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September 16, 2025Journal of Clinical InvestigationOpen Access

NR2F1 and mTORC1 provide the bridge between melanoma dormancy and therapeutic resistance

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Authors

NMNarsimha MamidiSDSwadesh K. DasPFPaul B. Fisher

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Overview

Observational analysis shows that NR2F1 and mTORC1 link dormancy and therapeutic resistance in melanoma, suggesting new treatment strategies.

Key Points

  • NR2F1 overexpression reduces treatment efficacy, contributing to therapeutic resistance in melanoma.
  • Elevated NR2F1 expression indicates persistent drug-tolerant cells in patients with minimal residual disease.
  • Combining BRAF and MEK inhibitors with mTORC1 inhibition may effectively target resistant melanoma cells.
  • These findings support exploring NR2F1 and mTORC1 as therapeutic targets in cutaneous melanoma.

Cite This Study

Mamidi et al. (2025) studied this question.

synapsesocial.com/papers/68d42336713b0b5dfea6b69bhttps://doi.org/10.1172/jci197764
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Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1Elevated NR2F1 underlies the persistence of invasive disease after treatment of BRAF-mutant melanoma.2025
  2. 2Molecular Basis of BRAF Inhibitor Resistance in Melanoma: A Systematic Review2025 · 18 citations
  3. 3<scp>PTRF</scp> Confers Melanoma‐Acquired Drug Resistance Through the Upregulation of <scp>EGFR</scp>2025
  4. 4Combination of the Novel <scp>RAF</scp> Dimer Inhibitor Brimarafenib With the <scp>MEK</scp> Inhibitor Mirdametinib Is Effective Against <scp>NRAS</scp> Mutant Melanoma2025 · 4 citations
  5. 5MAPK and mTORC1 signaling converge to drive cyclin D1 protein production to enable cell cycle reentry in melanoma persister cells2025