bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract B37: Negative affect and fruit/vegetable consumption: The nature of the relation differs by race/ethnicity
Authors: Kiviniemi MarcT. , Orom Heather , Giovino Gary A. 
Published: December 2010

Abstract
Dietary practices, including low fruit and vegetable consumption, are associated with risk for multiple cancers. Some work has shown that negative affectivity is associated with lower fruit and vegetable consumption. Previous work from our lab has shown that smoking behavior is differently associated with negative affectivity as a function of race/ethnicity. Given this evidence, it is plausible that the relationship between negative affectivity and fruit/vegetable consumption might also differ by race. To examine this question, data from the National Cancer Institute's Health Information National Trends Survey (HINTS) were used. Respondents reported current negative affect, daily fruit and vegetable consumption, and race. Linear regression analyses examined race, negative affect, and their interaction as predictors of fruit/vegetable consumption. Race analyses compared White (n=5445) to Black (n=687) respondents. Analyses controlled for demographics and were run in STATA10 using complex survey design techniques to account for the HINTS sampling design. For the overall sample, there was a significant relation between negative affect and fruit/vegetable consumption; r=-.15, p &lt; .05. However, this effect was qualified by a marginally significant race x negative affect interaction; f=1.74, p=0.08. When examined separately by race, the relation of negative affectivity to behavior was significant for White (f=2.73, p &lt; .05) but not Black respondents (f &lt; 1, ns). These findings indicate that the relation of negative affect to fruit/vegetable consumption may differ by race/ethnicity and may be more applicable to White individuals. This has implications for understanding factors that influence dietary behavior and for developing intervention strategies to address diet for members of racial/ethnic minority groups.
Citation Information: Cancer Epidemiol Biomarkers Prev 2010;19(10 Suppl):B37.
Abstract B46: Fear as a barrier to mammography for African American women
Authors: Hatcher Jennifer 
Published: December 2010

Abstract
Screening mammography is the single most effective method of early detection of breast cancer however mammography rates in America remain suboptimal among certain groups of women. African American women are one of those groups, experiencing high mortality rates and low rates of screening as compared to other ethnic groups. One of the factors related to inadequate screening is fear. Fear has been associated with participation in screening, however it is a concept that has been poorly explored within the context of culture. This report examined how African American women, who had been seen in the emergency department for non urgent complaints, describe their fear and its impact on their breast cancer screening patterns. Semi-structured interviews were used to gather data from 35 African American women, both screened and unscreened, between 2008 and 2010. Interview transcripts were analyzed and recurrent themes and patterns were identified. Most women expressed fear regarding cancer screening in some way, either fear of pain, fear of the unknown, or fear of finding out that something is wrong. This fear could be either a motivator or a barrier to mammography. This report illuminates that fear in the context of the other barriers and benefits to mammography experienced by these women. These findings will be important in the design of culturally relevant interventions that address the ongoing issue of inadequate screening mammography among African American women.
Citation Information: Cancer Epidemiol Biomarkers Prev 2010;19(10 Suppl):B46.
Abstract B54: Pregnancy and postpartum involution promote tumorigenesis in a preclinical model for triple negative/basal breast cancer
Authors: Russell Tanya D. , Fornetti Jaime , Schedin Pepper 
Published: December 2010

Abstract
Young African American women have an increased risk of developing and dying from “triple negative/basal breast cancer” compared to young Caucasian women, but the reason for this is unknown. Insight into this problem may be elucidated by the fact that breast cancers associated with a recent pregnancy are more likely to be metastatic. For all women, having had a recent pregnancy is an independent risk factor for poor prognosis. Epidemiologic data shows increased risk of triple negative/basal breast cancer with increased childbearing in African American women (Millikan et al 2008). We speculate that the hormones of pregnancy combined with the tissue-remodeling of the post-partum breast back to its pre-pregnant state (a normal process called postpartum involution that occurs after childbirth in the absence of breastfeeding, or at weaning in women who breastfeed) provides a two-hit tumor promotional tissue environment that results in increased metastasis of these tumors. Using an innovative, intraductal preclinical model developed in our laboratory, we tested whether a triple negative/basal breast cancer cell line (MCF10ADCIS.com) is promoted by pregnancy or postpartum involution. When these cells are injected into mammary ducts of nulliparous female mice, there is evidence of tumor progression from hyperplastic alveolar nodules to ductal carcinoma in situ to local invasion that is accompanied by progressive loss of the protective myoepithelial cell layer. Further, tumor burden in pregnancy and postpartum involution is much greater than their respective nulliparous controls. Importantly, with pregnancy and postpartum involution the protective myoepithelial cell layer surrounding tumors is compromised at earlier stages than in nulliparous controls. Physiologic changes to adherens junctions and myoepithelial cells occur during normal pregnancy and post-partum involution, respectively. These data suggest that the physiological environments of pregnant and involuting glands promote tumor progression and begin to unfold the biological mechanisms for the effects of parity on aggressive breast cancers.
Citation Information: Cancer Epidemiol Biomarkers Prev 2010;19(10 Suppl):B54.
Abstract B61: Phospholipid scramblase is a critical mediator of estrogen-induced apoptosis in antihormone resistant breast cancer cells
Authors: Lewis-Wambi Joan S. , King Tabitha , Smith Annalese 
Published: December 2010

