Advances and Challenges in RAS-Directed Cancer Therapy

A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Cancer Therapy".

Deadline for manuscript submissions: closed (10 August 2024) | Viewed by 224

Special Issue Editors


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Guest Editor
Department of Radiation Oncology, UT Southwestern Medical Center, Dallas, TX 75390, USA
Interests: RAS signaling; cancer therapy; structural biology; molecular simulation
Special Issues, Collections and Topics in MDPI journals

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Guest Editor
1. Department of Diagnostic and Therapeutic Ultrasonography, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Tianjin 300060, China
2. Key Laboratory of Cancer Prevention and Therapy, Tianjin's Clinical Research Center for Cancer, Tianjin 300060, China
Interests: ultrasound imaging; thyroid ablation; artificial intelligence; molecular imaging; tumor development

Special Issue Information

Dear Colleagues,

Oncogenic RAS mutations, such as G12C, G12D, G13D, and Q61H, are some of the most frequently mutated genes causing cancer. Multiple strategies have been developed to directly target the aberrant activation of RAS signaling to treat cancer, including prenylation inhibitors, PDEδ inhibitors, and SHP2 inhibitors, but none have advanced to use in the clinic. Recently approved KRAS G12C inhibitors justified KRAS as a target and, significantly, demonstrated that specific RAS mutant can be selectively targeted. However, KRAS G12C is the only RAS mutant that has been successfully targeted so far in human cancer patients, which limits its application for targeting other oncogenic RAS mutant-driven cancers.

Recently, new approaches have inspired optimism regarding targeting certain KRAS mutations, including G12D, G13D, and Q61H, based on epidemiological data suggesting that cancers harboring different RAS mutants exhibit distinct clinical behaviors. These differences suggest that unique functional classes of oncogenic RAS alleles will be differentially regulated and will have distinct vulnerabilities in cancer therapy. This concept may also apply to equivalent mutations in HRAS and NRAS.

This Special Issue will cover subjects related to recent progress in RAS-directed therapeutic approaches in cancer therapy and the underlying mechanisms for acquired drug resistance. The hope is that it will increase our understanding of the clinical efficacy and challenges of RAS targeting therapy in different cancers.

Dr. Zhiwei Zhou
Dr. Xi Wei
Guest Editors

Manuscript Submission Information

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Keywords

  • RAS
  • RAS targeting therapy
  • drug resistance
  • structural basis
  • cancer therapy

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Published Papers

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