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Progression of KRAS mutant pancreatic adenocarcinoma during vemurafenib treatment in a patient with metastatic melanoma
Author(s) -
Grey A.,
Cooper A.,
McNeil C.,
O'Toole S.,
Thompson J.,
Grimison P.
Publication year - 2014
Publication title -
internal medicine journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.596
H-Index - 70
eISSN - 1445-5994
pISSN - 1444-0903
DOI - 10.1111/imj.12415
Subject(s) - medicine , vemurafenib , metastatic melanoma , kras , metastatic adenocarcinoma , adenocarcinoma , melanoma , cancer research , oncology , mutant , metastasis , cancer , gene , colorectal cancer , chemistry , biochemistry
Vemurafenib is a tyrosine kinase inhibitor of BRAF that prolongs survival in patients with BRAF V 600‐mutant metastatic melanoma. Secondary cutaneous malignancies are a well‐documented toxicity of vemurafenib, thought to be mediated by enhanced ERK signalling in BRAF wild‐type, RAS ‐mutant cells. Vemurafenib could also promote growth of non‐cutaneous secondary malignancies by a similar mechanism. We present a case of an individual who received vemurafenib for metastatic melanoma and experienced rapid growth of a pre‐existing KRAS ‐ mutant pancreatic adenocarcinoma.