34% for PSA. Demographic factors related to never or rarely screened for DRE were: being single, younger age, no health insurance, and higher levels of education. Factors related to never or rarely screened for PSA were: younger age, no health insurance, and higher levels of education.
Conclusions: Since AA men have greater burden of prostate cancer among men, it is surprising that despite knowledge and awareness of screening and increased levels of education, approximately one-third of the men in this sample had neither a DRE or PSA ever or in 5 or more years. Additional studies are needed to further explore the relationship between prostate cancer knowledge and awareness, education attainment, and prostate cancer screening in AA men.
Citation Information: Cancer Prev Res 2010;3(1 Suppl):B29.
Abstract B5: Psychosocial mechanisms for explaining the relationship between physical activity and fatigue in breast cancer survivors
Authors: White Siobhan M. , McAuley Edward , Rogers Laura Q. , Courneya Kerry S. 
Published: May 2012

Abstract
Fatigue is one of the most commonly reported and enduring symptoms experienced as a result of breast cancer treatment. One important behavior that has been identified as having the potential to reduce breast cancer related fatigue is physical activity. However, few attempts have been made to fully understand this relationship and it is not known whether physical activity directly influences fatigue or operates through other factors. The purpose of this study was to examine the role of psychosocial mechanisms, self-efficacy and depression, as potential pathways from physical activity to fatigue in a cross-sectional sample of breast cancer survivors (N=192). Participants completed measures of health status, physical activity, depression, fatigue, and self-efficacy. Data were analyzed using path analysis within a covariance modeling framework. This model proposed that that physical activity's influence on fatigue is indirect through its direct effect on self-efficacy which, in turn, has both a direct effect on fatigue and an indirect effect through depression. The hypothesized path model provided an excellent fit to the data (Ξ2 = 1.48, df = 2, p =.48; SRMR = 0.02, CFI = 1.00). All of the proposed path coefficients of the hypothesized model were significant. Overall, the model accounted for 45.2% of the variation in fatigue. As a result of the robust relationship between fatigue and depression (β =.51), the analysis was re-run using a depression score which excluded items assessing “somatic and retarded activity” symptoms. The fit of the model was almost identical to the previously described model (Ξ2 = 1.48, df = 2, p =.45; SRMR = 0.03, CFI = 1.00). A final analysis was conducted on the original model to test effects of for demographics (i.e., age, education, employment, income), time since diagnosis, breast cancer stage, current treatment, menopausal status, body mass index, and comorbidities on model fit and path coefficients, as well as the model components themselves. This model also was an excellent fit to the data (Ξ2 = 2.10, df = 2, p =.35; SRMR = 0.01, CFI = 1.00). In general, the magnitude and direction of the hypothesized relationships were unaffected by the inclusion of the covariates in the model. Our findings suggest support for one set of psychosocial pathways from physical activity to fatigue, an important concern in breast cancer survivors. Subsequent work might replicate such associations in other survivor populations and attempt to determine whether model relations change with physical activity interventions, and the extent to which other known correlates of fatigue such as impaired sleep and inflammation can be incorporated into this model.
Citation Information: Cancer Prev Res 2010;3(1 Suppl):B5.
Abstract B54: The anticancer effects of calorie restriction on MC38 colon tumors are associated with decreased macrophage infiltration
Authors: Harvey Alison E. , Otto Glen , Nunez Nomeli P. , Perkins Susan N. , Hursting Stephen D. 
Published: May 2012

Abstract
Obesity is a risk factor for a number of chronic diseases including many types of cancer. The chronic, low-grade inflammation that develops as a result of obesity may be a primary mechanistic target underlying obesity-associated carcinogenesis. While the link between obesity and inflammation is not well understood, increases in adipose tissue macrophages may perpetuate and exacerbate a chronic inflammatory environment through production of inflammatory cytokines such as interleukin (IL)-6. In this study we tested the hypothesis that macrophage infiltration underlies our previously observed anticancer effects of calorie restriction (CR) in a mouse model of colon cancer. Six-week-old female C57BL/6 mice (n=30 per diet) were singly housed and randomized to either a control diet consumed ad libitum (which results in an overweight phenotype) or a 30% calorie-restricted diet regimen (CR) for 22 weeks, at which time 15 mice per group were euthanized and adiposity was measured using dual-energy X-ray absorptiometry (DXA). The remaining 15 mice/diet were then injected subcutaneously (flank) with 50,000 syngeneic mouse colon (MC)-38-adenocarcinoma cells and continued on their diet regimens while tumor growth was monitored for an additional 5 weeks. Excised tumors underwent histological analysis of macrophage infiltration (hematoxylin and eosin staining) and real-time RT-PCR analyses of macrophage (F4/80 and S100A9) and IL-6 gene expression. CR mice had lower body weight (20.3g +/− 0.2 vs. 26.0g +/− 0.5 (mean +/− SEM), p&lt;0.05) and body adiposity (22.9% +/− 1.2 vs. 29% +/− 1.7, p&lt;0.05) after 21 weeks on study compared to control mice. Additionally, CR mice had smaller tumors (100.3 mm^3 +/− 13.2 vs. 242.4 mm^3 +/− 28.3, p&lt;0.05) relative to controls. Tumors from CR mice, relative to controls, exhibited a 3-fold decrease in F4/80 and S100A9 gene expression and a 2.5 fold decrease in IL-6 (p&lt;0.05). Furthermore, HandE staining showed reduced macrophage infiltration in CR tumors compared to control tumors. These findings suggest that the inhibitory effects of CR on MC38 colon tumor growth are associated with reduced tumor infiltration of macrophages, which may lead to new targets for the prevention of colon cancer.
Citation Information: Cancer Prev Res 2010;3(1 Suppl):B54.
Abstract B6: Obesity risk in relation to quality of life: Baseline results from a worksite trial
Authors: Whisnant Stephanie , Beresford Shirley A.A. , Henderson Jo A. , McTiernan Anne , Xiao Liren , Patrick Donald L. , Wang C.Y. 
Published: May 2012

