THE ROLE OF OMEGA-3 PUFA IN CANCER PREVENTION

OMEGA-3 多不饱和脂肪酸在预防癌症中的作用

基本信息

  • 批准号:
    3190370
  • 负责人:
  • 金额:
    $ 13.03万
  • 依托单位:
  • 依托单位国家:
    美国
  • 项目类别:
  • 财政年份:
    1988
  • 资助国家:
    美国
  • 起止时间:
    1988-03-01 至 1991-09-29
  • 项目状态:
    已结题

项目摘要

The goals of this investigation are to determine whether isocaloric diets high in n-3 relative to n-6-fatty acids will have the chemopreventive effect in mouse skin carcainogenesis of reducing tumor initiation and promotion. It will be determined whether isocaloric diets containing 10% fat as either high n-6, n- 3, both or predominately saturated fatty acids alter tumor response to a metabolism-requiring carcinogen, 7,12- dimethylbenz(a)anthrene (DMBA) and a direct acting carcinogen, N-methyl-N-nitro-N-nitrosoquanidine (MNNG). Dietary effects on carcinogen binding to DNA and metabolite profiles in the epidermis will also be measured. The effect of these diets will also be studied with respect to tumor promotion, using 12-0- tetradecanyolphorbol-13-acetate (TPA) and benzoyl peroxide, as well as several parameters believed to be important to the promotion process: hyperplasia, inflammation and ornithine decarboxylase induction. Since it is expected that high n-6 fatty acid diets will enhance promotion, tumor experiments will be done in which the major arachidonate metabolites are applied to mice on the high n-3 fatty acid diets to attempt to partially restore promotion. Studies will also be carried out to determine whether the fatty acid effects seen above are epidermal in origin rather than due to changes in systemic parameters such as the immune system. This will be done by culturing mouse epidermal cells in a defined medium containing n-6 and/or n-3 fatty acids and measuring several parameters of growth and differentiation. Finally, it will also be determined if the different fatty acid diets affect the responsiveness of the immune system to challenge. Several parameters will be measured: delayed hypersensitivity, mitogen responsiveness, mixed lymphocyte reactions and natural killer cell activity.
这项调查的目的是确定是否

项目成果

期刊论文数量(0)
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SUSAN M FISCHER其他文献

SUSAN M FISCHER的其他文献

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{{ truncateString('SUSAN M FISCHER', 18)}}的其他基金

Obesity and Pancreatic Cancer: The Role of IGF-1
肥胖和胰腺癌:IGF-1 的作用
  • 批准号:
    8193238
  • 财政年份:
    2009
  • 资助金额:
    $ 13.03万
  • 项目类别:
Obesity and Pancreatic Cancer: The Role of IGF-1
肥胖和胰腺癌:IGF-1 的作用
  • 批准号:
    7653538
  • 财政年份:
    2009
  • 资助金额:
    $ 13.03万
  • 项目类别:
Obesity and Pancreatic Cancer: The Role of IGF-1
肥胖和胰腺癌:IGF-1 的作用
  • 批准号:
    8259466
  • 财政年份:
    2009
  • 资助金额:
    $ 13.03万
  • 项目类别:
Cyclooxygenase-2 Induced Pancreatic Cancer
环氧合酶 2 诱发胰腺癌
  • 批准号:
    8029551
  • 财政年份:
    2008
  • 资助金额:
    $ 13.03万
  • 项目类别:
Cyclooxygenase-2 Induced Pancreatic Cancer
环氧合酶 2 诱发胰腺癌
  • 批准号:
    8212143
  • 财政年份:
    2008
  • 资助金额:
    $ 13.03万
  • 项目类别:
Cyclooxygenase-2 Induced Pancreatic Cancer
环氧合酶 2 诱发胰腺癌
  • 批准号:
    7463485
  • 财政年份:
    2008
  • 资助金额:
    $ 13.03万
  • 项目类别:
Cyclooxygenase-2 Induced Pancreatic Cancer
环氧合酶 2 诱发胰腺癌
  • 批准号:
    7758221
  • 财政年份:
    2008
  • 资助金额:
    $ 13.03万
  • 项目类别:
Cyclooxygenase-2 Induced Pancreatic Cancer
环氧合酶 2 诱发胰腺癌
  • 批准号:
    7589786
  • 财政年份:
    2008
  • 资助金额:
    $ 13.03万
  • 项目类别:
COX-2 Driven Pancreatic Adenocarcinoma
COX-2驱动的胰腺腺癌
  • 批准号:
    7126617
  • 财政年份:
    2006
  • 资助金额:
    $ 13.03万
  • 项目类别:
COX-2 Driven Pancreatic Adenocarcinoma
COX-2驱动的胰腺腺癌
  • 批准号:
    7268125
  • 财政年份:
    2006
  • 资助金额:
    $ 13.03万
  • 项目类别:

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精神分裂症中的磷脂-花生四烯酸-类二十烷酸信号传导
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精神分裂症中的磷脂-花生四烯酸-类二十烷酸信号传导
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