Abstract
Phospholipid scramblase 1 (PLSCR1) is a mutiply palmitoylated protein which is localized in either the cell membrane or nucleus depending on its palmitoylated state and is responsible for the translocation of phospholipids between the two monolayers of a lipid bilayer of a cell membrane in a calcium (Ca2+)-dependent manner. There is evidence that PLSCR1 plays a role in cell signaling and apoptosis. In the present study, we investigated the functions of PLSCR1 in hormone-sensitive MCF-7 and T47D breast cancer cells versus antihormone-resistant MCF-7:5C and MCF-7:2A cells. We found that PLSCR1 protein and mRNA levels were dramatically increased in MCF-7:5C and MCF-7:2A cells compared to parental MCF-7 and T47D cells and suppression of PLSCR1 in these cells using small interfering RNA (siRNA) reduced their growth rate and altered their morphology to become more differentiated and spindle-shaped. Suppression of PLSCR1 also completely blocked estrogen-induced apoptosis in MCF-7:5C cells. Furthermore, we found that stable expression of PLSCR1 in MCF-7 cells enhanced their sensitivity to etoposide-induced apoptosis and that treatment of these cells with interferon-alpha 2 (IFN- 2) resulted in cell cycle arrest. Overall, these data show that PLSCR1 is overexpressed in antihormone-resistant breast cancer cells and they suggest that PLSCR1 plays an important role in sensitizing these cells to estrogen-induced apoptosis. These data also shed new insights into the biological and biochemical functions of PLSCR1 in breast cancer.
Citation Information: Cancer Epidemiol Biomarkers Prev 2010;19(10 Suppl):B61.
Abstract B63: Unraveling the paradoxes of ATM resensitized dynamics in LNCaP cell line via epigallocatechin-3-gallate (EGCG)
Authors: Farooqi Ammad A. , Bhatti Shahzad 
Published: December 2010

Abstract
Epigallocatechin-3-gallate (EGCG) is a major ingredient of green tea (GT) and Silibinin, the active component of Silymarin presumably hold a potential to prevent pathogenomics. Prostate cancer aggressiveness is triggered by fusion transcripts formed because of genomic instability induced by juxtapositioning of two genes. An abolished ATM dynamics is incapable of safeguarding integrity of DNA. In agreement with this assumption ATM and DNA PK were impaired in LNCaP cell line to confirm a tight interaction of ATM and DNA PK with the expression profile of TMPRSS2-ERG. Abolished ATM proved instrumental to expression of the fusion transcript. Similarly blunting of DNA PK downregulated the expression of the fusion transcript giving a notion that it is involved in the chromosomal translocation. LNCaP cell lines were analyzed for the effect of EGCG and silibinin on the expression profile of TMPRSS2-ERG. In this particular unprecedented study treatment of the LNCaP cell line with EGCG and Silibilin recapitulated ATM expression and activity and downregulated the fusion transcript generation. These results underscore the therapeutic effect of EGCG and SB in attenuating the exacerbation of the disease.
Citation Information: Cancer Epidemiol Biomarkers Prev 2010;19(10 Suppl):B63.
Abstract B96: Increasing access and utilization of supportive cancer care activities through health information technology: A prostate cancer example
Authors: Victorson David , Block Phoebe , Buono Sarah , Mason Thomas , Thomas Pete , Murray Marcus 
Published: December 2010

