Karimianpour Navaz, Mousavi-Shafaei Parisa, Ziaee Abed-Ali, Akbari Mohammad Taghi, Pourmand Gholamreza, Abedi Amirreza, Ahmadi Ali, Afshin Alavi Hossein
Institute of Biochemistry and Biophysics, Tehran University, Tehran, Iran.
Urol J. 2008 Fall;5(4):237-42.
Studies have shown different types of RAS mutations in human bladder tumors with a wide range of mutation frequencies in different patient populations. This study aimed to assess the frequency of specific-point mutations in the RAS gene family of a group of Iranian patients with bladder cancer.
We examined the tumor specimens of 35 consecutive patients with transitional cell carcinoma. The DNA samples were evaluated for the occurrence of HRAS, KRAS, and NRAS activation using a polymerase chain reaction-restriction fragment length polymorphism technique.
None of the patients had mutations in the RAS gene family "hot spots" including codons 12, 13, and 61.
We failed to find RAS mutations in our bladder tumor samples. These observations may reflect the involvement of different etiological factors in the induction of bladder tumor of which RAS mutation might not be present in all populations.
研究表明，人类膀胱肿瘤中存在不同类型的RAS突变，在不同患者群体中的突变频率范围广泛。本研究旨在评估一组伊朗膀胱癌患者RAS基因家族中特定点突变的频率。
我们检查了35例连续性移行细胞癌患者的肿瘤标本。使用聚合酶链反应-限制性片段长度多态性技术评估DNA样本中HRAS、KRAS和NRAS激活的发生情况。
所有患者的RAS基因家族“热点”（包括第12、13和61密码子）均未发生突变。
我们在膀胱肿瘤样本中未发现RAS突变。这些观察结果可能反映了不同病因因素在膀胱肿瘤诱导中的作用，其中RAS突变可能并非在所有人群中都存在。
