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

A. Grey; A. Cooper; C. Mcneil; Sandra O'Toole; J. Thompson; P. Grimison

doi:10.1111/imj.12415

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

A. Grey, A. Cooper, C. Mcneil, Sandra O'Toole, J. Thompson, P. Grimison

Royal Prince Alfred Hospital

Research output: Contribution to journal › Article › peer-review

17 Citations (Scopus)

Abstract

Vemurafenib is a tyrosine kinase inhibitor of BRAF that prolongs survival in patients with BRAF V600-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.

Original language	English
Pages (from-to)	597-600
Number of pages	4
Journal	Internal Medicine Journal
Volume	44
Issue number	6
DOIs	https://doi.org/10.1111/imj.12415
Publication status	Published - Jun 2014
Externally published	Yes

Keywords

BRAF inhibitor
Melanoma
Pancreatic adenocarcinoma
Secondary malignancy
Vemurafenib

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1111/imj.12415

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abstract = "Vemurafenib is a tyrosine kinase inhibitor of BRAF that prolongs survival in patients with BRAF V600-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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AU - Cooper, A.

AU - Mcneil, C.

AU - O'Toole, Sandra

AU - Thompson, J.

AU - Grimison, P.

PY - 2014/6

Y1 - 2014/6

N2 - Vemurafenib is a tyrosine kinase inhibitor of BRAF that prolongs survival in patients with BRAF V600-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.

AB - Vemurafenib is a tyrosine kinase inhibitor of BRAF that prolongs survival in patients with BRAF V600-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.

KW - BRAF inhibitor

KW - Melanoma

KW - Pancreatic adenocarcinoma

KW - Secondary malignancy

KW - Vemurafenib

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EP - 600

JO - Internal Medicine Journal

JF - Internal Medicine Journal

IS - 6

ER -

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

Abstract

Keywords

UN SDGs

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