BRAF-Mutated Colorectal Cancer: What Is the Optimal Strategy for Treatment?

被引:48
|
作者
Cohen, Romain [1 ]
Cervera, Pascale [1 ]
Svrcek, Magali [1 ]
Pellat, Anna [1 ]
Dreyer, Chantal [1 ]
de Gramont, Aimery [2 ]
Andre, Thierry [1 ,3 ]
机构
[1] St Antoine Hosp, AP HP, Dept Med Oncol, 184 Faubourg St Antoine, F-75012 Paris, France
[2] Inst Hosp Franco Britannique, Dept Med Oncol, 4 Kleber, F-92300 Levallois Perret, France
[3] GERCOR, Oncol Multidisciplinary Grp, 151 Faubourg St Antoine, F-75011 Paris, France
关键词
BRAFV600E; Colorectal cancer; Microsatellite instability; Checkpoint inhibitor; Vemurafenib; Dabrafenib; FOLFOXIRI PLUS BEVACIZUMAB; MISMATCH REPAIR STATUS; III COLON-CANCER; KRAS WILD-TYPE; 1ST-LINE TREATMENT; PHASE-II; MICROSATELLITE INSTABILITY; OPEN-LABEL; STAGE-II; INFUSIONAL FLUOROURACIL;
D O I
10.1007/s11864-017-0453-5
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
The BRAF activating mutation, harbored by approximately 10% of colorectal cancers (CRC), confers dramatic prognosis to advanced diseases. In early-stage setting, the identification of the BRAF mutation does not impact the therapeutic decision. Yet, the BRAF mutation could be considered as a stratification factor in adjuvant trials, because of its prognostic impact after relapse. Moreover, both BRAF mutation and mismatch repair (MMR) statuses should be determined in all CRC to help identify sporadic tumors versus Lynch syndromerelated tumors. Indeed, in patients with MMR-deficient (dMMR) tumors and MLH1 loss of expression, the BRAFV600E mutation indicates a sporadic origin. In advanced BRAFmutated CRC, the standard of care remains fluoropyrimidine-based cytotoxic regimen in combination with bevacizumab. Although a recent meta-analysis showed that there was insufficient data to justify the exclusion of anti-EGFR monoclonal antibodies,
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页数:14
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