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Search Results: 1 - 10 of 1970 matches for " Heather Feigelson "
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Future possibilities in the prevention of breast cancer: Role of genetic variation in breast cancer prevention
Heather Spencer Feigelson, Brian E Henderson
Breast Cancer Research , 2000, DOI: 10.1186/bcr69
Abstract: The traditional view of public health prevention strategies considers three broad categories. Primary prevention involves activities that are aimed at reducing and removing agents that increase risk. Secondary prevention includes early detection activities that are designed to reduce mortality. Finally, tertiary prevention aims to minimize or reduce long-term disability and suffering. Cancer prevention usually implies activities involved in primary or secondary prevention. For many cancer sites, we have made significant contributions in prevention. For example, the Pap smear has had a great impact on cervical cancer, and refrigeration and other safe food preservation practices have markedly reduced the incidence of stomach cancer. Largely because of the underlying hormonal etiology, however, primary prevention strategies for breast cancer have been limited.The biggest determinants of breast cancer risk are related to endogenous hormone levels and major reproductive events, and thus do not lend themselves to traditional prevention strategies. Table 1 lists the established breast cancer risk factors. Those with the greatest impact on risk are listed first, and unfortunately are the most difficult to modify by traditional public health measures. For example, surgical removal of the ovaries can hasten the onset of menopause, but is not considered a reasonable approach to reduce the risk of breast cancer. Age at menarche and the establishment of regular menstrual cycles may be delayed by vigorous physical activity and possibly diet, but rarely is breast cancer prevention a concern before menarche occurs.Limiting the use of alcohol, hormone replacement therapy (HRT), and oral contraceptives may reduce the risk of breast cancer, but the impact of these factors on breast cancer risk are modest. Furthermore, these agents have significant beneficial effects on the risks of other chronic diseases, and these risk-benefit ratios must be carefully weighed. Prolonged lactation may
A prospective study of XRCC1 (X-ray cross-complementing group 1) polymorphisms and breast cancer risk
Alpa V Patel, Eugenia E Calle, Alexandre L Pavluck, Heather Feigelson, Michael J Thun, Carmen Rodriguez
Breast Cancer Research , 2005, DOI: 10.1186/bcr1355
Abstract: Among the 21,965 women who were cancer-free in 1992 and gave blood between 1998 and 2001, 502 postmenopausal breast cancer cases were diagnosed between 1992 and 2001; 502 controls were matched to cases on age, race/ethnicity, and date of blood collection. Genotyping on DNA extracted from buffy coat was performed with Taqman. Conditional logistic regression was used to examine the association between each polymorphism and breast cancer risk controlling for breast cancer risk factors. We also examined whether factors associated with DNA damage, such as smoking and antioxidant intake, modified the association between XRCC1 polymorphisms and breast cancer.We observed a significant inverse association between Trp194 carriers (Trp/Trp and Trp/Arg) compared with Trp194 non-carriers in relation to breast cancer (Arg/Arg) (odds ratio (OR) 0.62, 95% confidence interval (CI) 0.40 to 0.95). The inverse association between breast cancer and Trp194 carriers compared with non-carriers was slightly stronger among smokers (OR 0.47, 95% CI 0.24 to 0.94) than never smokers (OR 0.78, 95% CI 0.43 to 1.40). An increased risk associated with the Arg399Gln polymorphism (Gln/Gln versus Arg/Arg) was observed only among women who reported ever smoking cigarettes (OR 2.76, 95% CI 1.36 to 5.63), and not in women who were lifelong non-smokers (OR 0.64, 95% CI 0.33 to 1.26). No other factor examined modified the association between XRCC1 polymorphisms and breast cancer risk.Our results support the hypothesis that genetic variation in XRCC1, particularly in Arg194Trp, may influence postmenopausal breast cancer risk. In our study, genetic variation in XRCC1 Arg399Gln was associated with breast cancer risk only among women with a history of smoking cigarettes.Base excision repair (BER) corrects localized DNA damage such as oxidized or fragmented lesions and non-bulky adducts [1]. Sources of oxidative damage include ionizing radiation and chemical carcinogens in tobacco smoke [1,2]. In the absence of
A Massive Young Star-Forming Complex Study in Infrared and X-ray: Mid-Infrared Observations and Catalogs
Michael A. Kuhn,Matthew S. Povich,Kevin L. Luhman,Konstantin V. Getman,Heather S. Busk,Eric D. Feigelson
Physics , 2013, DOI: 10.1088/0067-0049/209/2/29
Abstract: Spitzer IRAC observations and stellar photometric catalogs are presented for the Massive Young Star-Forming Complex Study in the Infrared and X-ray (MYStIX). MYStIX is a multiwavelength census of young stellar members of twenty nearby (d < 4 kpc), Galactic, star-forming regions that contain at least one O star. All regions have data available from the Spitzer Space Telescope, consisting of GLIMPSE or other published catalogs for eleven regions and results of our own photometric analysis of archival data for the remaining nine regions. This paper seeks to construct deep and reliable catalogs of sources from the Spitzer images. Mid-infrared study of these regions faces challenges of crowding and high nebulosity. Our new catalogs typically contain fainter sources than existing Spitzer studies, which improves the match rate to Chandra X-ray sources that are likely to be young stars, but increases the possibility of spurious point-source detections, especially peaks in the nebulosity. IRAC color-color diagrams help distinguish spurious detections of nebular PAH emission from the infrared excess associated with dusty disks around young stars. The distributions of sources on the mid-infrared color-magnitude and color-color diagrams reflect differences between MYStIX regions, including astrophysical e?ects such as stellar ages and disk evolution.
