Erlotinib can prolong survival in patients with non-small-cell lung cancer after first-line or second-line chemotherapy.

Patients with a colorectal tumor bearing mutated K-ras did not benefit from cetuximab, whereas patients with a tumor bearing wild-type K-ras did benefit from cetuximab. The mutation status of the K-ras gene had no influence on survival among patients treated with best supportive care alone. (ClinicalTrials.gov number, NCT00079066.)

BACKGROUND-Colon cancers with high-frequency microsatellite instability have clinical and pathological features that distinguish them from microsatellite-stable tumors. We investigated the usefulness of microsatellite-instability status as a predictor of the benefit of adjuvant chemotherapy with fluorouracil in stage II and stage III colon cancer.

Cetuximab improves overall survival and progression-free survival and preserves quality-of-life measures in patients with colorectal cancer in whom other treatments have failed. (ClinicalTrials.gov number, NCT00079066 [ClinicalTrials.gov].).

No abstract

As compared with placebo, letrozole therapy after the completion of standard tamoxifen treatment significantly improves disease-free survival.

Letrozole after tamoxifen is well-tolerated and improves both disease-free and distant disease-free survival but not overall survival, except in node-positive patients.

ECENT RETROSPECTIVE CORrelative analyses of metastatic colorectal cancer trials indicate that patients with KRAS-mutated tumors (NCBI Entrez Gene 3845) do not benefit from the anti-epidermal growth factor receptor (EGFR) monoclonal antibodies cetuximab and panitumumab. 1 These retrospective analyses were performed independently, and for each analysis, KRAS wild-type vs mutant were studied grouping codons 12 and 13 mutations together, without subgroup analysis. Health authorities in the United States and Europe have indicated that patients with KRAS codon 12-or KRAS codon 13-mutated tumors should not receive cetuximab or panitumumab. 2-4 However, indications exist that not all KRAS mutations are equal in their biological characteristics. First, the pattern of KRAS mutations is tumor-type spe-Author Affiliations are listed at the end of this article.