查詢結果分析
相關文獻
- Two-hit Hypothesis of Tumor Suppressor Gene and Revisions
- 以銀合歡種子內含成份Mimosine輔助提高化學治癌效果之研究
- 使用剝離細胞學檢測口腔鱗狀細胞癌之p 基因失去異質性
- P53抑癌基因與婦科腫瘤
- 抑癌基因在白血病發生發展中作用
- FHIT (fragile histidine triad)基因在子宮頸癌前期病變之分析
- P53抑癌基因在卵巢透亮細胞癌中不常發生
- Correlation of Elevated mRNA Expression of p53 Gene and Repair Genes with Lung Cancer Chemoresistance
- 以臺灣產茄科中藥調控肝細胞腫瘤中p53及Rb抑癌基因表現與調節修補DNA變異之酵素活性及其在抗腫瘤機轉上的研究
- 分子生物學在消化系醫學上之應用
頁籤選單縮合
題名 | Two-hit Hypothesis of Tumor Suppressor Gene and Revisions=抑癌基因的雙重打擊理論 |
---|---|
作者姓名(中文) | 俞志誠; 沈志陽; | 書刊名 | Journal of Medical Sciences |
卷期 | 22:1 2002.02[民91.02] |
頁次 | 頁13-18 |
分類號 | 415.138 |
關鍵詞 | 抑癌基因; 雙重打擊理論; 失去異質性; Loss of heterozygosity; Tumor suppressor gene; Two-hit model; |
語文 | 英文(English) |
英文摘要 | Knudson proposed his now famous two-hit hypothesis to explain mechanisms involved in inactivating tumor suppressor genes during tumorigenesis. Knudson suggested that two genetic events (hits) are required to abolish both alleles of a tumor suppressor gene, and, more importantly, both familial and sporadic forms of the same cancer are caused by mutations of the same tumor suppressor gene. Genomic loss is always the most common "hit" that inactivates a tumor suppressor gene. This is reflected in a genetic mechanism called loss of heterozygosity (LOH). As a result, the detection of recurrent LOH in a chromosomal region is now considered to be critical evidence for the localization of tumor suppressor genes. However, in sporadic cancers, with a few exceptions, the probability of fining somatic mutation in certain tumor suppressor genes with a high frequency of LOH has been shown to be extremely rare. Recent evidence has suggested two non-mutually exclusive possibilities provided support for a tumorigenic role for these genes defined solely by LOH. The first possibility is that a growing number of common tumor suppressor genes have been found to exhibit the haplo-insufficiency phenotype, which implies that homozygous inactivating mutations and complete loss of function are not necessary to cause defective tumor suppressor function. The second possibility is that other (epigenetic) inactivation mechanisms abrogating the function of these genes are implicated in tumorigenesis. For example, hyper-methylation of the promoter region has been found in some tumor suppressor genes. Based on a study seeking for two hits on E-Cadherine, a tumor suppressor gene associated with tumor metastasis, we suggest that maintaining a reversible mechanism, either by controlling the gene at the transcriptional level or by retaining an intact allele subsequent to LOH, might be important for tumor suppressor genes possessing diverse functions. Thus, inactivation of both alleles of a tumor suppressor gene might not be totally beneficial for tumor development. |
本系統之摘要資訊系依該期刊論文摘要之資訊為主。