P53--MARKER FOR ORAL CAVITY PREMALIGNANCY & CANCER RISK

P53——口腔癌前病变标志物

基本信息

  • 批准号:
    2100529
  • 负责人:
  • 金额:
    $ 14.84万
  • 依托单位:
  • 依托单位国家:
    美国
  • 项目类别:
  • 财政年份:
    1995
  • 资助国家:
    美国
  • 起止时间:
    1995-04-01 至 1996-01-31
  • 项目状态:
    已结题

项目摘要

The p53 tumor suppressor gene has been strongly implicated in the process of carcinogenesis. In particular, a strong association exists between mutations of the p53 gene and a variety of tobacco-related cancers, including cancers of head and neck, where p53 mutations were observed in up to 78% of head and neck squamous cell carcinomas from patients who were chronic smokers. The origin of p53 mutations during tumor progression has been studied by determining p53 mutation incidence in premalignant lesions of various organs and may be indicative of the tumorigenic potential of these lesions. We and others have obtained preliminary data demonstrating that premalignant lesions of the oral cavity may possess mutations at the p53 locus and that this may be dependent upon the degree of lesion dysplasia and/or malignant potential. These data suggest that p53 mutation may be an early event in oral cavity cancer progression. Since mutation of the p53 gene is highly correlated with the malignant phenotype, it may be an excellent candidate for risk assessment for oral cavity cancer in individuals with oral cavity preneoplastic lesions, and may serve as an intermediate biomarker in chemoprevention trials. In addition, we have demonstrated what appears to be a direct correlation between p53 mutation incidence in oral cavity premalignant lesions and a specific risk factor for oral cavity cancer - tobacco use. This must be confirmed using a larger subset of tumor tissue samples from tobacco users and non-users. We hypothesize that mutations of the p53 gene may be an important biomarker for determining the tumorigenic potential of premalignant lesions of the oral cavity. The overall goal of this research proposal is to examine the incidence of p53 mutations in premalignant lesions of the oral cavity and correlate this incidence with; i) the known tumorigenic potentials of different oral cavity premalignant lesion classes, ii) the degree of lesion dysplasia, and iii) specific risk factors. Premalignant oral cavity lesion samples will be obtained from patients recruited from five collaborating centers. Lesion tumorigenic potential will be assessed by diagnostic classification of lesions into categories of known tumorigenic potentials, and the degree of dysplasia will be determined histologically. P53 mutations will be assayed using sensitive molecular techniques such as polymerase chain reaction/single strand conformational polymorphism and DNA sequencing. To verify the causal relationship between p53 mutations and cancer in oral cavity premalignant lesions, we will also examine a small group of oral cavity premalignant lesions (in paraffin blocks) obtained prospectively from patients who later developed oral cavity cancer. The p53 mutational incidence and spectrum in these lesions will be compared to the incidence and spectrum observed in the tumors taken from the same patients. These studies should provide us with valuable information on p53 mutation as a biomarker for oral cavity cancer progression and etiology, and should indicate whether an analysis of the p53 mutational status of these lesions may be useful for both cynical diagnosis and patient prognosis and treatment. These studies should aid in the detection of oral cavity premalignant lesions with the highest tumorigenic potential in patients, and should ultimately lead to improved and more aggressive treatment modalities for such lesions.
p53肿瘤抑制基因与这一过程密切相关

项目成果

期刊论文数量(0)
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科研奖励数量(0)
会议论文数量(0)
专利数量(0)

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Philip Lazarus其他文献

Philip Lazarus的其他文献

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{{ truncateString('Philip Lazarus', 18)}}的其他基金

Gene-tobacco carcinogen interactions and lung cancer risk - a novel approach for precision cancer prevention
基因-烟草致癌物相互作用和肺癌风险——精准癌症预防的新方法
  • 批准号:
    10581340
  • 财政年份:
    2022
  • 资助金额:
    $ 14.84万
  • 项目类别:
The UGT2A and 3A metabolizing enzymes and tobacco-related cancer risk
UGT2A 和 3A 代谢酶与烟草相关癌症风险
  • 批准号:
    9131748
  • 财政年份:
    2015
  • 资助金额:
    $ 14.84万
  • 项目类别:
The UGT2A and 3A metabolizing enzymes and tobacco-related cancer risk
UGT2A 和 3A 代谢酶与烟草相关癌症风险
  • 批准号:
    9221216
  • 财政年份:
    2015
  • 资助金额:
    $ 14.84万
  • 项目类别:
The UGT2A and 3A metabolizing enzymes and tobacco-related cancer risk
UGT2A 和 3A 代谢酶与烟草相关癌症风险
  • 批准号:
    9278174
  • 财政年份:
    2015
  • 资助金额:
    $ 14.84万
  • 项目类别:
Role of pharmacogenetics on exemestane metabolism and toxicity
药物遗传学对依西美坦代谢和毒性的作用
  • 批准号:
    8727490
  • 财政年份:
    2012
  • 资助金额:
    $ 14.84万
  • 项目类别:
Role of pharmacogenetics on exemestane metabolism and toxicity
药物遗传学对依西美坦代谢和毒性的作用
  • 批准号:
    8915094
  • 财政年份:
    2012
  • 资助金额:
    $ 14.84万
  • 项目类别:
Role of pharmacogenetics on exemestane metabolism and toxicity
药物遗传学对依西美坦代谢和毒性的作用
  • 批准号:
    8372081
  • 财政年份:
    2012
  • 资助金额:
    $ 14.84万
  • 项目类别:
Role of pharmacogenetics on exemestane metabolism and toxicity
药物遗传学对依西美坦代谢和毒性的作用
  • 批准号:
    8527745
  • 财政年份:
    2012
  • 资助金额:
    $ 14.84万
  • 项目类别:
UDP-GLUCURONOSYLTRANSFERASE GENOTYPE AND CANCER RISK
UDP-葡萄糖醛酸基转移酶基因型和癌症风险
  • 批准号:
    7265009
  • 财政年份:
    2007
  • 资助金额:
    $ 14.84万
  • 项目类别:
UDP-GLUCURONOSYLTRANSFERASE GENOTYPE AND CANCER RISK
UDP-葡萄糖醛酸基转移酶基因型和癌症风险
  • 批准号:
    7612146
  • 财政年份:
    2007
  • 资助金额:
    $ 14.84万
  • 项目类别:

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