Establishment of patient-derived tumor organoids to functionally inform treatment decisions in metastatic colorectal cancer.

Background: Metastatic colorectal cancer (mCRC) patients tend to have modest benefits from molecularly driven therapeutics. Patient-derived tumor organoids (PDTOs) represent an unmatched model to elucidate tumor resistance to therapy, due to their high capacity to resemble tumor characteristics.

Materials And Methods: We used viable tumor tissue from two cohorts of patients with mCRC, naïve or refractory to treatment, respectively, for generating PDTOs.

Up-to-date role of aflibercept in the treatment of colorectal cancer.

: Colorectal cancer (CRC) is a major public health problem. Despite major progress understanding the biological basis of this tumor added to the incorporation of optimized diagnostic and therapeutic strategies, prognosis after progression on first-line standard treatment remains poor. Several antiangiogenic treatments have demonstrated improvement in overall survival (OS) in the second-line treatment being aflibercept, a fully humanized recombinant protein, one of them.

and inhibition as treatment strategies in V600E metastatic colorectal cancer.

Introduction: driver mutations are found in up to 15% of patients with colorectal cancer (CRC) and lead to constitutive activation of kinase and sustained pathway signaling. mutations define a sub-population characterized by a poor prognosis and dismal median survival. Following successful outcomes with inhibition in mutant metastatic melanoma, this approach was evaluated in metastatic colorectal cancer (mCRC).

Molecular subtypes and the evolution of treatment management in metastatic colorectal cancer.

Colorectal cancer (CRC) is a heterogeneous disease representing a therapeutic challenge, which is further complicated by the common occurrence of several molecular alterations that confer resistance to standard chemotherapy and targeted agents. Mechanisms of resistance have been identified at multiple levels in the epidermal growth factor receptor (EGFR) pathway, including mutations in , and , and in the HER2 and MET receptors. These alterations represent oncogenic drivers that may co-exist in the same tumor with other primary and acquired alterations a clonal selection process.