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Reversing vemurafenib-resistance in primary melanoma cells by combined romidepsin and type I IFN treatment through blocking of tumorigenic signals and induction of immunogenic effects.

Author: AscioneBarbara, BuoncervelloMaria, CaniniIrene, CaponeImerio, D'AtriStefania, FragaleAlessandra, GabrieleLucia, LicursiValerio, MatarresePaola, ParlatoStefania, PedaceLucia, PizziSimone, PresuttiCarlo, RemediGiacomo, RomagnoliGiulia, StellacciEmilia, TartagliaMarco

Journal ArticleAn article published in an academic or professional journal that reports original research or scholarly analysis.

Overview

BRAF<sup>V600</sup> mutations are common in melanoma cells and are often associated with resistance to BRAF inhibitors (BRAFi). This study found that the combination of the HDACi romidepsin and the immunomodulatory agent IFN-&#945;2b reduced melanoma proliferation, survival, and invasiveness, and overcame resistance to vemurafenib (VEM). This combination therapy also restored epigenetically silenced immune signals and induced both apoptosis and necroptosis in melanoma cells. These findings suggest that combined epigenetic-immune drugs may be a promising strategy for treating BRAFi-resistant metastatic melanoma.
Paper Details　
Original Abstract of the Article :
BRAF<sup>V600</sup> mutations are the most common oncogenic alterations in melanoma cells, supporting proliferation, invasion, metastasis and immune evasion. In patients, these aberrantly activated cellular pathways are inhibited by BRAFi whose potent antitumor effect and therapeutic potential are d...See full text at original site
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引用元：
https://doi.org/10.1002/ijc.34602

データ提供：米国国立医学図書館（NLM）

Reversing Vemurafenib-Resistance in Melanoma Cells

Melanoma, a type of skin cancer, often carries a mutation in the BRAF gene, specifically the V600E mutation, which fuels uncontrolled cell growth. Vemurafenib, a targeted therapy that inhibits BRAFV600, can be effective but often leads to resistance. This study investigates the potential of combining romidepsin, a histone deacetylase inhibitor (HDCAi), and IFN-α2b, an immunomodulatory agent, to overcome vemurafenib resistance in melanoma cells.

A Combined Approach: Overcoming Resistance in Melanoma

The researchers tested this drug combination on primary melanoma cell lines derived from metastatic patients, demonstrating its ability to reduce melanoma proliferation, long-term survival, and invasiveness. They found that the combination treatment not only reduced tumor growth but also restored epigenetically silenced immune signals, modulated MITF and AXL expression, and induced apoptosis and necroptosis in both sensitive and vemurafenib-resistant cells.

Hope for Resistance: Reprogramming Oncogenic and Immune Pathways

This study offers a beacon of hope in the desert of melanoma treatment. The researchers' findings suggest that combining epigenetic-immune drugs could be a valuable strategy for overcoming vemurafenib resistance. The combination treatment reprogrammed oncogenic and immune pathways, enhancing the body's natural defenses against melanoma cells. This study highlights the importance of exploring innovative drug combinations to address the challenge of resistance in cancer treatment.

Dr. Camel's Conclusion

This research is a testament to the power of combining forces in the fight against cancer. The researchers' findings suggest that combining epigenetic-immune drugs could be a potent weapon against vemurafenib resistance in melanoma. This study is a reminder that the desert of cancer research is vast and complex, but by exploring new pathways and forging innovative approaches, we can find solutions that bring hope to those battling this devastating disease.

Date :
  1. Date Completed 2023-07-17
  2. Date Revised 2023-11-16
Further Info :

Pubmed ID

37293858

DOI: Digital Object Identifier

10.1002/ijc.34602

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Article Analysis
・Effects of vemurafenib
SNS
PICO Info
in preparation
Languages

English

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