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Harvey JA , Santen RJ , Petroni GR , Bovbjerg VE , Smolkin ME , Sheriff FS , Russo J
Histologic changes in the breast with menopausal hormone therapy use: correlation with breast density, estrogen receptor, progesterone receptor, and proliferation indices
Menopause-the Journal of the North American Menopause Society. 2008 Jan-Feb;15(1) :67-73
AbstractObjective: This retrospective study systematically compared mammographic density with histology in women receiving or not receiving menopausal hormone therapy (HT). Design: This study was approved by the institutional review board. Twenty-eight postmenopausal women using HT were matched with 28 postmenopausal women not using HT at the time of breast cancer diagnosis. Noncancerous tissue from mastectomy specimens was examined histologically to quantitate the content of fibrous stroma, ducts, and lobule types 1, 2, and 3. Tissue samples were also evaluated for estrogen receptor, progesterone receptor, and Ki67 activity in the ducts and lobules. Breast density was quantified by digitizing the contralateral mammogram and computer-assisted interactive thresholding. Results: High breast density in women using HT was correlated with greater fibrous stroma (P = 0.020) and lobule type 1 (P = 0.016). Breast density also correlated with Ki67 activity in the ducts (P = 0.031) and lobules (P = 0.023) for both groups combined. Estrogen and progesterone receptors did not correlate with either breast density or HT use. Conclusions: Increased fibrous stroma and lobule type 1 are associated with increasing mammographic density in women using HT, independent of estrogen and progesterone receptor up-regulation. These findings suggest that increased breast density may be mediated through a paracrine effect. The increase in breast cancer risk with HT use may be due to an increase in target lobule type 1 cells.
NotesISI Document Delivery No.: 249YJ Times Cited: 0 Cited Reference Count: 39 Cited References: ANDERSON E, 1998, J MAMMARY GLAND BIOL, V3, P23 ANDERSON GL, 2004, JAMA-J AM MED ASSOC, V291, P1701 BANKS E, 2003, LANCET, V362, P419 BOYD NF, 1995, J NATL CANCER I, V87, P670 BOYD NF, 1998, CANCER EPIDEM BIOMAR, V7, P1133 BRISSON J, 2000, CANCER EPIDEM BIOMAR, V9, P911 BYNG JW, 1998, RADIOGRAPHICS, V18, P1587 BYRNE C, 1995, J NATL CANCER I, V87, P1622 BYRNE C, 2000, CANCER RES, V60, P3744 CHEN WY, 2006, ARCH INTERN MED, V166, P1027 CHRISTODOULAKOS GE, 2002, MENOPAUSE, V9, P110 CUZICK J, 2004, J NATL CANCER I, V96, P621 FREEDMAN M, 2001, J NATL CANCER I, V93, P51 GARMYSUSINI B, 2004, CIRC RES, V94, P1301 GOLD EB, 2001, AM J EPIDEMIOL, V153, P865 GREENDALE GA, 1999, ANN INTERN MED 1, V130, P262 GREENDALE GA, 2003, J NATL CANCER I, V95, P30 HARVEY JA, 2004, RADIOLOGY, V230, P29 HOFSETH LJ, 1999, J CLIN ENDOCR METAB, V84, P4559 JACKSON VP, 2003, AM J OBSTET GYNECOL, V188, P389 NAGATA C, 2005, BRIT J CANCER, V92, P2102 PAGE DL, 1986, AM J ROENTGENOL, V147, P487 PALMIERI C, 2004, J MOL ENDOCRINOL, V33, P35 PARMAR H, 2004, ENDOCR-RELAT CANCER, V11, P437 PERSSON I, 1997, J CLIN ONCOL, V15, P3201 PERSSON I, 1999, CANCER CAUSE CONTROL, V10, P253 PUROHIT A, 2005, J STEROID BIOCHEM, V94, P167 REED MJ, 2001, CLIN ENDOCRINOL, V54, P563 ROSS RK, 2000, J NATL CANCER I, V92, P328 ROSSOUW JE, 2002, JAMA-J AM MED ASSOC, V288, P321 RUSSO J, 1987, MAMMARY GLAND DEV RE, P67 RUSSO J, 1990, LAB INVEST, V62, P244 RUSSO J, 1999, BREAST CANCER RES TR, V53, P217 RUSSO J, 2004, BIOL MOL BASIS BREAS RUTTER CM, 2001, JAMA-J AM MED ASSOC, V285, P171 SCHAIRER C, 2000, JAMA-J AM MED ASSOC, V283, P485 SINGH A, 1997, J STEROID BIOCHEM, V61, P185 STEFANICK ML, 2006, JAMA-J AM MED ASSOC, V295, P1647 VACEK PM, 2004, CANCER EPIDEM BIOMAR, V13, P715 Harvey, Jennifer A. Santen, Richard J. Petroni, Gina R. Bovbjerg, Viktor E. Smolkin, Mark E. Sheriff, Fathima S. Russo, Jose LIPPINCOTT WILLIAMS & WILKINS; 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA