Table 3 Differentially expressed genes in chemoresistant patients respect to chemosensitive patients.

It is a component of apoptosome. The apoptosome has a role in chemioresistance in pancreatic cancer.

This gene is able to reduce the release of pro-apoptotic cytochrome c from mitochondria and block caspase activation. This gene is a direct transcription target of NF-kappa B and it acts in response to cytokine TNF and IL-1.

It acts as anti- or pro-apoptotic regulators. This gene is located on mitochondrial membrane and control VDAC opening, regulating the release of cytochrome C by mitochondria.

This gene is a member of a family of proteins that inhibits apoptosis by binding to tumor necrosis factor receptor-associated factors TRAF1 and TRAF2.

This gene is a member of a family of proteins that inhibits apoptosis by binding to tumor necrosis factor receptor-associated factors TRAF1 and TRAF2. In cells resistant to alkylating agent, it blocks through regulation of CHK2 and CDC2 proteins.

It regulates B cell function by engaging CD40 on the B cell surface.

CIDEB triggers DNA fragmentation and nuclear condensation. Its expression could be associated to resistance to apoptosis.

FAS/FASL ratio, after receiving chemotherapy, indicates chemosensitivity in several tumoral models. In addition, the decreasing ratio during chemotherapy treatment, despite the initial values, is related to acquired chemoresistance.

This receptor has been shown to stimulate NF-kappa B activity and regulate cell apoptosis. The signal transduction of this receptor is mediated by various death domains contained by adaptor proteins.

This protein preferentially induces apoptosis in transformed and tumoral cells and it is expressed at a significant level in the most of normal tissues. Its down regulation could impair the apoptosis induction.