Preprint Review Version 2 Preserved in Portico This version is not peer-reviewed

BRAF Mutations: Oncogenic Drivers in Solid Tumors

Version 1 : Received: 26 January 2024 / Approved: 29 January 2024 / Online: 29 January 2024 (04:43:19 CET)
Version 2 : Received: 9 February 2024 / Approved: 10 February 2024 / Online: 12 February 2024 (11:02:18 CET)

A peer-reviewed article of this Preprint also exists.

Roa, P.; Bremer, N.V.; Foglizzo, V.; Cocco, E. Mutations in the Serine/Threonine Kinase BRAF: Oncogenic Drivers in Solid Tumors. Cancers 2024, 16, 1215. Roa, P.; Bremer, N.V.; Foglizzo, V.; Cocco, E. Mutations in the Serine/Threonine Kinase BRAF: Oncogenic Drivers in Solid Tumors. Cancers 2024, 16, 1215.

Abstract

From their discovery in 2002, BRAF mutations have been identified as clear drivers of oncogenesis in several cancer types. Currently, their incidence rate is nearly 7% of all solid tumors with BRAF V600E constituting approximately 90% of these diagnoses [1]. In melanoma, thyroid cancer, and histiocytic neoplasms, BRAF hotspot mutations are found at a rate of about 50%, while in lung and colorectal cancers they range from 3 to 10% of reported cases [2-5]. Though present in other malignancies such as breast and ovarian cancers, they constitute a small portion of diagnoses (<1%). Given their frequency along with advancements in screening technologies, various methods are used for the detection of BRAF-mutant cancers. Among these are targeted next-generation sequencing (NGS) on tumor tissue or circulating tumor DNA (ctDNA) and immunohistochemistry (IHC)-based assays. With advancements in detection technologies, several approaches have been taken for the treatment of BRAF mutant cancers. In this review we retrace the milestones that led to the clinical development of targeted therapies currently available for these tumors.

Keywords

BRAF; solid tumors; NGS; targeted therapy; therapy resistance

Subject

Biology and Life Sciences, Biochemistry and Molecular Biology

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