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Molecular mechanisms of dietary and ...
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Ngo, Tung Hoang.
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Molecular mechanisms of dietary and exercise prevention of prostate cancer.
紀錄類型:
書目-語言資料,印刷品 : Monograph/item
正題名/作者:
Molecular mechanisms of dietary and exercise prevention of prostate cancer./
作者:
Ngo, Tung Hoang.
面頁冊數:
171 p.
附註:
Chair: R. James Barnard.
Contained By:
Dissertation Abstracts International63-07B.
標題:
Biology, Animal Physiology. -
電子資源:
http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3058531
ISBN:
0493743766
Molecular mechanisms of dietary and exercise prevention of prostate cancer.
Ngo, Tung Hoang.
Molecular mechanisms of dietary and exercise prevention of prostate cancer.
- 171 p.
Chair: R. James Barnard.
Thesis (Ph.D.)--University of California, Los Angeles, 2002.
Prostate cancer is the most commonly diagnosed cancer in Western men, but it is a rare malignancy in East Asian men. Small, latent prostate cancer incidence, however, is similar among countries around the world. Rates of prostate cancer in East Asian migrants to Western countries are much higher than the rates of prostate cancer in their countries of origin, with further increases in second-generation migrants. The Western lifestyle, including high-fat consumption and physical inactivity, is implicated in this trend of prostate cancer incidence. It has been unclear how lifestyle modifications affect prostate cancer cell growth and apoptosis at the molecular level. In an <italic>in vitro</italic> human study, fasting serum from men before and after participating in a healthy diet and exercise intervention (DE) was used to stimulate LNCaP prostate cancer cells. Serum factors were also analyzed for the effects of DE. Compared to serum obtained before DE, post-DE serum reduced LNCaP cell growth and induced apoptosis. DE reduced serum IGF-I and raised serum IGFBP-1. Adding IGF-I to LNCaP cell cultures stimulated growth, while adding IGFBP-1 resulted in inhibition of growth and activation of apoptosis. IGFBP-1 was shown to antagonize IGF-I action in an IGF-dependent manner. In an <italic>in vivo</italic> animal study, SCID mice were isocalorically fed either a high-fat (HF) or low-fat (LF) diet and injected subcutaneously with LAPC-4 prostate cancer cells, while still maintaining their respective diet throughout the experiment. LAPC-4 tumors in HF mice grew much more rapidly than tumors in LF mice. Serum from HF mice stimulated more growth of LAPC-4 cells <italic>in vitro</italic> than serum from LF mice. Serum IGF-I was higher, while serum IGFBP-1 was lower, in HF mice than in LF mice. Tumor IGF-I expression is still being analyzed, while tumor IGFBP-2 expression was higher in HF tumors compared to LF tumors. In conclusion, the effects of diet and exercise on prostate cancer growth were shown to be mediated through the IGF axis, especially IGF-I, IGFBP-1, and IGFBP-2. The interaction between these factors has specific effects on prostate cancer cell growth and apoptosis, and diet and exercise modify this interaction in favor of prostate cancer inhibition.
ISBN: 0493743766Subjects--Topical Terms:
1017835
Biology, Animal Physiology.
Molecular mechanisms of dietary and exercise prevention of prostate cancer.
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Prostate cancer is the most commonly diagnosed cancer in Western men, but it is a rare malignancy in East Asian men. Small, latent prostate cancer incidence, however, is similar among countries around the world. Rates of prostate cancer in East Asian migrants to Western countries are much higher than the rates of prostate cancer in their countries of origin, with further increases in second-generation migrants. The Western lifestyle, including high-fat consumption and physical inactivity, is implicated in this trend of prostate cancer incidence. It has been unclear how lifestyle modifications affect prostate cancer cell growth and apoptosis at the molecular level. In an <italic>in vitro</italic> human study, fasting serum from men before and after participating in a healthy diet and exercise intervention (DE) was used to stimulate LNCaP prostate cancer cells. Serum factors were also analyzed for the effects of DE. Compared to serum obtained before DE, post-DE serum reduced LNCaP cell growth and induced apoptosis. DE reduced serum IGF-I and raised serum IGFBP-1. Adding IGF-I to LNCaP cell cultures stimulated growth, while adding IGFBP-1 resulted in inhibition of growth and activation of apoptosis. IGFBP-1 was shown to antagonize IGF-I action in an IGF-dependent manner. In an <italic>in vivo</italic> animal study, SCID mice were isocalorically fed either a high-fat (HF) or low-fat (LF) diet and injected subcutaneously with LAPC-4 prostate cancer cells, while still maintaining their respective diet throughout the experiment. LAPC-4 tumors in HF mice grew much more rapidly than tumors in LF mice. Serum from HF mice stimulated more growth of LAPC-4 cells <italic>in vitro</italic> than serum from LF mice. Serum IGF-I was higher, while serum IGFBP-1 was lower, in HF mice than in LF mice. Tumor IGF-I expression is still being analyzed, while tumor IGFBP-2 expression was higher in HF tumors compared to LF tumors. In conclusion, the effects of diet and exercise on prostate cancer growth were shown to be mediated through the IGF axis, especially IGF-I, IGFBP-1, and IGFBP-2. The interaction between these factors has specific effects on prostate cancer cell growth and apoptosis, and diet and exercise modify this interaction in favor of prostate cancer inhibition.
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