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

机译:维拉非尼治疗转移性黑色素瘤患者中KRAS突变型胰腺腺癌的进展

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摘要

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.
机译:Vemurafenib是BRAF的酪氨酸激酶抑制剂,可延长BRAF V600突变型转移性黑色素瘤患者的生存期。继发性皮肤恶性肿瘤是vemurafenib的有据可查的毒性,据认为是由BRAF野生型RAS突变细胞中增强的ERK信号传导介导的。 Vemurafenib也可以通过类似的机制促进非皮肤继发性恶性肿瘤的生长。我们介绍了一个个体,该个体因转移性黑色素瘤接受维罗非尼治疗,并经历了预先存在的KRAS突变型胰腺腺癌的快速生长。

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