SMARCB1-Deficient Cancers: Novel Molecular Insights and Therapeutic Vulnerabilities.
SMARCB1-deficient cancer
chromatin
epigenetics
rhabdoid tumor
structure
therapeutics
Journal
Cancers
ISSN: 2072-6694
Titre abrégé: Cancers (Basel)
Pays: Switzerland
ID NLM: 101526829
Informations de publication
Date de publication:
27 Jul 2022
27 Jul 2022
Historique:
received:
25
06
2022
revised:
20
07
2022
accepted:
20
07
2022
entrez:
27
7
2022
pubmed:
28
7
2022
medline:
28
7
2022
Statut:
epublish
Résumé
SMARCB1 is a critical component of the BAF complex that is responsible for global chromatin remodeling. Loss of SMARCB1 has been implicated in the initiation of cancers such as malignant rhabdoid tumor (MRT), atypical teratoid rhabdoid tumor (ATRT), and, more recently, renal medullary carcinoma (RMC). These SMARCB1-deficient tumors have remarkably stable genomes, offering unique insights into the epigenetic mechanisms in cancer biology. Given the lack of druggable targets and the high mortality associated with SMARCB1-deficient tumors, a significant research effort has been directed toward understanding the mechanisms of tumor transformation and proliferation. Accumulating evidence suggests that tumorigenicity arises from aberrant enhancer and promoter regulation followed by dysfunctional transcriptional control. In this review, we outline key mechanisms by which loss of SMARCB1 may lead to tumor formation and cover how these mechanisms have been used for the design of targeted therapy.
Identifiants
pubmed: 35892904
pii: cancers14153645
doi: 10.3390/cancers14153645
pmc: PMC9332782
pii:
doi:
Types de publication
Journal Article
Review
Langues
eng
Subventions
Organisme : NIGMS NIH HHS
ID : T32GM008490
Pays : United States
Organisme : American Cancer Society
ID : MRSG-18-202-01
Organisme : Ian's Friends Foundation
ID : NA
Organisme : UnRavel Pediatric Cancer
ID : NA
Organisme : United States Department of Defense
ID : W81XWH-18-PRCRP-CDA
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