title: Significance of KRAS mutation in patients receiving mFOLFOX6 with or without bevacizumab for metastatic colorectal cancer.
abstract: OBJECTIVE
  KRAS mutation is an important prognostic factor for patients with metastatic colorectal cancer receiving anti-epidermal growth factor receptor therapy. However, the influence of KRAS mutation on the response to mFOLFOX6 ± bevacizumab remains unclear.
  
  
  METHODS
  We retrospectively analyzed 49 patients who received modified FOLFOX6 (mFOLFOX6) ± bevacizumab as first-line therapy. Genetic analysis showed that 30 patients had wild-type (WT) KRAS and 19 patients hadKRAS mutations (MT). These two groups were compared with regard to the response rate (RR), progression-free survival (PFS), and overall survival (OS).
  
  
  RESULTS
  The RR was not significantly different between the WT and MT groups, but PFS and OS were significantly better in the WT group than the MT group (PFS: 11.8 months vs. 8.7 months, p<0.01; OS: 37.8 months vs. 29.3 months, p<0.0385). A similar analysis of 27 patients who were treated with mFOLFOX6 + bevacizumab showed a better prognosis for WT patients. Multivariate analysis also revealed that KRAS mutation was an independent factor with a significant relation to PFS.
  
  
  CONCLUSIONS
  These results suggest that KRAS mutation may be a useful prognostic marker for patients with metastatic colorectal cancer receiving mFOLFOX6 ± bevacizumab therapy, especially for patients treated with mFOLFOX6 + bevacizumab.
authors.forename: Junichi
authors.initials: J
authors.lastname: Koike
authors.forename: Mitsunori
authors.initials: M
authors.lastname: Ushigome
authors.forename: Kimihiko
authors.initials: K
authors.lastname: Funahashi
authors.forename: Hiroyuki
authors.initials: H
authors.lastname: Shiokawa
authors.forename: Tomoaki
authors.initials: T
authors.lastname: Kaneko
authors.forename: Kenichiro
authors.initials: K
authors.lastname: Arai
authors.forename: Satoshi
authors.initials: S
authors.lastname: Matsuda
authors.forename: Satoru
authors.initials: S
authors.lastname: Kagami
authors.forename: Takayuki
authors.initials: T
authors.lastname: Suzuki
authors.forename: Akiharu
authors.initials: A
authors.lastname: Kurihara
authors.forename: Hideaki
authors.initials: H
authors.lastname: Shimada
authors.forename: Hironori
authors.initials: H
authors.lastname: Kaneko
mesh_terms: D000368:Aged; D061067:Antibodies, Monoclonal, Humanized / Q000008:administration & dosage*; D000971:Antineoplastic Combined Chemotherapy Protocols / Q000008:administration & dosage / Q000627:therapeutic use*; D000068258:Bevacizumab; D015179:Colorectal Neoplasms / Q000188:drug therapy* / Q000235:genetics / Q000401:mortality / Q000473:pathology; D005260:Female; D005472:Fluorouracil / Q000008:administration & dosage; D006801:Humans; D002955:Leucovorin / Q000008:administration & dosage; D008297:Male; D008875:Middle Aged; D009154:Mutation; D009362:Neoplasm Metastasis; D009944:Organoplatinum Compounds / Q000008:administration & dosage; D011518:Proto-Oncogene Proteins / Q000235:genetics*; D016283:Proto-Oncogene Proteins p21(ras); D012189:Retrospective Studies; D018631:ras Proteins / Q000235:genetics*
chemical_list: D061067:Antibodies, Monoclonal, Humanized; C117307:KRAS protein, human; D009944:Organoplatinum Compounds; D011518:Proto-Oncogene Proteins; D000068258:Bevacizumab; D016283:Proto-Oncogene Proteins p21(ras); D018631:ras Proteins; D002955:Leucovorin; D005472:Fluorouracil