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KRAS Mutation in Colon Ca Blocks Cetuximab


 

CHICAGO — Colorectal cancer patients whose tumors contain the wild-type KRAS gene responded better to treatment with cetuximab plus chemo- therapy than did patients with tumor KRAS mutations, according to data presented during a plenary presentation at the annual meeting of the American Society of Clinical Oncology.

More patients with wild-type KRAS tumors responded to cetuximab (Erbitux) plus the FOLFIRI (leucovorin, fluorouracil, and irinotecan) chemotherapy regimen (59%) than to FOLFIRI alone (43%), reported Dr. Eric Van Cutsem, the lead study author and professor of medicine at the University Hospital Gasthuisberg in Leuven, Belgium. The findings are based on a further analysis of data from the Cetuximab Combined with Irinotecan First-Line Therapy for Metastatic Colorectal Cancer (CRYSTAL) trial, which was presented at last year's ASCO meeting.

The original CRYSTAL trial data indicated that metastatic colorectal cancer patients who received a combination of cetuximab and FOLFIRI had a 15% reduced risk of disease progression. The researchers subsequently asked why some patients benefited from the regimen and others did not, Dr. Van Cutsem said.

In an effort to answer this question, they performed a retrospective analysis of the intent-to-treat population of the CRYSTAL trial. Using archived tumor material, the researchers were able to perform quantitative polymerase chain reaction-based KRAS mutation analysis of codons 12/13 for 540 patients from among the original 1,198 patients included in the trial. The research team disclosed receiving research funding from Merck & Co. and other financial relationships with the company, which markets cetuximab outside the United States and Canada.

KRAS tumor mutations were detected in about 35% of patients; about 65% of patients had KRAS wild type tumors. There were no significant differences in the baseline demographics between the wild-type KRAS tumor patients and the mutant KRAS group, Dr. Van Cutsem said.

Among the patients with wild-type KRAS tumors compared, the researchers found a significant benefit in favor of the cetuximab-FOLFIRI combination, compared with treatment with FOLFIRI alone. There was a 32% decreased risk for disease progression (hazard ratio 0.68) for combination therapy, which was statistically significant.

The median progression-free survival was 8.7 months for KRAS wild type patients treated with FOLFIRI only and 9.9 months for KRAS wild type patients treated with cetuximab plus FOLFIRI. In addition, among KRAS wild type patients, the progression-free survival rate at 1 year was 25% for FOLFIRI alone and 43% for the cetuximab-FOLFIRI combination.

Cetuximab made no difference in progression-free survival for the mutant KRAS population. “The benefit here was confined to the patients with the KRAS wild type tumor,” Dr. Van Cutsem said.

The evaluation of patient response to treatment, a secondary end point of the study, revealed that 59% of wild-type KRAS patients responded to treatment with cetuximab and FOLFIRI, compared with 43% of patients who responded to FOLFIRI alone. There was no significant difference in overall response between the treatment groups for patients with KRAS mutations.

The researchers also analyzed side effects and found no new signals of toxicity.

The results are consistent with previous research findings, Dr. Van Cutsem said. Several retrospective studies have shown that benefit from cetuximab was confined to KRAS wild type patients. Those with mutant tumors do not benefit from anti-epidermal growth factor receptor antibodies, these studies have found. “The data we report here today are in agreement with the biolog.”

Given the predictive value of the KRAS gene, Dr. Van Cutsem recommended that KRAS testing should become part of routine clinical practice. By knowing in advance if there is a KRAS mutation, physicians can avoid exposing patients to the unnecessary side effects of a treatment that will not be effective, he said.

KRAS testing should be fairly simple for clinicians, he said, because they can do it using archived tumor samples without performing fresh biopsies. Effective polymerase chain reaction-based assays are already commercially available.

Routine use of KRAS testing also got some recent support in Europe when the European Medicines Agency's Committee for Medicinal Products for Human Use issued a positive opinion on Merck's application to expand the use of cetuximab. The committee recommended the use of cetuximab in patients who have metastatic colorectal cancer with KRAS wild type tumors. The recommendation was for use in combination with chemotherapy and alone in patients who have failed oxaliplatin- and irinotecan-based therapy and who are intolerant to irinotecan.

The results of the CRYSTAL trial analysis, combined with other recent studies that point to the predictive value of KRAS mutation status, support routine KRAS testing for patients with metastatic colorectal cancer who are being considered for treatment with epidermal growth factor receptor inhibitors, Dr. S. Gail Eckhardt, head of medical oncology at the University of Colorado Cancer Center in Aurora, said during a discussion.

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