A dual pathway inhibition strategy using BKM120 combined with vemurafenib is poorly tolerated in BRAF V600 E/K mutant advanced melanoma-Reference-Cited by-同舟云学术

A dual pathway inhibition strategy using BKM120 combined with vemurafenib is poorly tolerated in BRAF V600 E/K mutant advanced melanoma

Published:2019-04-13 Issue:4 Volume:32 Page:603-606
ISSN:1755-1471
Container-title:Pigment Cell & Melanoma Research
language:en
Short-container-title:Pigment Cell Melanoma Res

Author:

Algazi Alain Patrick¹^ORCID,Rotow Julia¹,Posch Christian²³,Ortiz‐Urda Susana⁴,Pelayo Alyson¹,Munster Pamela N.¹,Daud Adil¹

Affiliation:

1. UCSF Hematology and Oncology San Francisco California

2. Department of Dermatology and Allergy Technical University of Munich Munich Germany

3. School of Medicine Sigmund Freud University Vienna Austria

4. UCSF Dermatology San Francisco California

Funder

Novartis

Publisher

Wiley

Subject

Dermatology,General Biochemistry, Genetics and Molecular Biology,Oncology

Link

https://onlinelibrary.wiley.com/doi/pdf/10.1111/pcmr.12777

Reference12 articles.

1. Dual MEK/AKT inhibition with trametinib and GSK2141795 does not yield clinical benefit in metastatic NRAS-mutant and wild-type melanoma

2. A phase Ib dose-escalation study of the oral pan-PI3K inhibitor buparlisib (BKM120) in combination with the oral MEK1/2 inhibitor trametinib (GSK1120212) in patients with selected advanced solid tumors;Bedard P.;Journal of Clinical Oncology,2015

3. Phase I, Dose-Escalation Study of BKM120, an Oral Pan-Class I PI3K Inhibitor, in Patients With Advanced Solid Tumors

4. BrafV600E cooperates with Pten loss to induce metastatic melanoma

5. PI3K and cancer: lessons, challenges and opportunities

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