Dose KRAS mutation status affect on the effect of VEGF therapy in metastatic colon cancer patients?

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Abstract

Purpose: Mutations affecting the KRAS gene are an established negative predictor for antiepidermal growth factor receptor (anti-EGFR) therapies in metastatic colorectal cancer (CRC). However, the role of KRAS mutation as a biomarker for anti-vascular endothelial growth factor (VEGF) remains controversial. Materials and Methods: We analyzed retrospective data from 32 CRC patients who were available for KRAS mutation status and received cytotoxic chemotherapy plus bevacizumab as a first-line therapy. Six of 32 patients received anti-EGFR therapies. We used KRAS mutation status as a predictive or prognostic factor in CRC patients receiving bevacizumab. Results: We observed mutations in KRAS in 59.4% of patients. Bevacizumab was used in combination with oxaliplatin based regimens. There was no significant difference for progression free survival (PFS) and overall survival (OS) in patients with oxaliplatin based cytotoxic chemotherapy plus bevacizumab according to the status of KRAS mutation. After first-line therapy, 28 patients (87.5%) received second-line therapy. In univariate analysis, KRAS mutations did not have a major prognostic value for PFS (hazard ratio, 1.007; 95% confidence interval [CI], 0.469 to 2.162; p > 0.05) or OS (hazard ratio, 0.548; 95% CI, 0.226 to 1.328; p > 0.05). In addition, anti-EGFR therapies did not affect the impact on OS. Conclusion: KRAS mutation is neither a predictive for bevacizumab nor a prognostic for OS in CRC patients receiving anti-VEGF therapy.

Original languageEnglish
Pages (from-to)48-54
Number of pages7
JournalCancer Research and Treatment
Volume46
Issue number1
DOIs
Publication statusPublished - 2014 Feb 20

Fingerprint

Colonic Neoplasms
Vascular Endothelial Growth Factor A
Mutation
oxaliplatin
Growth Factor Receptors
Colorectal Neoplasms
Survival
Therapeutics
Disease-Free Survival
Confidence Intervals
Drug Therapy
Biomarkers
Bevacizumab
Genes

Keywords

  • Colonic neoplasms
  • KRAS
  • Vascular endothelial growth factor

ASJC Scopus subject areas

  • Cancer Research
  • Oncology

Cite this

@article{f3619501fef34b35a622a28043b8d149,
title = "Dose KRAS mutation status affect on the effect of VEGF therapy in metastatic colon cancer patients?",
abstract = "Purpose: Mutations affecting the KRAS gene are an established negative predictor for antiepidermal growth factor receptor (anti-EGFR) therapies in metastatic colorectal cancer (CRC). However, the role of KRAS mutation as a biomarker for anti-vascular endothelial growth factor (VEGF) remains controversial. Materials and Methods: We analyzed retrospective data from 32 CRC patients who were available for KRAS mutation status and received cytotoxic chemotherapy plus bevacizumab as a first-line therapy. Six of 32 patients received anti-EGFR therapies. We used KRAS mutation status as a predictive or prognostic factor in CRC patients receiving bevacizumab. Results: We observed mutations in KRAS in 59.4{\%} of patients. Bevacizumab was used in combination with oxaliplatin based regimens. There was no significant difference for progression free survival (PFS) and overall survival (OS) in patients with oxaliplatin based cytotoxic chemotherapy plus bevacizumab according to the status of KRAS mutation. After first-line therapy, 28 patients (87.5{\%}) received second-line therapy. In univariate analysis, KRAS mutations did not have a major prognostic value for PFS (hazard ratio, 1.007; 95{\%} confidence interval [CI], 0.469 to 2.162; p > 0.05) or OS (hazard ratio, 0.548; 95{\%} CI, 0.226 to 1.328; p > 0.05). In addition, anti-EGFR therapies did not affect the impact on OS. Conclusion: KRAS mutation is neither a predictive for bevacizumab nor a prognostic for OS in CRC patients receiving anti-VEGF therapy.",
keywords = "Colonic neoplasms, KRAS, Vascular endothelial growth factor",
author = "Kim, {Seung Tae} and Park, {Kyong Hwa} and Shin, {Sang Won} and Kim, {Yeul Hong}",
year = "2014",
month = "2",
day = "20",
doi = "10.4143/crt.2014.46.1.48",
language = "English",
volume = "46",
pages = "48--54",
journal = "Cancer Research and Treatment",
issn = "1598-2998",
publisher = "Korean Society for Thoracic and Cardiovascular Surgery",
number = "1",