Abstract
Background: Prostate cancer (PCa) is a leading cause of cancer death in the United States, and certain racial/ethnic groups, such as African American men, are disproportionately affected. Treatment for clinically localized PCa can cause physical and functional problems like bowel, urinary and sexual dysfunction, as well as emotional symptoms such as anxiety, uncertainty and fear. Although not entirely avoidable, many of these negative aftereffects may be prevented or lessened through patient initiated behaviors. Symptom monitoring and self management (SMSM) support programs may increase access and utilization of needed supportive care and help men gain a greater sense of personal efficacy to address some of the associated difficulties of PCa.
Objective: To present patient focus group and expert survey findings that are the basis of a novel information technology-based application to increase access and utilization of self-care and symptom management in clinically localized PCa.
Study Design: We are currently developing culturally tailored multimedia-assisted self management interventions for bowel, urinary, sexual and anxiety domains based on a literature review, expert survey and patient focus groups. We are also using patient reported outcome measures of bowel, urinary and sexual function and anxiety for weekly symptom monitoring activity. Following this first study phase, we will beta test this system with a diverse sample of community end-users and pilot the new system in medical and community clinics with men representing primary PCa treatment approaches for localized disease (n=100). Over a 4 week period, participants will receive a weekly email with a link to complete brief self report questions on treatment side effects and disease symptoms. When a patient's scores surpass a designated severity cut-point in a given area, a multimedia-assisted self management intervention will be triggered. Participants will be able to read, listen to or watch interventions in real time or download them for later use.
Cancer Disparities Relevance: The proposed work can benefit men diagnosed with PCa gain increased access to utilization of important supportive care services though leveraging an innovative, culturally tailored information technology application. This study will offer new information on the feasibility, acceptance, and preliminary effectiveness of a patient-centered, internet-based system to provide real-time SMSM support during and following treatment.
Citation Information: Cancer Epidemiol Biomarkers Prev 2010;19(10 Suppl):B96.
Suppression of Signal Transducer and Activator of Transcription 3 Activation by Butein Inhibits Growth of Human Hepatocellular Carcinoma In Vivo
Authors: Rajendran Peramaiyan , Ong Tina H. , Chen Luxi , Li Feng , Shanmugam Muthu K. , Vali Shireen , Abbasi Taher , Kapoor Shweta , Sharma Ashish , Kumar Alan Prem , Hui Kam M. , Sethi Gautam 
Published: December 2010

Abstract
Purpose: Hepatocellular carcinoma (HCC) is the fifth most common malignancy worldwide and the third cause of global cancer mortality. Increasing evidence suggest that STAT3 is a critical mediator of oncogenic signaling in HCC and controls the expression of several genes involved in proliferation, survival, metastasis, and angiogenesis. Thus, the novel agents that can suppress STAT3 activation have potential for both prevention and treatment of HCC.
Experimental Design: The effect of butein on STAT3 activation, associated protein kinases, STAT3-regulated gene products, cellular proliferation, and apoptosis was investigated. The in vivo effect of butein on the growth of human HCC xenograft tumors in male athymic nu/nu mice was also examined.
Results: We tested an agent, butein, for its ability to suppress STAT3 activation in HCC cells and nude mice model along with prospectively testing the hypothesis of STAT3 inhibition in a virtual predictive functional proteomics tumor pathway technology platform. We found that butein inhibited both constitutive and inducible STAT3 activation in HCC cells. The suppression was mediated through the inhibition of activation of upstream kinases c-Src and Janus-activated kinase 2. Butein inhibited proliferation and significantly potentiated the apoptotic effects of paclitaxel and doxorubicin in HCC cells. When administered intraperitoneally, butein inhibited the growth of human HCC xenograft tumors in male athymic nu/nu mice.
Conclusions: Overall, cumulative results from experimental and predictive studies suggest that butein exerts its antiproliferative and proapoptotic effects through suppression of STAT3 signaling in HCC both in vitro and in vivo. Clin Cancer Res; 17(6); 1425–39. ©2010 AACR.
Phase I Safety, Pharmacokinetic, and Pharmacodynamic Study of ENMD-2076, a Novel Angiogenic and Aurora Kinase Inhibitor,in Patients with Advanced Solid Tumors
Authors: Diamond Jennifer R. , Bastos Bruno R. , Hansen Ryan J. , Gustafson Daniel L. , Eckhardt S. Gail , Kwak Eunice L. , Pandya Shuchi S. , Fletcher Graham C. , Pitts Todd M. , Kulikowski Gillian N. , Morrow Mark , Arnott Jamie , Bray Mark R. , Sidor Carolyn , Messersmith Wells , Shapiro Geoffrey I. 
Published: December 2010

