Abstract            Volume:13  Issue-10  Year-2025         Original Research Articles

Online ISSN : 2347 - 3215 Issues : 12 per year Publisher : Excellent Publishers Email : editorijcret@gmail.com

Pancreatic cancer (PC) is an aggressive malignancy arising from the uncontrolled proliferation of pancreatic exocrine or neuroendocrine cells. It is currently the seventh leading cause of cancer-related deaths globally and the third in many developed nations, with an overall 5-year survival rate of approximately 10%. Pancreatic ductal adenocarcinoma (PDAC), the most prevalent form of PC, is particularly lethal, as most patients present with unresectable or metastatic disease at diagnosis. Two major biological models have been proposed to explain PDAC progression. The clonal evolution theory suggests that random driver mutations emerge within tumor cells, with selective clonal expansion of variants that confer a growth advantage. In contrast, the cancer stem cell (CSC) model highlights a small subpopulation of pancreatic cancer stem cells (PCSCs), characterized by CD44?CD24?ESA? markers (representing 0.2–0.8% of tumor cells), which exhibit high tumorigenicity, self-renewal capacity, and the ability to differentiate into heterogeneous cell populations reflective of the primary tumor. These PCSCs also show elevated expression of developmental signaling regulators such as Sonic Hedgehog and Bmi-1. The interplay between PCSCs and the highly complex tumor microenvironment contributes significantly to therapeutic resistance, metastasis, and tumor relapse. Therefore, comprehensive understanding of the tumor microenvironment and global gene-expression profiling of cancer stem cells is essential for developing targeted and more effective therapeutic strategies for PDAC.

Download this article as