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Characteristics of BRAF V600K versus V600E: Effect of molecular weight change in melanoma

1 Sanitation 1, Medical Academic Center, Bangkok, Thailand
2 Department of Tropical Medicine, Hainan Medical University, Haikou, China

Correspondence Address:
Beuy Joob,
Sanitation 1, Medical Academic Center, Bangkok
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/jcrt.JCRT_433_18

How to cite this URL:
Joob B, Wiwanitkit V. Characteristics of BRAF V600K versus V600E: Effect of molecular weight change in melanoma. J Can Res Ther [Epub ahead of print] [cited 2019 Jul 18]. Available from: http://www.cancerjournal.net/preprintarticle.asp?id=257923


Melanoma is important cancer. The genetic underlying factor for the susceptibility/resistance of the cancer to treatment is very interesting. The effect of the genetic polymorphism should be discussed. Li et al. recently found that “elements of energy metabolism and protein translation pathways were upregulated” in V600K tumors compared with V600E tumors. We would like to share ideas on this finding. In fact, the energy requirement in metabolism can be altered as a result of the mutation, and this might affect the susceptibility/resistance of the tumor to treatment as well as the severity/prognosis of the disease.[1] Focusing on V600K and V600E mutations, the calculation for molecular weight change based on basic quantum calculation as presented in previous reports on important medical disorders[2],[3],[4] can show that the changes in V600K and V600E equal to 29 and 30/mol, respectively. This means the required energy per molecule to finalize the protein-translation pathway or the case of V600K should be slightly less than that of V600E. Hence, this finding is concordant and supports the observations in the study by Li et al.[1] Indeed, in a recent report by Hallmeyer et al.,[5] the response rate to treatment in V600K mutation is slightly higher than other mutation including to V600E. In fact, calculating the stability of BRAF dimers, either with itself or other RAF proteins which can make some senses. Still, it is clear how such stability calculations would translate into the differences in biology or clinical observations between V600K and V600E mutants. Here, it is clearly noted that “molecular weight change” contribute to the observe difference in susceptibility/resistance.

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 > References Top

Li Y, Umbach DM, Li L. Putative genomic characteristics of BRAF V600K versus V600E cutaneous melanoma. Melanoma Res 2017;27:527-35.  Back to cited text no. 1
Wiwanitkit V. Analysis of binding energy activity of imatinib and Abl tyrosine kinase domain based on simple consideration for conformational change: An explanation for variation in imatinib effect in mutated type. Indian J Cancer 2009;46:335-6.  Back to cited text no. 2
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Joob B, Wiwanitkit V. HSD11B1 rs846908 polymorphisms and tacrolimus concentrations: Quantum chemical analysis and implication in patients with renal transplantation. J Nephropharmacol 2017;6:19-20.  Back to cited text no. 3
Joob B, Wiwanitkit V. ATP-binding cassette, sub-family B (MDR/TAP), member 1 (ABCB1) polymorphism and clopidogrel concentration in acute coronary syndrome: Molecular change can explain the observed therapeutic concentration. Anatol J Cardiol 2016;16:303-4.  Back to cited text no. 4
Hallmeyer S, Gonzalez R, Lawson DH, Cranmer LD, Linette GP, Puzanov I, et al. Vemurafenib treatment for patients with locally advanced, unresectable stage IIIC or metastatic melanoma and activating exon 15 BRAF mutations other than V600E. Melanoma Res 2017;27:585-90.  Back to cited text no. 5


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