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Molecular Research in Pancreatic Cancer: Small Molecule Inhibitors, Their Mechanistic Pathways and Beyond
Shaila A Shetu1, Nneoma James1, Gildardo Rivera2
1Department of Chemistry, The University of Texas Rio Grande Valley, 1201 West University Drive, Edinburg, TX 78539, USA.
Abstract:
Pancreatic enzymes assist metabolic digestion, and hormones like insulin and glucagon play a critical role in maintaining our blood sugar levels. A malignant pancreas is incapable of doing its regular functions, which results in a health catastrophe. To date, there is no effective biomarker to detect early-stage pancreatic cancer, which makes pancreatic cancer the cancer with the highest mortality rate of all cancer types. Primarily, mutations of the KRAS, CDKN2A, TP53, and SMAD4 genes are responsible for pancreatic cancer, of which mutations of the KRAS gene are present in more than 80% of pancreatic cancer cases. Accordingly, there is a desperate need to develop effective inhibitors of the proteins that are responsible for the proliferation, propagation, regulation, invasion, angiogenesis, and metastasis of pancreatic cancer. This article discusses the effectiveness and mode of action at the molecular level of a wide range of small molecule inhibitors that include pharmaceutically privileged molecules, compounds under clinical trials, and commercial drugs. Both natural and synthetic small molecule inhibitors have been counted. Anti-pancreatic cancer activity and related benefits of using single and combined therapy have been discussed separately. This article sheds light on the scenario, constraints, and future aspects of various small molecule inhibitors for treating pancreatic cancer-the most dreadful cancer so far.
Insights
Targeting KRAS mutations in pancreatic cancer is crucial. This review explores small molecule inhibitors, including natural and synthetic compounds, for treating this deadly disease.
Area of Science:
- Oncology
- Molecular Biology
- Pharmacology
Background:
- Pancreatic cancer has the highest mortality rate due to lack of early detection biomarkers.
- Key gene mutations (KRAS, CDKN2A, TP53, SMAD4) drive pancreatic cancer, with KRAS mutations in over 80% of cases.
- The pancreas's metabolic and hormonal functions are critical, and malignancy leads to severe health consequences.
Purpose of the Study:
- To review the effectiveness and molecular mechanisms of small molecule inhibitors for pancreatic cancer.
- To discuss both natural and synthetic inhibitors, including those in clinical trials and commercial drugs.
- To explore the potential of single and combined therapies in treating pancreatic cancer.
Main Methods:
- Literature review of small molecule inhibitors targeting pancreatic cancer.
- Analysis of molecular mechanisms of action for various inhibitors.
- Discussion of clinical trial data and commercial drug applications.
Main Results:
- Small molecule inhibitors show promise in targeting KRAS and other key pathways in pancreatic cancer.
- Both natural and synthetic compounds exhibit anti-pancreatic cancer activity.
- Combined therapies may offer enhanced benefits over single-agent treatments.
Conclusions:
- There is a critical need for effective pancreatic cancer treatments, particularly targeting KRAS mutations.
- Small molecule inhibitors represent a promising therapeutic strategy for pancreatic cancer.
- Further research into novel inhibitors and combination therapies is essential for improving patient outcomes.
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