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Inhibition of the anti-apoptotic protein BCL2 in EML4-ALK cell models as a second proposed therapeutic target for non-small cell lung cancer.
PLoS One
January 2025
Department of Basic Sciences, Bioethics and Human Life, Faculty of Human Medicine, University of Piura, Miraflores, Lima, Perú.
The anaplastic lymphoma kinase (ALK) oncoprotein plays a crucial role in non-small cell lung cancer (NSCLC) by activating signaling pathways involved in cell proliferation and survival through constitutive phosphorylation. While first-line crizotinib can regulate phosphorylation, mutations in the ALK gene can lead to resistance against ALK inhibitors (ALKi) such as ceritinib and alectinib. On the other hand, overexpression of BCL2, a protein involved in cell death regulation, has been observed in NSCLC and is considered a potential therapeutic target.
View Article and Find Full Text PDFRepotrectinib: Redefining the therapeutic landscape for patients with ROS1 fusion-driven non-small cell lung cancer.
Clin Transl Med
October 2024
Department of Medicine, Early Drug Development Service, Memorial Sloan Kettering Cancer Center, New York, New York, USA.
Article Synopsis
- The ROS1 proto-oncogene is linked with receptor tyrosine kinases and plays a significant role in treating ROS1 fusion-positive non-small cell lung cancer (NSCLC) using FDA-approved TKIs like crizotinib and entrectinib, though these medications face challenges such as resistance and limited brain penetration.
- Repotrectinib, a new macrocyclic TKI, was created to tackle resistance mutations and enhance brain distribution, showing strong effectiveness in the TRIDENT-1 trial with high response rates in both TKI-naïve and TKI-pretreated patients.
- The trial showed that 79% of TKI-naïve patients achieved an objective response and had longer progression
Response to Crizotinib After Entrectinib Resistance in -Rearranged, -Amplified Lung Adenocarcinoma.
JCO Precis Oncol
October 2024
Lowe Center for Thoracic Oncology, Dana-Farber Cancer Institute, Boston, MA.
Crizotinib successfully overcomes MET amplification in ROS1-rearranged NSCLC after entrectinib failure.
View Article and Find Full Text PDFDiscovery of Oral Degraders of the ROS1 Fusion Protein with Potent Activity against Secondary Resistance Mutations.
J Med Chem
October 2024
Department of Chemistry, Xavier University of Louisiana, New Orleans, Louisiana 70125, United States.
The development of therapeutic resistance in the majority of patients limits the long-term benefit of ROS1 inhibitor treatment. On-target mutations of the ROS1 kinase domain confer resistance to crizotinib and lorlatinib in more than one-third of acquired resistance cases with no current effective treatment option. As an alternative to stoichiometric inhibition, proteolytic degradation of ROS1 could provide an effective tool to combat resistance generated by these mutations.
View Article and Find Full Text PDFAXL and SHC1 confer crizotinib resistance in patient-derived xenograft model of ALK-driven lung cancer.
iScience
September 2024
Department of Cardiovascular Surgery, the Second Xiangya Hospital of Central South University, Changsha, China.
Anaplastic lymphoma kinase (ALK) inhibitor crizotinib has dramatic effect in non-small cell lung cancer patients with ALK rearrangement. However, most patients eventually develop resistance. To discover therapeutic targets to overcome crizotinib resistance (CR), we generated patient-derived xenograft CR mice and subjected them to phosphorylation profiling, together with CR mice treated with ASP3026 or alectinib.
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