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. 2019 Aug 1;11(8):1093. doi: 10.3390/cancers11081093

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© 2019 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).

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p53 activator (PRIMA-1^Met) and BRAF inhibitor (vemurafenib) radiosensitise ^V600EBRAF mutant melanoma in vivo. (A) Swiss nude mice (nu/nu) were injected by either MM043 and treated with CTR (DMSO), vemurafenib (45 mg/kg), PRIMA-1^Met (50 mg/kg), or vemurafenib and PRIMA-1^Met. One day later, the mice were irradiated on the right leg. Data are presented as means ± SEM (n = 9) compared to untreated tumors (B) Tumor volume of mice, non-irradiated (left panel), irradiated (right panel), untreated or treated with vemurafenib and/or PRIMA-1^Met in the period between D0 and D36. ** p < 0.01, *** p < 0.001 (two-way ANOVA) compared to non-irradiated.

p53 activator (PRIMA-1^Met) and BRAF inhibitor (vemurafenib) radiosensitise ^V600EBRAF mutant melanoma in vivo. (A) Swiss nude mice (nu/nu) were injected by either MM043 and treated with CTR (DMSO), vemurafenib (45 mg/kg), PRIMA-1^Met (50 mg/kg), or vemurafenib and PRIMA-1^Met. One day later, the mice were irradiated on the right leg. Data are presented as means ± SEM (n = 9) compared to untreated tumors (B) Tumor volume of mice, non-irradiated (left panel), irradiated (right panel), untreated or treated with vemurafenib and/or PRIMA-1^Met in the period between D0 and D36. ** p < 0.01, *** p < 0.001 (two-way ANOVA) compared to non-irradiated.