Abstract
Purpose: ENMD-2076 is a unique orally bioavailable Aurora kinase and VEGFR inhibitor. The purpose of this phase 1 study of ENMD-2076 was to determine the MTD, pharmacokinetic, and pharmacodynamic profiles and preliminary antitumor activity.
Experimental Design: Patients with refractory advanced solid malignancies were treated with ENMD-2076 orally with continuous once daily dosing. Doses from 60 to 200 mg/m2 were evaluated using a standard 3 (to 4) + 3 design. Pharmacokinetic parameters were studied on days 1, 28, and 30 to 35 of cycle 1. Expanded MTD cohorts included patients with ovarian cancer, colorectal cancer, and refractory solid tumors.
Results: A total of 67 patients (46 F, 21M; ages 30–76) entered the study. Dose levels of 60, 80, 120, 200, and 160 mg/m2 were evaluated. Two patients experienced grade 3 hypertension at 200 mg/m2, and additional grade 3 neutropenia events limited tolerability at this dose. An intermediate dose of 160 mg/m2 was determined to be the MTD. The most common drug-related adverse events included hypertension, nausea/vomiting, and fatigue. The pharmacokinetics of ENMD-2076 were characterized by a rapid absorption phase (Tmax 3–7.8 hours), a t1/2 of 27.3 to 38.3 hours after a single dose, and dose proportional exposure. Decreased plasma sVEGFR2 was observed posttreatment. Two patients with platinum refractory/resistant ovarian cancer had RECIST partial responses.
Conclusions: ENMD-2076 was well tolerated, had a linear pharmacokinetic profile, and showed promising antitumor activity, particularly in ovarian cancer. The recommended phase 2 dose of ENMD-2076 is 160 mg/m2 administered orally once daily with continuous dosing. Clin Cancer Res; 17(4); 849–60. ©2010 AACR.
Distinctive Mechanism for Sustained TGF-β Signaling and Growth Inhibition: MEK1 Activation-Dependent Stabilization of Type II TGF-β Receptors
Authors: Chen Gang , Ghosh Paritosh , Longo Dan L. 
Published: December 2010

Abstract
There are multiple mechanisms by which cells evade TGF-β–mediated growth inhibitory effects. In this report, we describe a novel mechanism by which cells become resistant to TGF-β–mediated growth suppression. Although having all the components of the TGF-β signaling pathway, different cell lines, RL, HaCaT, and BJAB, have different sensitivities toward TGF-β–induced growth suppression. The TGF-β resistance of RL, a B-cell lymphoma cell line, was due to ligand-induced downregulation of TGF-β receptor II (TβRII) and only transient TGF-β induced nuclear translocation of Smad2 and Smad3. With low-dose phorbol 12-myristate 13-acetate (PMA) or anti-IgM treatment, TGF-β sensitivity was restored by stabilizing TβRII expression and sustaining TGF-β signaling. The MEK inhibitor, U0126, blocked both PMA- and anti-IgM–induced upregulation of TβRII. In HaCaT and BJAB, two TGF-β–sensitive cell lines, which had higher basal levels of phospho-MEK and TβRII compared with RL, U0126 induced downregulation of TβRII and blocked subsequent TGF-β signaling. Similar results were also obtained with normal B cells, where MEK1 inhibitor downregulated TβRII and subsequent TGF-β signaling. Constitutively active MEK1, but not constitutively active ERK2, induced upregulation of TβRII. Furthermore, TβRII physically interacted with the constitutively active MEK1, but not with wild-type MEK1, indicating involvement of active MEK1 in stabilizing TβRII. Collectively, our data suggest a novel mechanism for MEK1 in regulating the sensitivity to TGF-β signaling by stabilizing TβRII. Mol Cancer Res; 9(1); 78–89 ©2010 AACR.
Interactions with Fibroblasts Are Distinct in Basal-Like and Luminal Breast Cancers
Authors: Camp J. Terese , Elloumi Fathi , Roman-Perez Erick , Rein Jessica , Stewart Delisha A. , Harrell J. Chuck , Perou Charles M. , Troester Melissa A. 
Published: December 2010

