Acquired MTAP Loss Following Entrectinib Resistance in ROS1-Rearranged NSCLC With CD74 Exon 3-ROS1 Exon 34 Fusion
Mizuha Haraguchi Hashiguchi1, Maika Tanino1, Suzuyuki Yoneda1
1Division of Pulmonary Medicine, Department of Medicine, Keiyu Hospital, Yokohama, Japan.
Acquired methylthioadenosine phosphorylase (MTAP) loss can drive disease progression in ROS1-rearranged non-small cell lung cancer (NSCLC). Longitudinal genomic profiling is crucial for guiding treatment decisions, even with persistent CD74-ROS1 fusions.
Area of Science:
- Oncology
- Genomics
- Pharmacology
Background:
- ROS1-rearranged non-small cell lung cancer (NSCLC) is a distinct molecular subtype often treated with tyrosine kinase inhibitors.
- Resistance to targeted therapies like entrectinib can emerge, necessitating a deeper understanding of underlying mechanisms.
- Methylthioadenosine phosphorylase (MTAP) is a tumor suppressor enzyme whose loss has been implicated in various cancers.
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