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  • 1
    Online Resource
    Online Resource
    Relation of Serum Estrogen Metabolites with Terminal Duct Lobular Unit Involution Among Women Undergoing Diagnostic Image-Guided Breast Biopsy
    Springer Science and Business Media LLC ; 2016
    In:  Hormones and Cancer Vol. 7, No. 5-6 ( 2016-12), p. 305-315
    Details
    In: Hormones and Cancer, Springer Science and Business Media LLC, Vol. 7, No. 5-6 ( 2016-12), p. 305-315
    Type of Medium: Online Resource
    ISSN: 1868-8497 , 1868-8500
    URL: Article
    DOI: 10.1007/s12672-016-0265-2
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2016
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  • 2
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    Serum insulin‐like growth factor (IGF)‐I and IGF binding protein‐3 in relation to terminal duct lobular unit involution of the normal breast in Caucasian and African American women: The Susan G. Komen Tissue Bank
    Wiley ; 2018
    In:  International Journal of Cancer Vol. 143, No. 3 ( 2018-08), p. 496-507
    Details
    In: International Journal of Cancer, Wiley, Vol. 143, No. 3 ( 2018-08), p. 496-507
    Abstract: What's new? Insulin‐like growth factor (IGF)‐I signaling plays an important role in stimulating cell proliferation and inhibiting apoptosis. In this study, the authors examined normal mammary tissue in Caucasian and African American women, and found that increased levels of IGF‐binding protein (IGFBP)‐3 were associated with decreased involution of the mammary ducts in both groups. Because decreased involution is a known risk factor for breast cancer, and because these two groups express different levels of IGF‐I and IGFBP‐3, these results may help to explain the biological underpinnings of racial disparities in breast cancer.
    Type of Medium: Online Resource
    ISSN: 0020-7136 , 1097-0215
    URL: Issue
    URL: Article
    DOI: 10.1002/ijc.v143.3
    DOI: 10.1002/ijc.31333
    RVK:
    XA 10000
    Language: English
    Publisher: Wiley
    Publication Date: 2018
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  • 3
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    Relationship of Terminal Duct Lobular Unit Involution of the Breast with Area and Volume Mammographic Densities
    American Association for Cancer Research (AACR) ; 2016
    In:  Cancer Prevention Research Vol. 9, No. 2 ( 2016-02-01), p. 149-158
    Details
    In: Cancer Prevention Research, American Association for Cancer Research (AACR), Vol. 9, No. 2 ( 2016-02-01), p. 149-158
    Abstract: Elevated mammographic density (MD) is an established breast cancer risk factor. Reduced involution of terminal duct lobular units (TDLU), the histologic source of most breast cancers, has been associated with higher MD and breast cancer risk. We investigated relationships of TDLU involution with area and volumetric MD, measured throughout the breast and surrounding biopsy targets (perilesional). Three measures inversely related to TDLU involution (TDLU count/mm2, median TDLU span, median acini count/TDLU) assessed in benign diagnostic biopsies from 348 women, ages 40–65, were related to MD area (quantified with thresholding software) and volume (assessed with a density phantom) by analysis of covariance, stratified by menopausal status and adjusted for confounders. Among premenopausal women, TDLU count was directly associated with percent perilesional MD (P trend = 0.03), but not with absolute dense area/volume. Greater TDLU span was associated with elevated percent dense area/volume (P trend & lt;0.05) and absolute perilesional MD (P = 0.003). Acini count was directly associated with absolute perilesional MD (P = 0.02). Greater TDLU involution (all metrics) was associated with increased nondense area/volume (P trend ≤ 0.04). Among postmenopausal women, TDLU measures were not significantly associated with MD. Among premenopausal women, reduced TDLU involution was associated with higher area and volumetric MD, particularly in perilesional parenchyma. Data indicating that TDLU involution and MD are correlated markers of breast cancer risk suggest that associations of MD with breast cancer may partly reflect amounts of at-risk epithelium. If confirmed, these results could suggest a prevention paradigm based on enhancing TDLU involution and monitoring efficacy by assessing MD reduction. Cancer Prev Res; 9(2); 149–58. ©2015 AACR.
