scholarly journals Hormone Replacement Therapy and Colon Cancer among Members of a Health Maintenance Organization

Epidemiology ◽  
1999 ◽  
Vol 10 (4) ◽  
pp. 445-451 ◽  
Author(s):  
Eric J. Jacobs ◽  
Emily White ◽  
Noel S. Weiss ◽  
Susan R. Heckbert ◽  
Andrea LaCroix ◽  
...  
2020 ◽  
Vol 38 (15_suppl) ◽  
pp. e13599-e13599
Author(s):  
Nava Siegelmann-Danieli ◽  
Vered Rosenberg ◽  
Avital Bareket-Samish ◽  
Gabriel Chodick ◽  
Varda Shalev

e13599 Background: Trends in breast cancer (BC) incidence may be impacted by potentially competing variables (e.g., mammography rates, hormone-replacement therapy [HRT] use). Methods: This observational retrospective study examined trends/associations between BC incidence, mammography rates, and HRT use among female members of the Maccabi Healthcare Services (the second largest HMO in Israel).BC subtypes were determined based on therapies received by patients diagnosed after 2006 (following trastuzumab approval in the adjuvant setting). Results: Between 2002 and 2014, 14,092 BC cases (88% invasive, 12% in-situ) were identified. The age-adjusted incidence rate of invasive BC peaked in 2005, consistent with increased mammography screening that year, and decreased thereafter. HRT use among all female members aged≥45 years decreased from 13.2% in 2002 to 4.6% in 2014, consistent with the global trend after the Women's Health Initiative publication. Analysis by BC subtype involved 6,218 invasive BC patients diagnosed between 2007 and 2014 (luminal A, 47.5%; luminal B1 without human epidermal growth factor receptor 2 [HER2] over-expression, 25.7%; luminal B2 with HER2 over-expression, 7.7%; estrogen receptor [ER]-negative/HER2+, 4.9%; triple negative, 8.3%; unknown, 6.0%). Overall, 75-86% of patients across all subtypes did not have any HRT exposure vs 14-25% who were current users (within 1 year before the BC diagnosis), recent users (within 2-5 years), or past users ( > 5 years). Current and recent use of HRT was statistically significantly higher in luminal BC vs ER-negative tumors: rates in luminal A/B1/B2, 15.3%/12.1%/11.1% vs ER-negative HER2+/triple-negative/unknown, 8.9%/9.7%/7.7% ( P< 0.001). In BC patients (≥45 years) with HRT exposure, the preparations used were estrogen plus progesterone (62%), estrogen alone (24%), and tibolone (14%). In non-BC cases (≥45 years), the respective values were similar: 61%, 26%, and 13%. Conclusions: HRT current/recent exposure may contribute to increased incidence of luminal BC tumors.


2003 ◽  
Vol 14 (10) ◽  
pp. 979-984 ◽  
Author(s):  
Margaret T. Mandelson ◽  
Diana Miglioretti ◽  
Polly A. Newcomb ◽  
Robert Harrison ◽  
John D. Potter

2004 ◽  
Vol 181 (2) ◽  
pp. 327-337 ◽  
Author(s):  
Y Qiu ◽  
MJ Langman ◽  
MC Eggo

Epidemiological studies show a strong link between postmenopausal hormone replacement therapy and decreased incidence of colorectal cancer. The colon cancer cell line, COLO 205, develops sensitivity to 17beta-oestradiol (E(2)) in apoptosis assays with increasing passage number (>40), and we hypothesised that genes selectively regulated in multiply passaged cells were likely to be important in E(2)-related apoptosis. Gene array analysis was used to compare the patterns of genes up- or down-regulated in E(2)-sensitive and -insensitive cells. For some genes, changes in mRNA expression were confirmed by protein expression analyses. Changes found in response to E(2) in multiply passaged cells, but not minimally passaged cells, included induction of growth arrest and DNA damage-inducible protein 153 (GADD153), and repression of Kirsten-Ras 2B (K-Ras-2B), metastasis inhibition factor NM23 and vascular endothelial growth factor. A second group of genes was regulated with E(2) exposure in both cell types, and is unlikely to be critically involved in E(2)-associated apoptosis. These included up-regulation of butyrate response factor 1 (BRF1) and down-regulation of c-jun and the breast cancer associated ring domain gene known as BARD1. By comparing control arrays from the two cell populations, cAMP-response element-binding protein (CBP), which is associated with steroid receptor-dependent target gene transcription and the oncoprotein, tyrosine kinase-T3 (TRK-T3), were up-regulated whereas retinoic acid receptor alpha (RARalpha) was down-regulated in multiply passaged cells. This study provides evidence for selective regulation of genes in colon cancer cells by E(2), indicates which of those regulated are likely to be involved in induced apoptosis, and suggests genes likely to be responsible for facilitation.


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