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Updated: Jan 1, 2026

Spatial and Temporal Control of Murine Melanoma Initiation from Mutant Melanocyte Stem Cells
Published on: June 7, 2019
Beta Blockers and Melanoma
Aleksandra Vojvodic1, Petar Vojvodic2, Tatjana Vlaskovic-Jovicevic2
1Department of Dermatology and Venereology, Military Medical Academy, Belgrade, Serbia.
Abstract:
Understanding the mechanisms of cancer immune-tolerance is one of the most important challenges. Several studies have demonstrated the potential anticarcinogenic effects of beta-blockers, in patients with prostate cancer, breast cancer, and melanoma. At the other side variety of dermatoses may be caused or aggravated by β-blockers-psoriasis, lichen planus-like drug eruptions (LDE), acrocyanosis, alopecia etc. Beta-blockers have been shown to improve the prognosis of melanoma patients significantly. Propranolol inhibits melanoma by downregulating the tumour angiogenesis but also tumour cell proliferation, invasiveness and local immune suppression. Studies showed that only β3-but, not β2-adrenoceptors, were up-regulated under hypoxia in peripheral blood mononuclear cells and selectively expressed in immune cell sub-populations including Treg, MDSC, and NK. They increased NK and CD8 number and cytotoxicity. Catecholamines may retard melanoma progression and that β-blockers may have unrecognised potential as a therapeutic intervention for melanoma, in the prevention of the growth of melanoma in all stages and as adjuvant therapy with other targeted and immune therapies for melanoma.
Insights
Beta-blockers show promise in treating melanoma by inhibiting tumor growth and improving patient prognosis. They target tumor angiogenesis and immune suppression, offering potential as an adjuvant therapy.
Area of Science:
- Oncology
- Immunology
- Pharmacology
Background:
- Cancer immune-tolerance presents a significant challenge in oncology.
- Beta-blockers exhibit potential anticarcinogenic effects across various cancers, including melanoma.
- However, beta-blockers can also cause or exacerbate dermatological conditions.
Purpose of the Study:
- To investigate the mechanisms behind the anticarcinogenic effects of beta-blockers in melanoma.
- To explore the role of specific adrenoceptors in melanoma progression and immune response.
- To evaluate the therapeutic potential of beta-blockers as an adjuvant therapy for melanoma.
Main Methods:
- Analysis of beta-blocker effects on melanoma cell proliferation, angiogenesis, and invasiveness.
- Investigation of adrenoceptor expression (β2 and β3) in immune cells under hypoxic conditions.
- Assessment of changes in immune cell populations (Treg, MDSC, NK, CD8) and their cytotoxicity.
Main Results:
- Beta-blockers, particularly propranolol, significantly improve melanoma patient prognosis.
- Propranolol inhibits melanoma by reducing tumor angiogenesis, proliferation, and invasiveness, while mitigating local immune suppression.
- Hypoxia upregulates β3-adrenoceptors in peripheral blood mononuclear cells, specifically in immune cells like Treg, MDSC, and NK cells, enhancing NK and CD8 cell number and cytotoxicity.
Conclusions:
- Catecholamines may impede melanoma progression.
- Beta-blockers possess unrecognized therapeutic potential for melanoma prevention and treatment.
- Beta-blockers can serve as an effective adjuvant therapy alongside other melanoma treatments.
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