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Ultrasound-Guided Orthotopic Implantation of Murine Pancreatic Ductal Adenocarcinoma
Published on: November 19, 2019
Beyond KRAS: Practical Molecular Targets in Pancreatic Adenocarcinoma
Albert Grinshpun1, Yonaton Zarbiv1, Jason Roszik2
1Sharett Institute of Oncology, Hadassah-Hebrew University Medical Center, Jerusalem, Israel.
Abstract:
Pancreatic adenocarcinoma (PDAC) has a grim prognosis. Molecular and genomic analyses revealed that the striking majority of these tumors are driven by KRAS mutation, currently not amenable to targeted therapy. However, other driver mutations were found in a small fraction of patients. Herein we report of 3 cases of patients with metastatic PDAC and wildtype KRAS, found to harbor BRAF or RET pathogenic alterations. The patients were treated with targeted therapies with variable success. In our opinion, those proof-of-concept cases argue in favor of additional research and clinical trials' effort in this small but significant PDAC population with uncommon driver mutations.
Insights
Pancreatic cancer (PDAC) rarely has KRAS wildtype. Three metastatic PDAC patients with KRAS wildtype harbored BRAF or RET alterations and received targeted therapies with varied outcomes, suggesting further research is warranted.
Area of Science:
- Oncology
- Genomics
- Translational Research
Background:
- Pancreatic adenocarcinoma (PDAC) typically exhibits KRAS mutations, limiting targeted treatment options.
- A small subset of PDAC patients present with KRAS wildtype tumors, suggesting alternative driver mutations.
- Identifying these alternative drivers is crucial for developing novel therapeutic strategies.
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