Mesenchymal-epithelial transition (MET) is a member of a distinct subfamily of heterodimeric receptor tyrosine kinase receptors that specifically binds the hepatocyte growth factor (HGF). Binding to HGF leads to receptor dimerization/multimerization and phosphorylation, resulting in its catalytic activation. MET activation drives the malignant progression of several tumor types, including colorectal cancer (CRC), by promoting signaling cascades that mainly result in alterations of cell motility, survival, and proliferation. MET is aberrantly activated in many human cancers through various mechanisms, including point mutations, gene amplification, transcriptional up-regulation, or ligand autocrine loops. MET promotes cell scattering, invasion, and protection from apoptosis, thereby acting as an adjuvant pro-metastatic gene for many tumor types. In CRC, MET expression confers more aggressiveness and worse clinical prognosis. With all of this rationale, inhibitors that target the HGF/MET axis with different types of response have been developed. HGF and MET are new promising targets to understand the pathogenesis of CRC and for the development of new, targeted therapies.

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Presentamos el caso de un paciente varón de 62 años con masa dolorosa en hipocondrio izquierdo catalogado inicialmente como sarcoma irresecable, recibió quimioterapia y radioterapia sin respuesta, motivo por el cual se reintervino quirúrgicamente hallándose un tumor dependiente de bazo heterogéneo con perfil inmunohistoquímico de angioma de células litorales. El angioma de células litorales (ACL) es una lesión esplénica poco frecuente que se presenta asociado a síntomas genéricos como astenia, dolor regional y baja de peso, que requiere como manejo principal un abordaje quirúrgico. Suele ser una neoplasia asintomática de hallazgo incidental, afecta a ambos sexos por igual, cuyo diagnóstico es básicamente histológico e inmunohistoquímico con buen pronóstico luego de un abordaje quirúrgico inicial.

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