}

TY - JOUR

T1 - Dose KRAS mutation status affect on the effect of VEGF therapy in metastatic colon cancer patients?

AU - Kim, Seung Tae

AU - Park, Kyong Hwa

AU - Shin, Sang Won

AU - Kim, Yeul Hong

PY - 2014/2/20

Y1 - 2014/2/20

N2 - Purpose: Mutations affecting the KRAS gene are an established negative predictor for antiepidermal growth factor receptor (anti-EGFR) therapies in metastatic colorectal cancer (CRC). However, the role of KRAS mutation as a biomarker for anti-vascular endothelial growth factor (VEGF) remains controversial. Materials and Methods: We analyzed retrospective data from 32 CRC patients who were available for KRAS mutation status and received cytotoxic chemotherapy plus bevacizumab as a first-line therapy. Six of 32 patients received anti-EGFR therapies. We used KRAS mutation status as a predictive or prognostic factor in CRC patients receiving bevacizumab. Results: We observed mutations in KRAS in 59.4% of patients. Bevacizumab was used in combination with oxaliplatin based regimens. There was no significant difference for progression free survival (PFS) and overall survival (OS) in patients with oxaliplatin based cytotoxic chemotherapy plus bevacizumab according to the status of KRAS mutation. After first-line therapy, 28 patients (87.5%) received second-line therapy. In univariate analysis, KRAS mutations did not have a major prognostic value for PFS (hazard ratio, 1.007; 95% confidence interval [CI], 0.469 to 2.162; p > 0.05) or OS (hazard ratio, 0.548; 95% CI, 0.226 to 1.328; p > 0.05). In addition, anti-EGFR therapies did not affect the impact on OS. Conclusion: KRAS mutation is neither a predictive for bevacizumab nor a prognostic for OS in CRC patients receiving anti-VEGF therapy.

AB - Purpose: Mutations affecting the KRAS gene are an established negative predictor for antiepidermal growth factor receptor (anti-EGFR) therapies in metastatic colorectal cancer (CRC). However, the role of KRAS mutation as a biomarker for anti-vascular endothelial growth factor (VEGF) remains controversial. Materials and Methods: We analyzed retrospective data from 32 CRC patients who were available for KRAS mutation status and received cytotoxic chemotherapy plus bevacizumab as a first-line therapy. Six of 32 patients received anti-EGFR therapies. We used KRAS mutation status as a predictive or prognostic factor in CRC patients receiving bevacizumab. Results: We observed mutations in KRAS in 59.4% of patients. Bevacizumab was used in combination with oxaliplatin based regimens. There was no significant difference for progression free survival (PFS) and overall survival (OS) in patients with oxaliplatin based cytotoxic chemotherapy plus bevacizumab according to the status of KRAS mutation. After first-line therapy, 28 patients (87.5%) received second-line therapy. In univariate analysis, KRAS mutations did not have a major prognostic value for PFS (hazard ratio, 1.007; 95% confidence interval [CI], 0.469 to 2.162; p > 0.05) or OS (hazard ratio, 0.548; 95% CI, 0.226 to 1.328; p > 0.05). In addition, anti-EGFR therapies did not affect the impact on OS. Conclusion: KRAS mutation is neither a predictive for bevacizumab nor a prognostic for OS in CRC patients receiving anti-VEGF therapy.

KW - Colonic neoplasms

KW - KRAS

KW - Vascular endothelial growth factor

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