Reliability of KRAS mutation testing in metastatic colorectal cancer patients across five laboratories
Heather Feigelson, Katrina AB Goddard, Monique A Johnson, Kellyan C Funk, Alanna Rahm, Tia L Kauffman, Dhananjay A Chitale, Loic Le Marchand, C Richards
BMC Research Notes , 2012, DOI: 10.1186/1756-0500-5-196
Abstract: Twenty formalin-fixed paraffin-embedded human colorectal cancer samples from colon resections previously tested for KRAS mutations were selected based on mutation status (6 wild type, 8 codon 12 mutations, and 6 codon 13 mutations). We found good agreement across laboratories despite differences in mutation detection methods. Eighteen of twenty samples (90%) were concordant across all five labs. Discordant results are likely not due to laboratory error, but instead to tumor heterogeneity, contamination of the tumor sample with normal tissue, or analytic factors affecting assay sensitivity.Our results indicate commercial and academic laboratories provide reliable results for the common KRAS gene mutations at codons 12 and 13 when an adequate percentage of tumor cells is present in the sample.Anti-epidermal growth factor receptor (EGFR) monoclonal antibodies are approved for the treatment of metastatic colorectal cancer (CRC). However, these anti-EGFR therapies do not benefit patients whose tumors harbor a KRAS mutation [1]. Genetic testing for the presence of KRAS mutations has been recommended to guide treatment for these patients [2].Several factors can influence KRAS mutation testing results in CRC specimens [3-5]. The purpose of this study was to evaluate comparability and consistency of clinical KRAS test results among laboratories used to determine KRAS mutation status in a large multi-center study. Three commercial laboratories (Genzyme, Clarient, Quest Diagnostics), one clinical academic laboratory (Henry Ford Health System), and one academic research laboratory (Molecular and Medical Genetics, Oregon Health and Science University) were contracted to analyze KRAS mutation status for comparison with previous clinical results. While all five laboratories are Clinical Laboratories Improvement Act (CLIA) certified, they have different sample preparation and mutation detection methods. Our aim was not to certify these laboratories, but to ensure that we could comb
Polymorphisms in the vascular endothelial growth factor gene and breast cancer in the Cancer Prevention Study II cohort
Eric J Jacobs, Heather Feigelson, Elizabeth B Bain, Kerri A Brady, Carmen Rodriguez, Victoria L Stevens, Alpa V Patel, Michael J Thun, Eugenia E Calle
Breast Cancer Research , 2006, DOI: 10.1186/bcr1400
Abstract: We examined the association between these four VEGF polymorphisms and risk for breast cancer among postmenopausal women in CPS-II (Cancer Prevention Study II) Nutrition Cohort. This cohort was established in 1992 and participants were invited to provide a blood sample between 1998 and 2001. Included in this analysis were 501 postmenopausal women who provided a blood sample and were diagnosed with breast cancer between 1992 and 2001 (cases). Control individuals were 504 cancer-free postmenopausal women matched to the cases with respect to age, race/ethnicity, and date of blood collection (controls).We found no association between any of the polymorphisms examined and overall breast cancer risk. However, associations were markedly different in separate analyses of invasive cancer (n = 380) and in situ cancer (n = 107). The -2578C and -1154G alleles, which are both hypothesized to increase expression of VEGF, were associated with increased risk for invasive breast cancer (odds ratio [OR] 1.46, 95% confidence interval [CI] 1.00–2.14 for -2578 CC versus AA; OR 1.64, 95% CI 1.02–2.64 for -1154 GG versus AA) but they were not associated with risk for in situ cancer. The +936C allele, which is also hypothesized to increase VEGF expression, was not clearly associated with invasive breast cancer (OR 1.21, 95% CI 0.88–1.67 for +936 CC versus TT/CT), but it was associated with reduced risk for in situ cancer (OR 0.59, 95% CI 0.37–0.93 for CC versus TT/CT). The -634 C/G polymorphism was not associated with either invasive or in situ cancer.Our findings provide limited support for the hypothesis that the -2578C and -1154G VEGF alleles are associated with increased risk for invasive but not in situ breast cancer in postmenopausal women.Angiogenesis, the development of new blood vessels, is required for the growth of microscopic cancers into larger, clinically relevant tumors [1]. Vascular endothelial growth factor (VEGF) is believed to play a central role in angiogenesis through a
Genetic variation in candidate obesity genes ADRB2, ADRB3, GHRL, HSD11B1, IRS1, IRS2, and SHC1 and risk for breast cancer in the Cancer Prevention Study II
