2013
DOI: 10.1073/pnas.1205575110
|View full text |Cite
|
Sign up to set email alerts
|

BCL2A1 is a lineage-specific antiapoptotic melanoma oncogene that confers resistance to BRAF inhibition

Abstract: Although targeting oncogenic mutations in the BRAF serine/threonine kinase with small molecule inhibitors can lead to significant clinical responses in melanoma, it fails to eradicate tumors in nearly all patients. Successful therapy will be aided by identification of intrinsic mechanisms that protect tumor cells from death. Here, we used a bioinformatics approach to identify drug-able, "driver" oncogenes restricted to tumor versus normal tissues. Applying this method to 88 short-term melanoma cell cultures, w… Show more

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
2
1
1
1

Citation Types

13
193
0

Year Published

2014
2014
2019
2019

Publication Types

Select...
9
1

Relationship

1
9

Authors

Journals

citations
Cited by 200 publications
(206 citation statements)
references
References 46 publications
(43 reference statements)
13
193
0
Order By: Relevance
“…3). These results are consistent with other work implicating MITF in melanoma survival (Haq et al 2013) 754 Genome Research www.genome.org therefore regulates two contrary effects of BRAF inhibition, namely, induction of melanocyte differentiation, which is an anti-tumorigenic effect important for immune cell recognition of melanoma (Kono et al 2006;Boni et al 2010;Liu et al 2013), and the pro-tumorigenic effect of engaging innate drug resistance to BRAF inhibition.…”
Section: Resultssupporting
confidence: 81%
“…3). These results are consistent with other work implicating MITF in melanoma survival (Haq et al 2013) 754 Genome Research www.genome.org therefore regulates two contrary effects of BRAF inhibition, namely, induction of melanocyte differentiation, which is an anti-tumorigenic effect important for immune cell recognition of melanoma (Kono et al 2006;Boni et al 2010;Liu et al 2013), and the pro-tumorigenic effect of engaging innate drug resistance to BRAF inhibition.…”
Section: Resultssupporting
confidence: 81%
“…Consistent with these findings, SCLCCs usually express high levels of anti-apoptotic proteins, DNA repair enzymes and ATP-binding cassette (ABC) transporters, which help SCLCCs survive the drug attack [6][7][8]. Thus, unraveling the roles of SCLCCs in tumorigenesis and drug resistance has changed our view on chemotherapy and aided the development of new therapeutic strategies against cancers [9][10][11]. Multiple signaling pathways, including WNT, TGF-β, Notch and Hedgehog pathways, have been found to play important roles in SCLCCs [12].…”
Section: Introductionmentioning
confidence: 58%
“…In contrast, BCL2A1 has been confirmed as a lineage-specific anti-apoptotic melanoma oncogene with amplification, which confers resistance to BRAF inhibition (29). In addition, BCL2A1 is also regulated by the melanoma-specific oncogene, MITF, which is also amplified specifically in melanoma UACC62 and UACC257 cells (30). In the present study, MITF mRNA and protein were also suppressed by CR (data not shown), supporting the functional significance of the MITF/BCL2A1 axis in CR-induced apoptosis.…”
Section: Discussionmentioning
confidence: 99%