Abstract 49P
Background
We aimed to investigate the effects of RAS and BRAF analyses and mutations on survival in patients diagnosed with metastatic colorectal cancer (mCRC), which we followed in our clinic for last 5 years.
Methods
186 patients followed up in our clinic with mCRC were reviewed retrospectively.
Results
The median age of 186 patients followed up with mCRC was 58 (44–76). 118 (63%) were men and 68 (37%) were women. At the end of the mean 40.3(8-122) months follow-up period, 74 (40%) of patients were alive, while 112 (60%) were passed away. Primary tumor localization and metastasis areas (liver, lymph nodes, lung, peritoneal carsinomatosis) of the patients were examined at the time of diagnosis. The overall survival of 47 KRAS mutant patients was 32 months, shorter than that of KRAS wild-type patients (P=0.66). The overall survival of three NRAS mutant patients was 33 months, shorter than that of NRAS wild patients (P=0.68). In accordance with the literature, the survival of BRAF mutant patients was shorter at 17.5 months (P=0.33).
Conclusions
There was no significant difference in survival between RAS/BRAF mutant patients treated with doublet plus anti-EGFR agent or doublet plus anti-VEGF agent. However, one of the BRAF mutant patients was also MSI-high (MSI-H) and treated with doublet plus anti-VEGF therapy; the survival time was significantly longer than that of the other BRAF mutant patients at 28 months (p < 0.05). According to the literature, Ras-wild patients were initially treated with doublets plus anti-EGFR agents. In our study, according to the RAS analysis, no treatment option had a statistically significant effect on survival. The overall survival of 47 KRAS mutant patients was 32 months, shorter than that of KRAS wild-type patients (P=0.66). While the patients in the RAS/BRAF wild group were observed to live longer than the other, no statistical significance was detected (36 months ± 13.7 x 30.5 months ± 10.5, p=0.728). The use of intensive chemotherapy regimens in BRAF mutant and MSI-H patients with a low incidence and poor prognosis of mCRC, the inclusion of anti-VEGF therapy in the first-line treatment, and the selection of new targeted therapies based on new genomic discoveries can increase effectiveness.
Clinical trial identification
Editorial acknowledgement
Legal entity responsible for the study
M. Özkan.
Funding
Has not received any funding.
Disclosure
All authors have declared no conflicts of interest.
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Abstract