探討在中台灣地區的白血病病患中beta-catenin和N-ras之突變率

因為基因突變而引起前致癌基因的活化造成細胞不正常的生長最後會導致腫瘤的形成是常見的現象。前致癌基因如：beta-catenin及N-ras分別參與在Wnt傳遞路徑及MAPK的活化，此二者蛋白的突變在許多的腫瘤組織中已被發表，本研究主要探討在中部地區的白血病病患中此二種前致癌基因突變的頻率。我們抽取22位病患的體DNA(genomic DNA)進行聚合連鎖反應(polymerase chain reaction, PCR)，接著利用DNA定序的方式去偵測此二者的突變。本實驗顯示在22病患中只有兩位有beta-catenin基因突變而16位病患中有一位病患被偵測出N-ras的突變情形。我們的研究指出在中部地區的白血病生成過程中beta-catenin和N-ras的突變扮演極微小的角色。
Mutation of proto-oncogene commonly results in their activation, triggering abnormal cell growth leading to formation of cancers caused formation of cancers. The protooncogene beta-catenin is involved in Wnt signal transduction and N-ras in the activation of MAPK. Both have been found to be mutated in several human tumors. In this study investigating the mutation frequency of these two genes in leukemia patients in central part of Taiwan, we performed PCR amplification and DNA sequencing analysis on twenty-two genomic DNAs derived from leukemia patients. We found that two out of the twenty-two patients harbored beta-catenin mutation and one out of sixteen harbored N-ras mutation. Our data suggests that mutation of beta-catenin and N-ras may play only a minor role in the tumorigenesis of leukemia.