    Type of Medium: Online Resource
    ISSN: 1940-6207 , 1940-6215
    URL: Article
    DOI: 10.1158/1940-6207.CAPR-15-0282
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2016
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  • 4
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    Abstract A36: Serum insulin-like growth factor (IGF)-I and IGF binding protein-3 in relation to terminal duct lobular unit involution in Caucasian and African American women: The Susan G. Komen Tissue Bank
    American Association for Cancer Research (AACR) ; 2018
    In:  Cancer Epidemiology, Biomarkers & Prevention Vol. 27, No. 7_Supplement ( 2018-07-01), p. A36-A36
    Details
    In: Cancer Epidemiology, Biomarkers & Prevention, American Association for Cancer Research (AACR), Vol. 27, No. 7_Supplement ( 2018-07-01), p. A36-A36
    Abstract: Background: Insulin-like growth factor (IGF)-I and IGF binding protein (IGFBP)-3 play important roles in carcinogenesis, particularly for breast cancer. However, little is known about whether the IGF system influences histologic characteristics of normal glandular tissue and whether relationships vary by race. Lesser degrees of age-related terminal duct lobular unit (TDLU) involution, as reflected by higher numbers of TDLUs and acini per TDLU, have been associated with higher breast cancer risk. We examined the associations of IGF measures with TDLU involution of normal breast using standardized TDLU measures. Methods: Among 715 Caucasian and 283 African American (AA) women with normal breast tissue samples from the Komen Tissue Bank, serum concentrations of IGF-I and IGFBP-3 were quantified using enzyme-linked immunosorbent assay (ELISA). Hematoxilyn and eosin-stained tissue sections were assessed for numbers of TDLUs (“TDLU count”) and acini/TDLU. Zero-inflated Poisson regression models with a robust variance estimator were used to estimate associations of IGF-I, IGFBP-3, and IGF-I:IGFBP-3 molar ratio (tertiles) with TDLU count by race and menopausal status, adjusting for potential confounders. We also tested for interactions by race using likelihood ratio tests. Results: AA (vs. Caucasian) women had higher age-adjusted mean levels of serum IGF-I (137 vs. 131 ng/mL, p=0.07) and lower levels of IGFBP-3 (4165 vs. 4684 ng/mL, p & lt;0.0001); the differences persisted after adjustment for additional covariates including BMI and parity/age at first birth. Postmenopausal IGFBP-3 was inversely associated with TDLU count among both AA (RR T3vs.T1=0.49, 95% CI=0.28-0.84, p-trend=0.04) and Caucasian (RR T3vs.T1=0.63, 95% CI=0.41-0.99, p-trend=0.04) women. In premenopausal women, higher IGF-I:IGFBP-3 ratios were associated with higher TDLU count in Caucasians (OR T3vs.T1=1.33, 95% CI=1.01-1.31, p-trend=0.04) but not in AA (OR T3vs.T1=0.65, 95% CI=0.42-1.00, p-trend=0.05) women. There was no statistically significant interaction by race (p-interaction≥0.10). Conclusions: Our data suggest the potential role of the IGF system, particularly IGFBP-3, in TDLU involution of the normal breast among both Caucasian and AA women. Citation Format: Hannah OH, Ruth M. Pfeiffer, Roni T. Falk, Hisani N. Horne, Jackie Xiang, Michael Pollak, Louise A. Brinton, Anna Maria V. Storniolo, Mark E. Sherman, Gretchen L. Gierach, Jonine D. Figueroa. Serum insulin-like growth factor (IGF)-I and IGF binding protein-3 in relation to terminal duct lobular unit involution in Caucasian and African American women: The Susan G. Komen Tissue Bank [abstract]. In: Proceedings of the Tenth AACR Conference on the Science of Cancer Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; 2017 Sep 25-28; Atlanta, GA. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2018;27(7 Suppl):Abstract nr A36.
