Progression of   KRAS   mutant pancreatic adenocarcinoma during vemurafenib treatment in a patient with metastatic melanoma | Zendy

Grey A. | Zendy; Cooper A. | Zendy; McNeil C. | Zendy; O'Toole S. | Zendy; Thompson J. | Zendy; Grimison P. | Zendy

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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.

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