Association between KRAS, NRAS, and BRAF mutations and tumor localization in colorectal cancer patients in BSMMU
DOI:
https://doi.org/10.18203/2349-2902.isj20243539Keywords:
Colorectal cancer, KRAS, NRAS, BRAF, DNA isolation, PCR amplificationAbstract
Background: Colorectal cancer (CRC) is a common malignancy with significant genetic heterogeneity. Mutations in proto-oncogenes such as KRAS, NRAS, and BRAF play a pivotal role in CRC development, impacting prognosis and treatment. This study aims to correlate mutations in these genes with tumor localization in both primary and metastatic CRC in the Bangabandhu Sheikh Mujib medical university (BSMMU) cohort.
Methods: This prospective cross-sectional study was conducted between July 2023 and June 2024 at BSMMU. A total of 30 CRC patients, confirmed via histopathology, were included. Purposive sampling was used to select patients. Tumor tissue samples were collected and analyzed for KRAS, NRAS, and BRAF mutations using DNA isolation, PCR amplification, and sequencing techniques.
Results: Among the 30 patients, the majority were male (66.7%) with a mean age of 50.4 years. KRAS mutations were found in 5 patients (16.7%), while no mutations in NRAS or BRAF were detected. Rectal cancer was the most frequent tumor location (36.7%), followed by hepatic and splenic flexure (16.7% each). No significant correlation was observed between KRAS mutations and tumor localization.
Conclusions: There was no statistically significant correlation between KRAS, NRAS, and BRAF mutations and tumor localization in the BSMMU CRC patient cohort. The study highlights the need for larger sample sizes to better understand the genetic landscape of CRC in Bangladesh. Small sample size may limit the ability to detect significant associations. Further large-scale studies could offer more conclusive insights.
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References
Siegel RL, Miller KD, Jemal A. Cancer statistics, 2019. CA Cancer J Clin. 2019;69(1):7-34.
Kuellmer A, Mueller J, Caca K, Aepli P, Albers D, Schumacher B, et al. Endoscopic full-thickness resection for early colorectal cancer. Gastrointest Endosc. 2019;89(6):1180-9.
Dhillon AS, Hagan S, Rath O, Kolch W. MAP kinase signalling pathways in cancer. Oncogene. 2007;26(22):3279-90.
Markman B, Javier Ramos F, Capdevila J, Tabernero J. EGFR and KRAS in colorectal cancer. Adv Clin Chem. 2010;51:71-119.
Uprety D, Adjei AA. KRAS: From undruggable to a druggable cancer target. Cancer Treat Rev. 2020;89:102070.
Sanz-Garcia E, Argiles G, Elez E, Tabernero J. BRAF mutant colorectal cancer: prognosis, treatment, and new perspectives. Ann Oncol. 2017;28(11):2648-57.
Li Y, Shen L, Li J. Analysis of KRAS, NRAS, and BRAF mutations in East Asian patients with early colorectal cancer: A cohort study. Front Oncol. 2022;12:897548.
Fearon ER, Vogelstein B. A genetic model for colorectal tumorigenesis. Cell. 1990;61(5):759-67.
Bożyk A, Krawczyk P, Reszka K, Kinga K, Agnieszka K, Sławomir M, et al. Correlation between KRAS, NRAS, and BRAF mutations and tumor localization in patients with primary and metastatic colorectal cancer. Arch Med Sci. 2022;18(5):1221-30.
Andreyev HJ, Norman AR, Cunningham D, Oates JR, Clarke PA. Kirsten ras mutations in patients with colorectal cancer: the multicenter "RASCAL" study. J Natl Cancer Inst. 1998;90(9):675-84.
Kopetz S, Grothey A, Yaeger R, Van Cutsem E, Desai J, Yoshino T, et al. Encorafenib, binimetinib, and cetuximab in BRAF V600E–mutated colorectal cancer. N Engl J Med. 2019;381(17):1632-43.
Mattiuzzi C, Sanchis-Gomar F, Lippi G. Concise update on colorectal cancer epidemiology. Ann Transl Med. 2019;7(21):609.