    Type of Medium: Online Resource
    ISSN: 1055-9965 , 1538-7755
    URL: Article
    DOI: 10.1158/1538-7755.DISP17-A36
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2018
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  • 5
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    Online Resource
    Inactivation of the MAL Gene in Breast Cancer Is a Common Event That Predicts Benefit from Adjuvant Chemotherapy
    American Association for Cancer Research (AACR) ; 2009
    In:  Molecular Cancer Research Vol. 7, No. 2 ( 2009-02-01), p. 199-209
    Details
    In: Molecular Cancer Research, American Association for Cancer Research (AACR), Vol. 7, No. 2 ( 2009-02-01), p. 199-209
    Abstract: Dysregulation of MAL (myelin and lymphocyte protein) has been implicated in several malignancies including esophageal, ovarian, and cervical cancers. The MAL protein functions in apical transport in polarized epithelial cells; therefore, its disruption may lead to loss of organized polarity characteristic of most solid malignancies. Bisulfite sequencing of the MAL promoter CpG island revealed hypermethylation in breast cancer cell lines and 69% of primary tumors analyzed compared with normal breast epithelial cells. Differential methylation between normal and cancer DNA was confined to the proximal promoter region. In a subset of breast cancer cell lines including T47D and MCF7 cells, promoter methylation correlated with transcriptional silencing that was reversible with the methylation inhibitor 5-aza-2′-deoxycytidine. In addition, expression of MAL reduced motility and resulted in a redistribution of lipid raft components in MCF10A cells. MAL protein expression measured by immunohistochemistry revealed no significant correlation with clinicopathologic features. However, in patients who did not receive adjuvant chemotherapy, reduced MAL expression was a significant predictive factor for disease-free survival. These data implicate MAL as a commonly altered gene in breast cancer with implications for response to chemotherapy. (Mol Cancer Res 2009;7(2):199–209)
    Type of Medium: Online Resource
    ISSN: 1541-7786 , 1557-3125
    URL: Article
    DOI: 10.1158/1541-7786.MCR-08-0314
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2009
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  • 6
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    FDA Approval Summary: Niraparib for the Maintenance Treatment of Patients with Recurrent Ovarian Cancer in Response to Platinum-Based Chemotherapy
    American Association for Cancer Research (AACR) ; 2018
    In:  Clinical Cancer Research Vol. 24, No. 17 ( 2018-09-01), p. 4066-4071
    Details
    In: Clinical Cancer Research, American Association for Cancer Research (AACR), Vol. 24, No. 17 ( 2018-09-01), p. 4066-4071
    Abstract: The FDA approved niraparib, a poly(ADP-ribose) polymerase (PARP) inhibitor, on March 27, 2017, for maintenance treatment of patients with recurrent epithelial ovarian, fallopian tube, or primary peritoneal cancer who are in response to platinum-based chemotherapy. Approval was based on data from the NOVA trial comparing niraparib with placebo in two independent cohorts, based on germline BRCA mutation status (gBRCAm vs. non-gBRCAm). Progression-free survival (PFS) in each cohort was the primary endpoint. In the gBRCAm cohort, estimated median PFS on niraparib was 21 months versus 5.5 months on placebo [HR, 0.26; 95% confidence interval (CI), 0.17–0.41; P & lt; 0.0001]. In the non-gBRCAm cohort, estimated median PFS for niraparib and placebo was 9.3 and 3.9 months, respectively (HR, 0.45; 95% CI, 0.34–0.61; P & lt; 0.0001). Common adverse reactions ( & gt;20% and higher incidence in the niraparib arm) with niraparib included thrombocytopenia, anemia, neutropenia, nausea, constipation, vomiting, mucositis, fatigue, decreased appetite, headache, insomnia, nasopharyngitis, dyspnea, rash, and hypertension. There were five cases of myelodysplastic syndrome and acute myeloid leukemia (1.4%) in patients treated with niraparib compared with two cases (1.1%) on placebo. Niraparib is the first PARP inhibitor approved as maintenance therapy for patients with ovarian, fallopian tube, or primary peritoneal cancer, with improvement in PFS, regardless of gBRCAm status. Clin Cancer Res; 24(17); 4066–71. ©2018 AACR. See related commentary by Konstantinopoulos and Matulonis, p. 4062