Abstract
Introduction: Obesity, a risk factor for certain cancers, can also be related to reduced health-related quality of life and productivity. We examined eating physical activity behaviors, and body mass index (BMI), as predictors of health-related quality of life and productivity.
Methods: MOVE ‘M is a worksite-randomized trial targeting diet and physical activity to reduce weight gain. Secondary outcomes include Obesity and Weight Loss Quality of Life (OWLQOL) and productivity. Baseline data collection occurred from 2006–2008, and data were analyzed in 2009.
Results: Baseline data were analyzed for individual-level associations using linear mixed models. Since gender was found to be an effect modifier, data were analyzed separately for men (n=288) and women (n=281). BMI was negatively associated with OWLQOL in both women (p&lt;0.001) and men (p&lt;0.001). The linear effect estimate for OWLQOL score associated with one category increase in BMI was 32% (95% CI: 27%, 37%) for women and 12% (95% CI: 8%, 17%) for men. Physical activity was associated (p=0.007) with OWLQOL only in women. Eating while doing another activity was negatively associated with OWLQOL scores only in men (p=0.0003) and with productivity only in women (p=0.004).
Conclusion: Our results suggest obese persons, particularly women, experience diminished OWLQOL. If longitudinal analyses confirm these findings, there may be additional work-related and general health benefits from reducing weight and increasing physical activity.
Citation Information: Cancer Prev Res 2010;3(1 Suppl):B6.
Abstract B61: Ha-RAS mutations in fibroblast of the cervical stroma of squamous neoplasias of the uterine cervix
Authors: Moreno-Acosta Pablo , Serrano Martha , Carrillo Schyrly , Nuñez, Diana , Romero-Rojas Alfredo 
Published: May 2012

Abstract
The stroma is maintained, renovated, and repaired by resident fibroblasts, supports and instructs the epithelium, and is essential for epithelial function. Now recognized that stromal changes are necessary for the establishment of cancer and previously considered as a spectator in front of the clonal expansion and acquisition of malignant characteristics of tumor cells. Most studies on the stroma and t its relationship with the generation, progression and metastasis of cancer in which involve multiple steps of tumorigenesis and the microenvironment, have focused especially on cancers such as breast and others as cancer of prostate, gastric, colorectal and cervical cancer. Reports of cervical cancer specifically address issues such as clonality and genomic features in cervical carcinogenesis. However, the presence of mutations Ha-RAS oncogen in stromal cells and their contribution to the generation and progression of cervical squamous neoplasia has not yet been reported. The aim of this study was detect and determine the frequency of mutations Ha-RAS in stromal fibroblasts from biopsies of the transformation zone of the uterine cervix. We selected eight samples of fresh frozen tissue of patients diagnosed with cervical intraepithelial neoplasia squamous (CIN I, CIN II, CIN III), cancer in situ and invasive squamous cell carcinoma, tissue in which it was represented only the stroma, without evidence of residual tumoral epithelial component, and each of whom had cervical tissue in paraffin-embedded control confirming the presence of cervical squamous neoplasia. The detection of Ha-ras mutations in codon 12 was performed using a nonradioactive PCR-SSCP and restriction enzyme analysis. The mutation found for a substitution of a glycine by a valine at codon 12 of Ha-RAS was detected in alone sample (12.5%), CIN III. The non-detection of the GTC mutation in the remaining seven samples could be due to somatic mutation that this represented only a small fraction (approximately 15%) of total DNA analyzed (33), as well as a topographical heterogeneity likely distribution of these mutations. The presence of a point mutation of Ha-RAS oncogene in the stroma of one case studied, represents an important change, this mutation prevents the conversion of active to inactive form, and suggest an alternative pathway involving stromal genetic instability in the generation of intraepithelial neoplasia and progression of the cervical cancer.
Citation Information: Cancer Prev Res 2010;3(1 Suppl):B61.