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
- 来源:
- 关键词:alcoholic beverage consumption biochemistry biomarker cancer prevention cancer risk dietary constituent early diagnosis gene mutation histopathology human subject interview longitudinal human study neoplasm /cancer classification /staging neoplastic process nucleic acid sequence oral pharyngeal neoplasm polymerase chain reaction preneoplastic state questionnaires single strand conformation polymorphism tobacco abuse tumor suppressor genes
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)
专著数量(0)
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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