    Type of Medium: Online Resource
    ISSN: 1078-0432 , 1557-3265
    URL: Article
    DOI: 10.1158/1078-0432.CCR-18-0042
    RVK:
    XA 36791
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2018
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  • 7
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    Weighing the Evidence: Variant Classification and Interpretation in Precision Oncology, US Food and Drug Administration Public Workshop—Workshop Proceedings
    American Society of Clinical Oncology (ASCO) ; 2019
    In:  JCO Precision Oncology , No. 3 ( 2019-12), p. 1-7
    Details
    In: JCO Precision Oncology, American Society of Clinical Oncology (ASCO), , No. 3 ( 2019-12), p. 1-7
    Abstract: Next-generation sequencing (NGS) oncology panels are becoming integral in hospital and academic settings to guide patient treatment and enrollment in clinical trials. Although NGS technologies have revolutionized decision-making for cancer therapeutics, physicians may face many challenges in parsing and prioritizing NGS-based test results to determine the best course of treatment for individual patients. On January 29, 2018, the US Food and Drug Administration held a public workshop entitled, “Weighing the Evidence: Variant Classification and Interpretation in Precision Oncology.” Here, we discuss the presentations and discussion highlights across the four sessions of the workshop. METHODS The goal of the public workshop was to engage stakeholders and solicit input from experts in precision oncology to discuss the integration of complex NGS data into patient management and regulatory innovation within the precision oncology community. The US Food and Drug Administration gathered representatives from academia, industry, patient advocacy, government, and professional organizations for a series of presentations followed by panel discussions. After the workshop, the transcript and speaker presentation slides were reviewed and summarized for manuscript preparation. RESULTS Speakers and panelists provided diverse perspectives on the integration of NGS technology into patient care for oncology and on the complexities that surround data interpretation and sharing. Discussions highlighted the challenges with standardization for variant classification while expressing the utility of consensus recommendations among stakeholders in oncology for driving innovation in the era of precision medicine. CONCLUSION As precision medicine advances, clear communication within the field of precision oncology will be key to creating an environment that facilitates the generation and sharing of data that have value to patients. [Box: see text]
    Type of Medium: Online Resource
    ISSN: 2473-4284
    URL: Article
    DOI: 10.1200/PO.18.00314
    Language: English
    Publisher: American Society of Clinical Oncology (ASCO)
    Publication Date: 2019
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  • 8
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    Abstract B11: Effect of patient navigation on colorectal cancer screening in a community-based randomized controlled trial of urban African American Medicare beneficiaries
    American Association for Cancer Research (AACR) ; 2011
    In:  Cancer Epidemiology, Biomarkers & Prevention Vol. 20, No. 10_Supplement ( 2011-09-01), p. B11-B11
    Details
    In: Cancer Epidemiology, Biomarkers & Prevention, American Association for Cancer Research (AACR), Vol. 20, No. 10_Supplement ( 2011-09-01), p. B11-B11
