According to a Kaiser Permanente study, HIV-positive subjects had a 2.1-fold higher risk for basal cell carcinomas and a 2.6-fold higher risk for squamous cell carcinomas, compared to HIV-negative subjects. Squamous cell carcinomas were associated with lower CD4 counts, a measure of immunodeficiency. Prior antiretroviral therapy was not found to be associated with the incidence of either squamous cell carcinomas or basal cell carcinomas
- LDH levels
Melanoma researchers from the U.S. and Australia highlight that the recent success of targeted agents and immunotherapies for treatment of melanoma should be tested in combination clinical trials, particularly in the adjuvant setting
A 2nd publication from a German group also find mutations in TERT, in 74% of non-inherited melanoma cases. Together with the publication from the Harvard group in the same journal, these results are likely a starting point for targeting TERT, the enzyme responsible for adding extra ends onto chromosomes.
GSK has started its COMBI-AD phase III study evaluating its BRAF inhibitor, dabrafenib with trametinib, its MEK inhibitor as adjuvant therapy for melanoma. The global study will investigate whether the combo can delay or prevent the recurrence of melanoma in patients with Stage IIIa, IIIb, or IIIc BRAF V600E or V600K mutation-positive melanoma that has been completely removed by surgery.
Retrospective analysis of 520 melanoma patients with a negative sentinel lymph node biopsy showed an overall recurrence rate of 16%, with median follow-up of 61 months. For recurrences in the sampled nodal basin, the false-negative rate was 4%. Age, Breslow thickness, ulceration, and head and neck lesions significantly predicted recurrence.
Pharmaceutical giant GlaxoSmithKline (NYSE: GSK ) announced in a press release that it has begun a phase 3 study to find out whether two of its drugs — its BRAF inhibitor dabrafenid and MEK inhibitor trametinib — can combine to work as a successful therapy for melanoma.
Review of genetics of melanoma including analysis of the mutational signatures of melanoma tumors continues to cement the causative role of UV exposure in melanoma pathogenesis. Melanomas from sun-exposed skin areas have distinct mutational signatures including C to T transitions indicative of UV-induced damage. It is thus necessary to continue spreading awareness on how to decrease the risk factors of developing the disease while at the same time working for a cure.
Review of the available data to best guide initial treatment choice and the sequence of treatments for patients with BRAF Val600 mutant melanoma.
Study finds phosphorylation of Mps1 by BRAFV600E prevents Mps1 degradation and contributes to chromosome instability in melanoma. The results raise the possibility that targeting the oncogenic BRAF and S281-phosphorylated Mps1, especially when used in combination could potentially provide great therapeutic opportunities for cancer treatment.