Abstract
The world is suffering from a pandemic of Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which was ruined in Wuhan (China) and consequently spread worldwide...
Highlights
Pancreatic cancer, including Pancreatic Adenocarcinoma and PNET (Pancreatic Neuroendocrine Tumor), is known to be one of the most common and deadly cancers [1] in our society
The study found the various effects of co-occurring genomic alterations on survival in patients with KRAS-Mutant Pancreatic cancer
As the pattern of co-occurring mutations may describe different biological subsets of patients with KRAS-mutant pancreatic cancer, we explored the effects of co-occurring mutations on patient survival rates
Summary
Pancreatic cancer, including Pancreatic Adenocarcinoma and PNET (Pancreatic Neuroendocrine Tumor), is known to be one of the most common and deadly cancers [1] in our society. Numerous studies [2] have shown a strong relationship between mutations in the KRAS gene, a gene that codes for a protein that regulates the propagation of growth factors and cell signaling molecules, and the development of pancreatic cancer. Mutant forms of the KRAS gene induces an uninterrupted activation of the protein despite the lack of extracellular signals; the excessive activation of KRAS causes the formation of tumor in the pancreas. While the significance of KRAS and its mutant form in promoting pancreatic cancer is heavily studied, there have been few studies analyzing the role of genes that co-occur with mutant-KRAS. The following study analyzes the relationship between mutations in the co-occurring genes and the development of pancreatic cancer. We explore the effects of comutations on patient survivability and on various other pathways
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