    Abstract: Background: In recent years, colorectal cancer screening rates have increased steadily in the United States, though racial and ethnic disparities persist. We investigated the effect of a patient navigation intervention on adherence to colorectal cancer screening guidelines among African American older adults in Baltimore, MD. Methods: We examined data collected from the Cancer Prevention and Treatment Demonstration (CPTD), a community-based randomized, controlled trial. Our study population consisted of 661 African American men and women aged 65 to 75 years who were Medicare beneficiaries and residents of Baltimore City. Participants were randomized to receive either printed educational materials only (PEM) or the addition of a patient navigator (NAV). The Johns Hopkins trained and certified patient navigator assisted participants with identifying and overcoming potential barriers to cancer screening. Self-reported colorectal cancer screening data were collected at baseline and at one-year follow-up through inperson interviews. Rates of screening between the two groups were examined using multivariable logistic regression modeling. All participants irrespective of their baseline screening status were included in calculating the adjusted odds of completing colorectal cancer screening during the follow-up period. Results: At baseline, 68% of the PEM group and 71% of the NAV group (P = 0.45) reported being up-to-date with colorectal cancer screening, defined as having either a fecal occult blood test (FOBT) within one year or colonoscopy/sigmoidoscopy within ten years of randomization. At the one-year follow-up visit, participants in the NAV group were more likely to report having undergone any colorectal cancer screening during the previous year, compared to the PEM group, 54% versus 46%, though this did not reach statistical significance (P = 0.12). After adjusting for age, gender, number of co-morbidities, education, participants’ health perception and level of health literacy, individuals in the NAV group were more likely to report being screened by colonoscopy/sigmoidoscopy (OR, 1.53; 95% CI, 1.07–2.18) compared to those in the PEM group. Individuals who underwent patient navigation did not have a statistically significant change in the likelihood of reporting a FOBT compared to the PEM group. Conclusions: In a population of urban African American older adults, patient navigation was effective in increasing the likelihood of screening by colonoscopy/sigmoidoscopy but not fecal occult blood testing at one-year follow-up. The lack of effect on screening by FOBT likely represents the relatively low rate of provider utilization of this screening modality in the target population. Citation Information: Cancer Epidemiol Biomarkers Prev 2011;20(10 Suppl):B11.
    Type of Medium: Online Resource
    ISSN: 1055-9965 , 1538-7755
    URL: Article
    DOI: 10.1158/1055-9965.DISP-11-B11
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2011
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  • 9
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    FDA Approval Summary: Rucaparib for the Treatment of Patients with Deleterious BRCA Mutation–Associated Advanced Ovarian Cancer
    American Association for Cancer Research (AACR) ; 2017
    In:  Clinical Cancer Research Vol. 23, No. 23 ( 2017-12-01), p. 7165-7170
    Details
    In: Clinical Cancer Research, American Association for Cancer Research (AACR), Vol. 23, No. 23 ( 2017-12-01), p. 7165-7170
    Abstract: On December 19, 2016, the FDA granted accelerated approval to rucaparib (RUBRACA; Clovis Oncology, Inc.) for the treatment of patients with deleterious BRCA mutation (germline and/or somatic)–associated advanced ovarian cancer who have been treated with two or more chemotherapies. The FDA also approved the FoundationFocus CDxBRCA test (Foundation Medicine, Inc.), the first next-generation sequencing-based companion diagnostic, for identifying patients with advanced ovarian cancer eligible for treatment with rucaparib based on detection of deleterious BRCA1 and/or BRCA2 mutations in tumor tissue. Rucaparib's approval was based primarily on efficacy data from 106 patients with BRCA mutation–associated ovarian cancer who had prior treatment with two or more chemotherapies and safety data from 377 patients with ovarian cancer treated with rucaparib 600 mg orally twice daily on two open-label, single-arm trials. Investigator-assessed objective response rate was 54% [57/106; 95% confidence interval (CI), 44–64], and median duration of response was 9.2 months (95% CI, 6.6–11.7). The approved companion diagnostic verified tumor BRCA mutation status retrospectively in 96% (64/67) of patients. Common adverse reactions (≥20%) to rucaparib were nausea, fatigue, vomiting, anemia, abdominal pain, dysgeusia, constipation, decreased appetite, diarrhea, thrombocytopenia, and dyspnea. This article summarizes the FDA review and data supporting rucaparib's accelerated approval. Clin Cancer Res; 23(23); 7165–70. ©2017 AACR. See related commentary by Kohn et al., p. 7155
