BACKGROUND: We aimed to investigate the molecular features of synchronous colorectal cancer (CRC). MATERIALS AND METHODS: Out of 1,262 patients with CRC, 130 lesions in 59 patients with synchronous CRC were retrospectively analyzed. Microsatellite, v-Ki-Ras2 Kristen rat sarcoma viral oncogene homolog (KRAS), v-raf murine sarcoma viral oncogene homolog B1 (BRAF), tumor protein 53 (TP53) and β-catenin status were evaluated and compared between synchronous CRC lesions in each patient. RESULTS: The subtypes of instability, BRAF and β-catenin subtypes was significant but low. Patients with discordant KRAS and TP53 were not concordant between lesions in the same patient, and concordance of microsatellite KRAS/BRAF subtypes comprised 50.8% of those with synchronous CRC. The rate of patients with lesions containing both mutL homolog 1 (MLH1) methylation and microsatellite stable status was 66.7% in those with synchronous CRC, with at least one lesion with high microsatellite instability. CONCLUSION: The present study on synchronous CRC demonstrated a low concordance of molecular subtypes between lesions in the same patient. A molecular analysis of metastatic lesions is warranted for molecular targeted therapy of metastatic synchronous CRC. Copyright
BACKGROUND: We aimed to investigate the molecular features of synchronous colorectal cancer (CRC). MATERIALS AND METHODS: Out of 1,262 patients with CRC, 130 lesions in 59 patients with synchronous CRC were retrospectively analyzed. Microsatellite, v-Ki-Ras2 Kristen ratsarcoma viral oncogene homolog (KRAS), v-raf murine sarcoma viral oncogene homolog B1 (BRAF), tumor protein 53 (TP53) and β-catenin status were evaluated and compared between synchronous CRC lesions in each patient. RESULTS: The subtypes of instability, BRAF and β-catenin subtypes was significant but low. Patients with discordant KRAS and TP53 were not concordant between lesions in the same patient, and concordance of microsatellite KRAS/BRAF subtypes comprised 50.8% of those with synchronous CRC. The rate of patients with lesions containing both mutL homolog 1 (MLH1) methylation and microsatellite stable status was 66.7% in those with synchronous CRC, with at least one lesion with high microsatellite instability. CONCLUSION: The present study on synchronous CRC demonstrated a low concordance of molecular subtypes between lesions in the same patient. A molecular analysis of metastatic lesions is warranted for molecular targeted therapy of metastatic synchronous CRC. Copyright
Authors: Ruba A Hamed; Sam Marks; Helen Mcelligott; Roshni Kalachand; Hawa Ibrahim; Said Atyani; Greg Korpanty; Nemer Osman Journal: Mol Clin Oncol Date: 2021-12-21