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Previous studies have demonstrated an anti-tumoral effect of beta-adrenergic blocking agents on cutaneous melanoma (CM). The aim of this study was to investigate if beta-adrenergic blocking agents have an impact on survival in Swedish patients with melanoma. A population-based retrospective registry study including all patients diagnosed with a primary invasive melanoma between 2009 and 2013 was performed. Data from the Swedish Melanoma Register were linked to the Swedish Prescribed Drug Registry and the Swedish Cause of Death Register. Cox regression analyses including competing risk assessments were performed. There were 12,738 patients included, out of which 3702 were exposed to beta-blockers vs. 9036 non-exposed patients. Age, male sex, Breslow thickness, ulceration, and nodal status were independent negative prognostic factors for melanoma-specific survival (MSS). Adding beta-blockers to the analysis did not add any prognostic value to the model (HR 1.00, p = 0.98), neither when adjusting for competing risks (HR 0.97, p = 0.61). When specifically analyzing the use of non-selective beta-blockers, the results were still without statistical significance (HR 0.76, p = 0.21). In conclusion, this population-based registry study could not verify that the use of beta-adrenergic blocking agents improve survival in patients with melanoma.

BackgroundThe survival in metastatic melanoma has dramatically improved after the introduction of immune checkpoint‐ (ICIs) and MAPKinase inhibitors (MAPKis).ObjectiveOur aim was to describe therapy response and survival in a real‐world population as well as to assess the associations between clinical variables and therapy outcome for patients with metastatic melanoma receiving first‐line ICIs or MAPKis.MethodsA total of 252 patients with metastatic (stage IV) melanoma were prospectively followed between 1 January 2010 and 3 December 2017 with follow‐up until 31 March 2019, at the Karolinska University Hospital, Sweden. Hazard ratios (HRs) for progression‐free survival (PFS) and overall survival (OS) were analysed with Cox regression, and logistic regression was used to estimate odds ratios (ORs) for therapy response.ResultsPatients receiving ICIs (n = 138) experienced longer PFS compared to patients that received MAPKis (n = 114; median PFS for ICIs was 6.8 months, and median PFS for MAPKis was 5.3 months). In the multivariable analyses of clinical markers, increasing M‐stage (OR 0.65; 95% CI 0.45–0.94; P = 0.022) and male sex (OR 0.41; 95% CI 0.19–0.90; P = 0.027) were significantly associated with lower response to ICIs. Lower baseline albumin levels (OR 0.90; 95% CI 0.83–0.98; P = 0.019) and male sex (OR 0.33; 95% CI 0.12–0.93; P = 0.036) were related with lower response to MAPKis. For ICIs, increasing M‐stage (HR 1.34; 95% CI 1.07–1.68; P = 0.010), increasing LDH (HR 1.73; 95% CI 1.19–2.50; P = 0.004) and decreasing albumin (HR 1.06; 95% CI 1.01–1.10; P = 0.011) were significantly associated lower PFS in the adjusted model. The corresponding markers for MAPKis were increasing LDH (HR 1.44; 95% CI 1.08–1.92; P = 0.013) and decreasing albumin (HR 1.05; 95% CI 1.02–1.09; P = 0.005) for PFS.ConclusionICIs and MAPKis were effective in this real‐world population, and we could confirm the importance of previously reported clinical prognostic markers. Albumin values may be associated with therapy outcome but need further validation.