Mutations of RAS gene family in specimens of bladder cancer

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

Role of PTEN gene in progression of Prostate Cancer

The aim of this study was to clarify the role of PTEN gene in progression of prostate cancer. A total of 51 formalin-fixed paraffin-embedded specimens of prostate cancer were analyzed for PTEN mutations. Tissue microdissection and polymerase chain reaction/ single-strand conformation polymorphism methods were used. Clinical and pathologic data of the patients were reviewed with regard to PTEN mutation. The Gleason score [GS] was less than 7 in 29 [56.8%], 7 in 11 [21.6%], and greater than 7 in 11 [21.6%]. Tumor stage was IIa, IIb, IIc, and IV in 14 [27.4%], 4 [7.8%], 21 [41.2%], and 12 [23.6%] patients, respectively. Eleven of 12 stage IV tumors had metastases at the time of presentation. Six of 51 cases [11.6%] showed mutation in PTEN which had involved exones 1,2, and 5. Two of these cases had localized and the others had advanced prostate cancer. One case of the tumors with PTEN mutation had a GS of 7 and 5 had GSs greater than 7. Patients with a positive mutation of PTEN had a significantly greater GS [P<.001], lower survival rate [P=.001], higher tendency to metastasis [P=.002], and higher prostate-specific antigen [p=.03]. Cox proportional hazard model showed that only GS was significantly correlated with mortality [P=.03]. Patients with prostate cancer who had PTEN mutation had also a significantly greater GS, poorer prognosis, and higher rate of metastasis. However, this mutation cannot predict the prognosis and the GS is a more precise factor