    Type of Medium: Online Resource
    ISSN: 1078-0432 , 1557-3265
    URL: Article
    DOI: 10.1158/1078-0432.CCR-17-1337
    RVK:
    XA 36791
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2017
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  • 10
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    Abstract LB-336: Association of variant rs2046210 at 6q25.1 (ESR1) with breast cancer risk suggests heterogeneity by E-cadherin tumor tissue expression
    American Association for Cancer Research (AACR) ; 2012
    In:  Cancer Research Vol. 72, No. 8_Supplement ( 2012-04-15), p. LB-336-LB-336
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 72, No. 8_Supplement ( 2012-04-15), p. LB-336-LB-336
    Abstract: Background: E-cadherin is a cell-cell adhesion protein that functions as a cancer tumor suppressor gene based on in vitro and in vivo evidence showing that loss of this gene can lead to tumor progression and invasion. E-cadherin loss is strongly associated with breast tumors of lobular histology, which are more likely to be estrogen receptor-alpha (ESR1) positive and more frequently metastasize to the gastrointestinal tract and ovary compared to ductal tumors. We sought to determine if relative risk estimates for 19 established breast cancer susceptibility loci were modified by E-cadherin expression levels and tumor histology. Methods: Analyses included up to 1885 invasive breast cancer cases and 2366 age and site matched controls aged 20-74 years, from a population-based case-control study conducted in Poland from 2000-2003. Genotyping of the 19 single nucleotide polymorphisms (SNPs) was performed using TaqMan assays. Tissue expression of E-cadherin was assessed using immunohistochemical (IHC) staining of tissue microarrays and IHC results were scored as the product of percent positive tumor cells x intensity. Tumors with a score of & lt;10 were classified as E-cadherin low and scores ≥10 as E-cadherin high. Polytomous logistic regression models adjusted for age and study site were used to estimate odds ratios (OR) and 95% confidence intervals (95% CI) for each breast cancer subtype, defined by E-cadherin expression levels, compared to controls. Logistic regression models restricted to cases were used to test for heterogeneity by tumor characteristics. Results: We observed significant associations with breast cancer risk overall for the following SNPs: 1p11.2 (NOTCH2/FCGR1B), 2q35 (TNP1/IGFBP5/IGFBP2/TNS1), 6q25.1 (ESR1), 8q24 (FAM84B/c-MYC/POU5F1P1), 9p21 (CDKN2B), 10p14 (CASP8), 10q21.2 (ZNF365), 10q26 (FGFR2), 11q13 (ORAOV1), 14q24.1 (RAD51L1) and two SNPs at 5p12 (MRPS30/FGFR10). One SNP rs2046210 at 6q25.1 (ESR1) displayed significant heterogeneity by E-cadherin expression after Bonferroni adjustment (Pheterogeneity= 0.002), showing stronger associations with breast tumors that had low E-cadherin expression levels compared to high. The estimated OR per A-allele for E-cadherin low (N = 136) tumors was 1.53 (95% CI = 1.19-1.98) and 0.99 for E-cadherin high tumors (N = 566) (95% CI = 0.86-1.14). These differences were not explained by lobular/ductal histology [per A-allele ORs (95% CI) for E-cadherin low lobular = 1.60 (1.15-2.22) and, for E-cadherin low ductal = 1.45 (0.88-2.40)] or ER status. Conclusions: Our data suggest that associations for breast cancer susceptibility loci vary by E-cadherin expression in breast cancer tumor tissues. Specifically, our results suggest that the genetic marker rs2046210 SNP at 6q25.1 may preferentially increase risk for tumors with low or absent E-cadherin expression, which requires replication in other datasets. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr LB-336. doi:1538-7445.AM2012-LB-336
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2012-LB-336
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2012
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