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Identifying Actionable Alterations in KRAS Wild-Type Pancreatic Cancer
Ahmed Elhariri1, Jaydeepbhai Patel1, Himil Mahadevia1
1Division of Hematology-Oncology, Department of Medicine, Mayo Clinic Florida, 4500 San Pablo Rd, Jacksonville, FL, 32224, USA.
Abstract:
The 5-year relative survival rate for pancreatic cancer is currently the lowest among all cancer types with a dismal 13%. A Kirsten rat sarcoma virus (KRAS) gene mutation is present in approximately 90% of patients with pancreatic cancer; however, KRAS-specific drugs are not yet widely used in clinical practice for pancreatic cancer, specifically the KRASG12D variant. Advances in genomic testing revealed an opportunity to detect genetic alterations in a subset of patients with no KRAS mutation termed KRAS wild-type. Patients with KRAS wild-type tumors have a propensity to express driver alterations, hence paving the way for utilizing a targeted therapy approach either via clinical trials or standard-of-care drugs. These alterations include fusions, amplifications, translocations, rearrangements and microsatellite instability-high tumors and can be as high as 11% in some studies. Here, we discuss some of the most notable alterations in KRAS wild-type and highlight promising clinical trials.
Insights
Pancreatic cancer has a low survival rate, with most cases driven by KRAS mutations. However, KRAS wild-type pancreatic tumors may respond to targeted therapies, offering new treatment avenues.
Area of Science:
- Oncology
- Genetics
- Molecular Biology
Background:
- Pancreatic cancer exhibits the lowest 5-year survival rate (13%) among all cancers.
- Approximately 90% of pancreatic cancers harbor Kirsten rat sarcoma virus (KRAS) gene mutations, yet KRAS-specific therapies are underutilized, particularly for the KRAS G12D variant.
Purpose of the Study:
- To explore targeted therapy opportunities in KRAS wild-type pancreatic tumors.
- To identify and discuss notable genetic alterations in KRAS wild-type pancreatic cancer.
- To highlight promising clinical trials for this patient subset.
Main Methods:
- Genomic testing to identify genetic alterations in KRAS wild-type tumors.
- Review of current literature on KRAS wild-type pancreatic cancer alterations.
- Analysis of clinical trial data for targeted therapies.
Main Results:
- KRAS wild-type pancreatic tumors can present with driver alterations like fusions, amplifications, translocations, rearrangements, and microsatellite instability-high status (up to 11% in some studies).
- These alterations present actionable targets for therapy.
Conclusions:
- Targeted therapy approaches, including clinical trials and standard-of-care drugs, show promise for patients with KRAS wild-type pancreatic cancer.
- Genomic profiling is crucial for identifying these targetable alterations and guiding treatment decisions.
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