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Abstract
Genetic alterations, especially the K-Ras mutation, carry the heaviest burden in the progression of pancreatic precursor lesions into pancreatic ductal adenocarcinoma (PDAC). The tumor microenvironment is one of the challenges that hinder the therapeutic approaches from functioning sufficiently and leads to the immune evasion of pancreatic malignant cells. Mastering the mechanisms of these two hallmarks of PDAC can help us in dealing with the obstacles in the way of treatment. In this review, we have analyzed the signaling pathways involved in PDAC development and the immune system’s role in pancreatic cancer and immune checkpoint inhibition as next-generation therapeutic strategy. The direct targeting of the involved signaling molecules and the immune checkpoint molecules, along with a combination with conventional therapies, have reached the most promising results in pancreatic cancer treatment.
Highlights
Because of its poor prognosis, pancreatic cancer causes almost as many deaths (466,000)as cases (496,000) and is the seventh leading cause of cancer death in both men and women
The Zeb family of transcription factors is one of the best evaluated EMT induction agents. Both tumor-associated stroma and pancreatic cancer cells demonstrated a great level of Zeb-1 expression, which was linked with poor prognosis in pancreatic ductal adenocarcinoma (PDAC) patients
PDAC is marked by a stromal reaction known as desmoplasia, in which overactive cancer-associated fibroblasts deposit an excessive amount of extracellular matrix (ECM), the majority of which is fibrillar type I collagen
Summary
Because of its poor prognosis, pancreatic cancer causes almost as many deaths (466,000). The first example of a biomarker identified subpopulation of pancreatic cancer patients that can drive therapeutic decision making is represented by BRCA1, BRCA2, or PALB2 mutations. In this context, platinum-based therapy with or without a PARP inhibitor has achieved a significant response [9,10]. Whole-genome sequencing of pancreatic cancers revealed that 119 somatic chromosomal structural variants were found in each patient This is an overstatement, since researchers believed that the number of mutations already exceeds 63 [12]. This review will focus on different types of mutations, signaling pathways, along with a glance at immune system-based therapies, as well as potential therapeutic targets in pancreatic ductal adenocarcinoma
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