Caracterización Del Infiltrado Linfocitario (Cd3, Cd4, Cd8, Cd45ro Y Foxp3) E Inestabilidad Micro-Satelital en Pacientes Con Cáncer Colorrectal

Abstract

Lymphocyte infiltration and microsatellite instability in colorectal cancer patients Background: In colorectal cancer (CRC) patients, lymphocyte infiltration (LI) and microsatellite instability (MSI) have been associated with better prognosis. aim: To analyze the association between components of LI (CD3/CD4/CD8/CD45R0/FoxP3) and MSI status with metastatic stages in CRC patients. material and methods: Prospective study of 109 patients diagnosed with CRC. The expression of CD3, CD4, CD8, CD45R0 and FoxP3 markers, was evaluated by immunohistochemical analysis, and tumors were classified into negative, low and intense expression. The MSI was assessed with seven markers amplified by PCR from normal and tumoral DnA. Tumors were grouped in MSS (stable)/MSI-low and MSI-high. Statistical analysis was performed with Fischer's exact test. results: 29%, 28%, 12% and 86% of tumors exhibits intense expression of CD3+, CD4+, CD8+ and CD45RO+ lymphocytes, respectively. 84% of the tumors presented MSS/ MSI-low and 16% had MSI-high. Tumors that show a high density of T cells (CD3+, CD4+ y CD45R0+) are associated with early stage tumors (I and II) (p = 0.023; p = 0.030 and p = 0.003, respectively). Additionally, there was a significant association between the MSS/MSI-low tumors and a reduced ability to recruit CD8+ cytotoxic T lymphocytes (p = 0.037) and CD3+ (p = 0.064). conclusion: There is an association between high densities of CD3+, CD4+ and CD45RO+ lymphocytes and non-metastatic tumors. In addition, MSS/ MSI-low tumors are associated with a lower recruitment of CD8+ and CD3+ lymphocytes.

Caracterización de pacientes con cáncer colorrectal esporádico basado en la nueva subclasificación molecular de consenso

“…Se ha descrito como lesión precursora a los pólipos sésiles aserrados 36 . Estos tumores presentan una alta respuesta de infiltrado intratumoral, lo cual confiere a estos pacientes un buen pronós-tico y, según lo reportado, se sugiere que ello se debería a la presencia de linfocitos T citotóxicos CD8+ [37][38][39][40] . Por otra parte, se ha establecido que la mutación activante en el oncogen BRAF (V600E) provoca la activación constitutiva de la vía EGFR y en consecuencia una ineficiente respuesta al tratamiento con cetuximab o panitumumab.…”