1. Introduction
tumor, cancer of the pancreas [, cancer, pancreatic tumors, pancreatic cancer, tumors, arrest, pancreatic adenocarcinoma
TUMOR, LYSIS, PANCREATIC DUCTAL ADENOCARCINOMA, TISSUE INVASION, PROLIFERATION, CANCER, GROWTH SUPPRESSION, TUMOR GROWTH, CYTOTOXICITY, DISEASES, PANCREATIC TUMOR, PANCREATIC CANCER, METASTASIS, PANCREATIC TUMORS, DISEASE, CANCER OF THE PANCREAS, TUMORS, ARREST, PANCREATIC ADENOCARCINOMA
In 2020, pancreatic cancer (of 36 most common types of cancer) was ranked the 14The most used cytotoxic drug for the treatment of pancreatic adenocarcinoma has been gemcitabine, as monotherapy or combined with other treatments. The combination of gemcitabine plus nab-paclitaxel results more effective for locally advanced diseases than the rest of the combinations. The selection of the most appropriate regimen for each patient continues to depend on clinicopathologic stratification, and the development of appropriate biomarkers remains as a challenge [The molecular characterization, the epigenomic, and the genomic profile of pancreatic adenocarcinoma have allowed a better understanding of the disease and have opened the doors to the study of other therapeutic approaches. The deeply immunosuppressive tumor microenvironment of pancreatic ductal adenocarcinoma, the dense stroma, the presence of inhibitory cytokines, few inhibitory T cells, and the low mutational tumor burden have played an important role in the failure of immunotherapy for the treatment of cancer of the pancreas [The epidermal growth factor receptor (EGFR) is overexpressed in pancreatic tumor cells where it is believed to promote cell survival, proliferation, tissue invasion, and metastasis formation while inhibiting apoptosis [Nimotuzumab is a humanized monoclonal antibody that mainly exerts its mechanism of action by competitively inhibiting the binding of the EGF ligand to the extracellular domain of the EGFR. The binding to EGFR leads to a further inhibition of the homodimerization or heterodimerization of this receptor and subsequent autophosphorylation of its tyrosine residues. The consequent inhibition of different canonical and noncanonical ligand-induced signal-transduction pathways results in suppression of tumor growth, inhibition of the mitogenic stimulation of malignant cells, and, therefore, their persistent proliferation and invasiveness. The processes of angiogenesis and metastasis are also inhibited, and apoptosis is activated. Nimotuzumab also elicits other immune responses such as the activation of natural killer (NK) cells and tumor cell lysis through antibody-dependent cellular cytotoxicity (ADCC). Furthermore, nimotuzumab activates adaptive immunity through tumor antigen- (TA-) specific CD8+ T cells and increases the expression of the human leukocyte antigen (HLA) class I-dependent antigen presentation molecule (known as signal 1) that allows induced T cells to recognize and kill EGFR+ tumor cells, reversing one EGFR-mediated mechanism of immune escape that can benefit tumors [Nimotuzumab has been evaluated in clinical trials for the treatment of different types of cancer, obtaining evidence of benefits in terms of therapeutic effect and a broad safety profile [Gao et al. found that nimotuzumab combined with gemcitabine-based chemoradiation promotes the enhancement of the cell cycle arrest, growth suppression, and apoptosis of EGFR-overexpressed pancreatic cancer cell lines PANC-1 [The present study was carried out to evaluate the safety and effect of nimotuzumab combined with gemcitabine in unresectable locally advanced or metastatic pancreatic tumors in a Cuban real-world conditions.