Heather Feigelson, Lauren R Teras, W Ryan Diver, Weining Tang, Alpa V Patel, Victoria L Stevens, Eugenia E Calle, Michael J Thun, Mark Bouzyk
Breast Cancer Research , 2008, DOI: 10.1186/bcr2114
Abstract: We conducted a nested case-control study among postmenopausal women from the American Cancer Society Cancer Prevention Study II Nutrition Cohort to determine whether genes associated with obesity increase risk for breast cancer. Tagging single nucleotide polymorphisms (SNPs) were selected to capture common variation across seven candidate genes that encode adipose-related proteins: ADRB2, ADRB3, GHRL, HSD11B1, IRS1, IRS2, and SHC1. Thirty-nine SNPs were genotyped in 648 cases and 659 controls. Logistic regression models were used to examine the association between each tagging SNP and risk for breast cancer while adjusting for matching factors and potential confounders. We also examined whether these SNPs were associated with measures of adult adiposity.Two out of five tagging SNPs in HSD11B1 were associated with breast cancer (rs11807619, P = 0.006; rs932335, P = 0.0001). rs11807619 and rs932335 were highly correlated (r2 = 0.74) and, when modeled as a haplotype, only haplotypes containing the rs932335 C allele were associated with breast cancer. The rs932335 C allele was associated with a nearly twofold increased risk for breast cancer (odds ratio = 1.83, 95% confidence interval = 1.01–3.33 for C/C versus G/G). Three of the 11 SNPs for IRS2 were associated with breast cancer (rs4773082, P = 0.007; rs2289046, P = 0.016; rs754204, P = 0.03). When these three SNPs were examined as a haplotype, only the haplotype that included the G allele of rs2289046 was associated with breast cancer (odds ratio = 0.76, 95% confidence interval = 0.63–0.92 for TGC versus CAT). IRS2 rs2289046, rs754204, and rs12584136 were also associated with adult weight gain but only among cases. None of the other SNPs in any gene investigated were associated with breast cancer or adiposity.Our findings suggest that these tagging SNPs in HSD11B1 and IRS2 mark regions of the genome that may harbor risk alleles for breast cancer, and these associations are probably independent of adiposity.Obesity is
Vitamin D pathway gene polymorphisms, diet, and risk of postmenopausal breast cancer: a nested case-control study
Marjorie L McCullough, Victoria L Stevens, William R Diver, Heather S Feigelson, Carmen Rodriguez, Robin M Bostick, Michael J Thun, Eugenia E Calle
Breast Cancer Research , 2007, DOI: 10.1186/bcr1642
Abstract: We conducted a nested case-control study within the Cancer Prevention Study II Nutrition Cohort of associations between breast cancer and four VDR single-nucleotide polymorphisms (SNPs), Bsm1,Apa1,Taq1, and Fok1, a poly(A) microsatellite, and associated haplotypes (baTL and BAtS). We also examined one SNP in the 24-hydroxylase gene (CYP24A1) and two in the vitamin D-binding protein (group-specific component [GC]) gene. Participants completed a questionnaire on diet and medical history at baseline in 1992. This study includes 500 postmenopausal breast cancer cases and 500 controls matched by age, race/ethnicity, and date of blood collection.Incident breast cancer was not associated with any genotype examined. However, women with the Bsm1 bb SNP who consumed greater than the median intake of total calcium (≥902 mg/day) had lower odds of breast cancer compared to women with the Bb or BB genotype and less than the median calcium intake (odds ratio 0.61, 95% confidence interval 0.38 to 0.96; pinteraction = 0.01). Similar interactions were observed for Taq1 (T allele) and the poly(A) (LL) repeat.We found no overall association between selected vitamin D pathway genes and postmenopausal breast cancer risk. However, certain VDR gene polymorphisms were associated with lower risk in women consuming high levels of calcium, suggesting that dietary factors may modify associations by VDR genotype.Vitamin D has been associated with a lower risk of several types of cancer, including breast cancer [1,2]. Its action is mediated through the vitamin D receptor (VDR), a nuclear transcription-regulating factor that signals the synthesis of proteins involved in bone mineral homeostasis and cell-cycle regulation [2]. The receptor is present in most cell types, including normal and neoplastic breast tissue [3]. Clinically, breast tumors with greater VDR expression relapse more slowly after first diagnosis [4].The VDR gene contains several polymorphisms. Three single-nucleotide polymorphisms
Utilization of Neoadjuvant Chemotherapy Varies in the Treatment of Women with Invasive Breast Cancer
Adedayo A. Onitilo, Jill K. Onesti, Richard M. Single, Jessica M. Engel, Ted A. James, Erin J. Aiello Bowles, Heather Spencer Feigelson, Tom Barney, Laurence E. McCahill
