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Sex Differences in Hepatotoxic, Infl...

Hanna, Daniel.

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Sex Differences in Hepatotoxic, Inflammatory and Proliferative Responses in Mouse Models of Liver Carcinogenesis.

Record Type:	Electronic resources : Monograph/item
Title/Author:	Sex Differences in Hepatotoxic, Inflammatory and Proliferative Responses in Mouse Models of Liver Carcinogenesis./
Author:	Hanna, Daniel.
Published:	Ann Arbor : ProQuest Dissertations & Theses, : 2018,
Description:	170 p.
Notes:	Source: Dissertations Abstracts International, Volume: 80-05, Section: B.
Contained By:	Dissertations Abstracts International80-05B.
Subject:	Toxicology. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=10842162
ISBN:	9780438670259

Sex Differences in Hepatotoxic, Inflammatory and Proliferative Responses in Mouse Models of Liver Carcinogenesis.
Hanna, Daniel.

Sex Differences in Hepatotoxic, Inflammatory and Proliferative Responses in Mouse Models of Liver Carcinogenesis. - Ann Arbor : ProQuest Dissertations & Theses, 2018 - 170 p.

Source: Dissertations Abstracts International, Volume: 80-05, Section: B.

Thesis (Ph.D.)--University of Toronto (Canada), 2018.

This item must not be sold to any third party vendors.

Liver cancer is the third most common cause of cancer-related death in humans and is 2-4 times more common in men than in women for reasons that are not clear. Chronic inflammation is a critical driving force for liver cancer and may play a role in the increased risk in men. Postnatal exposure of mice to liver procarcinogens like 4-aminobiphenyl (ABP) or diethylnitrosamine (DEN), or in genetically modified mice such as the hepatitis B virus transgenic (HBVTg) mouse, also produces more liver cancer in males than in females. Liver damage, inflammation and proliferation are central characteristics of liver cancer, and were previously found to be acutely higher in adult male mice than in females after high-dose exposure to DEN. However, postnatal exposure of mice to tumor-inducing doses of either ABP or DEN produces no acute response. It is not known whether sex differences may develop chronically after sexual maturation. We compared specific biomarkers of liver damage, inflammation and cell proliferation between male and female mice exposed to ABP or DEN postnatally, and in HBVTg mice, throughout the time period that mice are maintained in standard liver tumor studies. Postnatal exposure to ABP or DEN produced no chronic liver damage, inflammation or proliferation in either male or female mice. HBVTg mice had increased liver damage and proliferation and a modest increase in inflammation with age, but no sex difference. We show that chronic liver damage, inflammation and proliferation are not detectable in standard chemical-induced liver tumor induction models and are increased in HBVTg mice, but with no sex differences. Our results suggest that while chronic liver damage, inflammation and proliferation may be necessary for liver tumor development, they do not appear to be necessary contributors to the observed sex difference in liver tumor risk.

ISBN: 9780438670259Subjects--Topical Terms:

556884
Toxicology.
Subjects--Index Terms:

Hepatotoxicity

Sex Differences in Hepatotoxic, Inflammatory and Proliferative Responses in Mouse Models of Liver Carcinogenesis.
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520 $a Liver cancer is the third most common cause of cancer-related death in humans and is 2-4 times more common in men than in women for reasons that are not clear. Chronic inflammation is a critical driving force for liver cancer and may play a role in the increased risk in men. Postnatal exposure of mice to liver procarcinogens like 4-aminobiphenyl (ABP) or diethylnitrosamine (DEN), or in genetically modified mice such as the hepatitis B virus transgenic (HBVTg) mouse, also produces more liver cancer in males than in females. Liver damage, inflammation and proliferation are central characteristics of liver cancer, and were previously found to be acutely higher in adult male mice than in females after high-dose exposure to DEN. However, postnatal exposure of mice to tumor-inducing doses of either ABP or DEN produces no acute response. It is not known whether sex differences may develop chronically after sexual maturation. We compared specific biomarkers of liver damage, inflammation and cell proliferation between male and female mice exposed to ABP or DEN postnatally, and in HBVTg mice, throughout the time period that mice are maintained in standard liver tumor studies. Postnatal exposure to ABP or DEN produced no chronic liver damage, inflammation or proliferation in either male or female mice. HBVTg mice had increased liver damage and proliferation and a modest increase in inflammation with age, but no sex difference. We show that chronic liver damage, inflammation and proliferation are not detectable in standard chemical-induced liver tumor induction models and are increased in HBVTg mice, but with no sex differences. Our results suggest that while chronic liver damage, inflammation and proliferation may be necessary for liver tumor development, they do not appear to be necessary contributors to the observed sex difference in liver tumor risk.
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