Abstract
Basal-like breast cancers have several well-characterized distinguishing molecular features, but most of these are features of the cancer cells themselves. The unique stromal–epithelial interactions, and more generally, microenvironmental features of basal-like breast cancers have not been well characterized. To identify characteristic microenvironment features of basal-like breast cancer, we performed cocultures of several basal-like breast cancer cell lines with fibroblasts and compared these with cocultures of luminal breast cancer cell lines with fibroblasts. Interactions between basal-like cancer cells and fibroblasts induced expression of numerous interleukins and chemokines, including IL-6, IL-8, CXCL1, CXCL3, and TGFβ. Under the influence of fibroblasts, basal-like breast cancer cell lines also showed increased migration in vitro. Migration was less pronounced for luminal lines; but, these lines were more likely to have altered proliferation. These differences were relevant to tumor biology in vivo, as the gene set that distinguished luminal and basal-like stromal interactions in coculture also distinguishes basal-like from luminal tumors with 98% accuracy in 10-fold cross-validation and 100% accuracy in an independent test set. However, comparisons between cocultures where cells were in direct contact and cocultures where interaction was solely through soluble factors suggest that there is an important impact of direct cell-to-cell contact. The phenotypes and gene expression changes invoked by cancer cell interactions with fibroblasts support the microenvironment and cell–cell interactions as intrinsic features of breast cancer subtypes. Mol Cancer Res; 9(1); 3–13 ©2010 AACR.
Locus of Control and Metabolic Control of Diabetes
Authors: Hummer Kimberly , Vannatta Jerry , Thompson David 
Published: December 2010

Purpose The purpose of this meta-analysis was to investigate whether locus of control (LOC) for internal LOC, powerful others, or chance is correlated with how well people control diabetes (measured by H1C). Methods The literature search included Medline, CINAHL, PsychINFO, PsychArticles, Health Source, Academic Search Elite, EMBASE, Current Contents, and BIOsis databases, which yielded 296 articles. Selection criteria for inclusion were adult participants with diabetes mellitus, use of glycosylated hemoglobin (H1C) as a measure of glycemic control, measurement of a locus-of control scale, and a Pearson correlation (r) value. Seventeen articles met all inclusion criteria. The R package “metacor,” was used to perform a random effects meta-analysis and estimate correlation coefficients between the 3 LOC measurements and H1C. Results The strength of subjects ascribing an internal LOC (across 13 studies) was uncorrelated with H1C ( r = −0.0099; 95% confidence interval [CI], −0.1092, 0.0893). A LOC ascribed to powerful others LOC (across 9 studies) was similarly uncorrelated with H1C (r = 0.0928; 95% CI, −0.0136, 0.1993). Ascribing LOC to chance (across 9 studies) was also uncorrelated with H1C (r = 0.0926; 95% CI, −0.0398, 0.2250). Conclusions This meta-analysis of 17 studies found no correlation between the control of diabetes and LOC. At best, there may be a weak correlation between powerful others and chance LOC with the metabolic control of diabetes. The use of LOC as a means of designing diabetes care can be discarded as this random effects meta-analysis found no significant correlation with effectiveness of diabetes control in adult patients.
Goal setting and action planning in the rehabilitation setting: development of a theoretically informed practice framework
Authors: Scobbie Lesley , Dixon Diane , Wyke Sally 
Published: December 2010

Background: Setting and achieving goals is fundamental to rehabilitation practice but has been criticized for being a-theoretical and the key components of replicable goal-setting interventions are not well established. Purpose: To describe the development of a theory-based goal setting practice framework for use in rehabilitation settings and to detail its component parts. Methods: Causal modelling was used to map theories of behaviour change onto the process of setting and achieving rehabilitation goals, and to suggest the mechanisms through which patient outcomes are likely to be affected. A multidisciplinary task group developed the causal model into a practice framework for use in rehabilitation settings through iterative discussion and implementation with six patients. Results: Four components of a goal-setting and action-planning practice framework were identified: (i) goal negotiation, (ii) goal identification, (iii) planning, and (iv) appraisal and feedback. The variables hypothesized to effect change in patient outcomes were self-efficacy and action plan attainment. Conclusions: A theory-based goal setting practice framework for use in rehabilitation settings is described. The framework requires further development and systematic evaluation in a range of rehabilitation settings.