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Estrogen Inhibits Colon Polyp Formation in a Benzo(a)Pyrene‐Induced Colon Cancer Rat Model
Author(s) -
Harris Kenneth J.,
AmosLandgraf James,
Archibong Anthony E.,
Adunyah Samuel E.,
Ramesh Aramandla
Publication year - 2019
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2019.33.1_supplement.812.10
Subject(s) - estrogen , colorectal cancer , medicine , carcinogen , endocrinology , incidence (geometry) , cancer , estrogen receptor , benzo(a)pyrene , gastroenterology , oncology , chemistry , breast cancer , biochemistry , physics , optics
Colorectal cancer (CRC) is the third most common diagnosed cancer and the third leading cause of cancer‐related deaths in the United States. The incidence and mortality rates of colorectal cancer are higher in men than in women. Epidemiological evidence show estrogen might influence the incidence of CRC in women by acting in a protective role. Whether estrogen acts via estrogen receptor beta (ERβ) to render its protective effect or through some other mechanism is not yet known. Using the Polyposis in Rat Colon (PIRC) animal model, we have demonstrated that male animals develop twice as many polyps in the colon than female animals when treated with the food toxicant, Benzo(a)pyrene [B(a)P]. In this study, to assess the potential protective role of estrogen against polyp formation in the colon, we treated female PIRC rats, depleted of ovarian steroids by ovariectomy (OVX), with B(a)P and measured polyp development. We found that B(a)P treatment of OVX‐female PIRC rats increased the polyp numbers when compared to control OVX‐female animals. Estrogen replacement in these B(a)P‐treated OVX PIRC rats significantly decreased total colon polyp numbers. These results suggest that estrogen does provide protection against B(a)P‐induced colon carcinogenesis. Support or Funding Information This research was funded by NIH grants 5R25GM059994‐3, U54CA163069‐04 and G12MD007586‐29. This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .