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Not All Kirsten Rat Sarcoma Viral Oncogene Homolog Mutations Predict Poor Survival in Patients With Unresectable Colorectal Liver Metastasis

Objective: To assess the characteristics of Kirsten rat sarcoma viral oncogene homolog (KRAS) mutations and investigated whether all KRAS mutations predict poor prognosis in patients with unresectable colorectal liver metastasis (CRLM). Methods: Correlations between KRAS-mutation status and clinicop...

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Autores principales: Lin, Zhizun, Liu, Yi, Cai, Shaoxin, Yang, Changshun, Zhou, Liyuan, Li, Weihua
Formato: Online Artículo Texto
Lenguaje:English
Publicado: SAGE Publications 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8532248/
https://www.ncbi.nlm.nih.gov/pubmed/34669528
http://dx.doi.org/10.1177/15330338211039131
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author Lin, Zhizun
Liu, Yi
Cai, Shaoxin
Yang, Changshun
Zhou, Liyuan
Li, Weihua
author_facet Lin, Zhizun
Liu, Yi
Cai, Shaoxin
Yang, Changshun
Zhou, Liyuan
Li, Weihua
author_sort Lin, Zhizun
collection PubMed
description Objective: To assess the characteristics of Kirsten rat sarcoma viral oncogene homolog (KRAS) mutations and investigated whether all KRAS mutations predict poor prognosis in patients with unresectable colorectal liver metastasis (CRLM). Methods: Correlations between KRAS-mutation status and clinicopathological characteristics of 93 patients with unresectable CRLM at our institution between 2010 and 2018 were retrospectively analyzed. Kaplan–Meier and Cox proportional hazard models were used to evaluate the prognostic significance of KRAS mutations. Results: KRAS were primarily single-point mutations, identified in 41.9% of patients. There were no significant differences in clinicopathological characteristics between wild-type KRAS and mutant KRAS. Patients with mutant KRAS had significantly worse overall survival (OS) and progression-free survival (PFS) than those with wild-type KRAS. Moreover, patients with codon 12 mutations had worse OS and PFS than those with wild-type KRAS, whereas mutations in codon 13 were not associated with a worse prognosis. Among the 5 most common mutations in codons 12, G12V, and G12D were associated with worse OS, furthermore, G12C mutation seemed to associated with worse PFS than patients with wild-type KRAS. Conclusion: KRAS codon 12 mutations were predictive for a poor prognosis in patients with unresectable CRLM. G12D and G12V mutations were associated with worse OS, whereas G12C mutation seemed to be associated with decreased PFS.
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spelling pubmed-85322482021-10-23 Not All Kirsten Rat Sarcoma Viral Oncogene Homolog Mutations Predict Poor Survival in Patients With Unresectable Colorectal Liver Metastasis Lin, Zhizun Liu, Yi Cai, Shaoxin Yang, Changshun Zhou, Liyuan Li, Weihua Technol Cancer Res Treat Original Article Objective: To assess the characteristics of Kirsten rat sarcoma viral oncogene homolog (KRAS) mutations and investigated whether all KRAS mutations predict poor prognosis in patients with unresectable colorectal liver metastasis (CRLM). Methods: Correlations between KRAS-mutation status and clinicopathological characteristics of 93 patients with unresectable CRLM at our institution between 2010 and 2018 were retrospectively analyzed. Kaplan–Meier and Cox proportional hazard models were used to evaluate the prognostic significance of KRAS mutations. Results: KRAS were primarily single-point mutations, identified in 41.9% of patients. There were no significant differences in clinicopathological characteristics between wild-type KRAS and mutant KRAS. Patients with mutant KRAS had significantly worse overall survival (OS) and progression-free survival (PFS) than those with wild-type KRAS. Moreover, patients with codon 12 mutations had worse OS and PFS than those with wild-type KRAS, whereas mutations in codon 13 were not associated with a worse prognosis. Among the 5 most common mutations in codons 12, G12V, and G12D were associated with worse OS, furthermore, G12C mutation seemed to associated with worse PFS than patients with wild-type KRAS. Conclusion: KRAS codon 12 mutations were predictive for a poor prognosis in patients with unresectable CRLM. G12D and G12V mutations were associated with worse OS, whereas G12C mutation seemed to be associated with decreased PFS. SAGE Publications 2021-10-20 /pmc/articles/PMC8532248/ /pubmed/34669528 http://dx.doi.org/10.1177/15330338211039131 Text en © The Author(s) 2021 https://creativecommons.org/licenses/by-nc/4.0/This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License (https://creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access page (https://us.sagepub.com/en-us/nam/open-access-at-sage).
spellingShingle Original Article
Lin, Zhizun
Liu, Yi
Cai, Shaoxin
Yang, Changshun
Zhou, Liyuan
Li, Weihua
Not All Kirsten Rat Sarcoma Viral Oncogene Homolog Mutations Predict Poor Survival in Patients With Unresectable Colorectal Liver Metastasis
title Not All Kirsten Rat Sarcoma Viral Oncogene Homolog Mutations Predict Poor Survival in Patients With Unresectable Colorectal Liver Metastasis
title_full Not All Kirsten Rat Sarcoma Viral Oncogene Homolog Mutations Predict Poor Survival in Patients With Unresectable Colorectal Liver Metastasis
title_fullStr Not All Kirsten Rat Sarcoma Viral Oncogene Homolog Mutations Predict Poor Survival in Patients With Unresectable Colorectal Liver Metastasis
title_full_unstemmed Not All Kirsten Rat Sarcoma Viral Oncogene Homolog Mutations Predict Poor Survival in Patients With Unresectable Colorectal Liver Metastasis
title_short Not All Kirsten Rat Sarcoma Viral Oncogene Homolog Mutations Predict Poor Survival in Patients With Unresectable Colorectal Liver Metastasis
title_sort not all kirsten rat sarcoma viral oncogene homolog mutations predict poor survival in patients with unresectable colorectal liver metastasis
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8532248/
https://www.ncbi.nlm.nih.gov/pubmed/34669528
http://dx.doi.org/10.1177/15330338211039131
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