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Updated: Jun 26, 2026

An Orthotopic Bladder Cancer Model for Gene Delivery Studies
Published on: December 1, 2013
Mutations of RAS gene family in specimens of bladder cancer
Navaz Karimianpour1, Parisa Mousavi-Shafaei, Abed-Ali Ziaee
1Institute of Biochemistry and Biophysics, Tehran University, Tehran, Iran.
Introduction:
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.
Materials And Methods:
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.
Results:
None of the patients had mutations in the RAS gene family "hot spots" including codons 12, 13, and 61.
Conclusion:
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.
Insights
This study found no RAS gene mutations in Iranian bladder cancer patients, suggesting varying causes for bladder tumors across populations. RAS mutations may not be a universal factor in bladder cancer development.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- RAS gene mutations are implicated in various human cancers, including bladder tumors.
- Mutation frequencies of RAS genes differ significantly across diverse patient cohorts.
- Understanding RAS mutation prevalence is crucial for targeted therapies and etiological research in bladder cancer.
Purpose of the Study:
- To determine the frequency of specific point mutations within the RAS gene family (HRAS, KRAS, NRAS) in a cohort of Iranian bladder cancer patients.
- To investigate the role of RAS mutations in the development of bladder transitional cell carcinoma in this specific population.
Main Methods:
- Tumor specimens from 35 consecutive patients diagnosed with transitional cell carcinoma were analyzed.
- Polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) was employed to detect HRAS, KRAS, and NRAS gene mutations.
- Specific "hot spots" in codons 12, 13, and 61 of the RAS genes were targeted for mutation analysis.
Main Results:
- No mutations were detected in the RAS gene family's common mutation sites (codons 12, 13, and 61) among the 35 analyzed bladder tumor samples.
- The study found a complete absence of detectable RAS gene mutations in the investigated Iranian patient group.
Conclusions:
- The absence of RAS mutations in this cohort suggests that RAS gene alterations may not be a significant factor in bladder cancer development for this Iranian population.
- These findings highlight the potential role of diverse etiological factors in bladder cancer, indicating that RAS mutations are not universally present in all bladder tumor cases.
- Further research is warranted to explore alternative genetic and environmental factors contributing to bladder cancer in populations where RAS mutations are infrequent.
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