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0084535
Abstract: Background Treatment with neoadjuvant chemotherapy (NAC) has made it possible for some women to be successfully treated with breast conservation therapy (BCT ) who were initially considered ineligible. Factors related to current practice patterns of NAC use are important to understand particularly as the surgical treatment of invasive breast cancer has changed. The goal of this study was to determine variations in neoadjuvant chemotherapy use in a large multi-center national database of patients with breast cancer. Methods We evaluated NAC use in patients with initially operable invasive breast cancer and potential impact on breast conservation rates. Records of 2871 women ages 18-years and older diagnosed with 2907 invasive breast cancers from January 2003 to December 2008 at four institutions across the United States were examined using the Breast Cancer Surgical Outcomes (BRCASO) database. Main outcome measures included NAC use and association with pre-operatively identified clinical factors, surgical approach (partial mastectomy [PM] or total mastectomy [TM]), and BCT failure (initial PM followed by subsequent TM). Results Overall, NAC utilization was 3.8%l. Factors associated with NAC use included younger age, pre-operatively known positive nodal status, and increasing clinical tumor size. NAC use and BCT failure rates increased with clinical tumor size, and there was significant variation in NAC use across institutions. Initial TM frequency approached initial PM frequency for tumors >30-40mm; BCT failure rate was 22.7% for tumors >40mm. Only 2.7% of patients undergoing initial PM and 7.2% undergoing initial TM received NAC. Conclusions NAC use in this study was infrequent and varied among institutions. Infrequent NAC use in patients suggests that NAC may be underutilized in eligible patients desiring breast conservation.
The MYStIX InfraRed-Excess Source Catalog
Matthew S. Povich,Michael A. Kuhn,Konstantin V. Getman,Heather A. Busk,Eric D. Feigelson,Patrick S. Broos,Leisa K. Townsley,Robert R. King,Tim Naylor
Physics , 2013, DOI: 10.1088/0067-0049/209/2/31
Abstract: The MYStIX project (Massive Young Star-Forming Complex Study in Infrared and X-rays) provides a comparative study of 20 Galactic massive star-forming complexes (d = 0.4 to 3.6 kpc). Probable stellar members in each target complex are identified using X-ray and/or infrared data via two pathways: (1) X-ray detections of young/massive stars with coronal activity/strong winds; or (2) infrared excess (IRE) selection of young stellar objects (YSOs) with circumstellar disks and/or protostellar envelopes. We present the methodology for the second pathway, using Spitzer/IRAC, 2MASS, and UKIRT imaging and photometry. Although IRE selection of YSOs is welltrodden territory, MYStIX presents unique challenges. We combine IR spectral energy distribution (SED) fitting with IR color cuts and spatial clustering analysis to identify IRE sources and isolate probable YSO members in each MYStIX target field from the myriad types of contaminating sources that can resemble YSOs: extragalactic sources, evolved stars, nebular knots, and even unassociated foreground/background YSOs. Applying our methodology consistently across 18 of the target complexes, we produce the MYStIX IRE Source (MIRES) Catalog comprising 20,719 sources, including 8686 probable stellar members of the MYStIX target complexes. We also classify the SEDs of 9365 IR counterparts to MYStIX X-ray sources to assist the first pathway, the identification of X-ray detected stellar members. The MIRES catalog provides a foundation for follow-up studies of diverse phenomena related to massive star cluster formation, including protostellar outflows, circumstellar disks, and sequential star formation triggered by massive star feedback processes.
Identifying Young Stars in Massive Star-Forming Regions for the MYStIX Project
Patrick S. Broos,Konstantin V. Getman,Matthew S. Povich,Eric D. Feigelson,Leisa K. Townsley,Tim Naylor,Michael A. Kuhn,R. R. King,Heather A. Busk
Physics , 2013, DOI: 10.1088/0067-0049/209/2/32
Abstract: The Massive Young star-forming Complex Study in Infrared and X-rays (MYStIX) project requires samples of young stars that are likely members of 20 nearby Galactic massive star-forming regions. Membership is inferred from statistical classification of X-ray sources, from detection of a robust infrared excess that is best explained by circumstellar dust in a disk or infalling envelope, and from published spectral types that are unlikely to be found among field stars. We present the MYStIX membership lists here, and describe in detail the statistical classification of X-ray sources via a \Naive Bayes Classi
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