Resumen
Thymic carcinomas are the most aggressive thymic epithelial tumors. While thymic carcinomas do not have a single specific cause, various aspects of their growth have been evaluated at the molecular level. In this review, we organize the recent findings according to what have been defined as the hallmarks of cancer. The identification of the molecular alterations that drive the growth of these tumors is crucial for the development of effective target therapies. Inactivation of CDKN2A, TP53, and CDKN2B by somatic mutation or deletion is most common in thymic carcinomas. In advanced tumors, mutations in genes that regulate epigenetic and chromatin remodeling can occur. On the contrary, mutations in tyrosine kinase receptors and other oncogenes are only occasional, with those of KIT being the most common and present in only 10% of thymic carcinomas. Thymic carcinomas present an enhanced and aberrant vasculature that has been targeted in clinical trials with promising results. Additionally, thymic carcinomas evade the control of the immune system, with some tumors showing a response to immune checkpoint inhibitors.