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Addressing Biases in Analysis of Time of Infusion: NCI/SWOG Trial S1404 Among Participants With High-Risk Resectable Melanoma Who Received Adjuvant Anti-PD-1 Therapy.

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RAS(ON) Multiselective Inhibition Drives Antitumor Immunity in Preclinical Models of NRAS-Mutant Melanoma.

Larissa Anastacio Da Costa Carvalho1, Nataliya Tovbis Shifrin2, Manali S Phadke1

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A new targeted therapy, daraxonrasib, shows promise for NRAS-mutant melanoma by activating anti-tumor immunity. This RAS(ON) inhibitor promotes T-cell responses and tumor regression, offering a potential new treatment option.

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Area of Science:

  • Oncology
  • Immunology
  • Pharmacology

Background:

  • NRAS-mutant melanoma lacks effective targeted therapies.
  • RAS(ON) signaling pathways are crucial in melanoma development.

Purpose of the Study:

  • To evaluate the efficacy of RMC-7977, a preclinical RAS(ON) multiselective inhibitor (daraxonrasib), in NRAS-mutant melanoma models.
  • To investigate the immune mechanisms underlying RMC-7977's antitumor activity.
  • To assess combination therapy with anti-PD-1 and clinical responses.

Main Methods:

  • In vivo studies using NRAS-mutant melanoma models.
  • Assessment of MAPK signaling, immune cell infiltration (CD4+, CD8+ T cells), MHC and PD-L1 expression.
  • Combination therapy with RMC-7977 and anti-PD-1.
  • Analysis of clinical data from a Phase I/Ib trial.

Main Results:

  • RMC-7977 induced rapid tumor regressions and potent antitumor immune responses.
  • Treatment upregulated MHC and PD-L1, enhancing T-cell infiltration and activity.
  • Resistance was associated with reduced T-cell infiltration and altered myeloid cell populations.
  • Combination therapy overcame resistance and improved survival.
  • Two patients with NRAS-mutant melanoma showed objective clinical responses.

Conclusions:

  • RAS(ON) multiselective inhibition with daraxonrasib is a promising strategy for NRAS-mutant melanoma.
  • The drug elicits antitumor immunity dependent on adaptive T-cell responses.
  • Combination therapy may overcome resistance to PD-1 blockade.
  • Further clinical evaluation of daraxonrasib is warranted.