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This study investigated whether oncogenic and tumor-suppressive gene mutations are involved in the differential outcomes of patients with rectal carcinoma receiving neoadjuvant chemoradiotherapy (nCRT). Genomic DNA was obtained from formalin-fixed paraffin-embedded (FFPE) specimens of patients with rectal carcinoma who received a complete nCRT course. Gene mutation status was examined in specimens from patients before and after nCRT by using the AmpliSeq platform. Our data revealed that the nonsynonymous <i>p53</i>, <i>APC</i>, <i>KRAS</i>, <i>CDKN2A</i>, and <i>EGFR</i> mutations were observed in 93.1%, 65.5%, 48.6%, and 31% of the patients with rectal adenocarcinoma, respectively. <i>BRAF</i>, <i>FBXW7</i>, <i>PTEN</i>, and <i>SMAD4</i> mutations were observed in 20.7% of patients with rectal carcinoma. The following 12 gene mutations were observed more frequently in the patients exhibiting a complete response than in those demonstrating a poor response before nCRT: <i>ATM</i>, <i>BRAF</i>, <i>CDKN2A</i>, <i>EGFR</i>, <i>FLT3</i>, <i>GNA11</i>, <i>KDR</i>, <i>KIT</i>, <i>PIK3CA</i>, <i>PTEN</i>, <i>PTPN11</i>, <i>SMAD4</i>, and <i>TP53</i>. In addition, <i>APC</i>, <i>BRAF</i>, <i>FBXW7</i>, <i>KRAS</i>, <i>SMAD4</i>, and <i>TP53</i> mutations were retained after nCRT. Our results indicate a complex mutational profile in rectal carcinoma, suggesting the involvement of <i>BRAF</i>, <i>SMAD4</i>, and <i>TP53</i> genetic variants in the outcomes of patients with nCRT.