Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5783571 | PMC |
| http://dx.doi.org/10.1016/j.ccell.2017.12.011 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Molecular and pathological landscape of the AT-rich interaction domain 1A (ARID1A) mutation in hepatocellular carcinoma.
Pathol Res Pract
December 2024
Department of Oncology, Dianjiang People's Hospital of Chongqing, Chongqing, China.
Article Synopsis
- Hepatocellular carcinoma (HCC) is a major cause of cancer deaths globally, with complex causes and significant genetic variations.
- ARID1A mutations, found in about 7.9% of HCC cases, often lead to tumor aggressiveness, larger sizes, and worse patient outcomes due to their loss-of-function effects.
- The dual role of ARID1A as both a tumor suppressor and facilitator of early tumor development highlights its importance in HCC, suggesting that tailored therapies targeting its functions could improve treatment effectiveness.
ARID1A loss is associated with increased NRF2 signaling in human head and neck squamous cell carcinomas.
PLoS One
February 2024
Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill School of Medicine, Chapel Hill, North Carolina, United States of America.
Prior to the next generation sequencing and characterization of the tumor genome landscape, mutations in the SWI/SNF chromatin remodeling complex and the KEAP1-NRF2 signaling pathway were underappreciated. While these two classes of mutations appeared to independently contribute to tumor development, recent reports have demonstrated a mechanistic link between these two regulatory mechanisms in specific cancer types and cell models. In this work, we expand upon these data by exploring the relationship between mutations in BAF and PBAF subunits of the SWI/SNF complex and activation of NRF2 signal transduction across many cancer types.
View Article and Find Full Text PDFTargeting the BAF complex in advanced prostate cancer.
Expert Opin Drug Discov
February 2021
Urology Research Group, CRUK Beatson Institute, Glasgow, UK.
Introduction: The BRG1/BRM associated factors (BAF) complex is a chromatin remodeling SWI/SNF which is mutated in 20% of cancers. This complex has many interchangeable subunits which may have oncogenic or tumor suppressor activity in a context-dependent manner. The BAF complex is mutated in 35-50% of metastatic prostate cancer (PC); however, its role in advanced disease is unclear.
View Article and Find Full Text PDFARID1A/BAF250a is significantly overexpressed in primary invasive breast cancer.
Transl Cancer Res
June 2020
Department of Pathology, Wroclaw Medical University, Wroclaw, Poland.
Background: ARID1A (also known as BAF250a, p270 or SMARCF1) is a major component of the mammalian SWI/SNF family that is involved in the regulation of the chromatin structure. ARID1A gene mutations have been associated with many types of malignancies, including breast cancer. This study aimed to explore the expression of BAF250a protein in breast cancer and its association with the clinical and pathological characteristics and prognosis of breast cancer.
View Article and Find Full Text PDFSWI/SNF protein and claudin-4 expression in anaplastic carcinomas arising in mucinous tumours of the ovary and retroperitoneum.
Histopathology
August 2020
Pathology Service, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
Aims: Anaplastic carcinoma arising in a mucinous tumour of the ovary and rarely in the retroperitoneum is an uncommon neoplasm with three morphological patterns; rhabdoid, sarcomatoid and pleomorphic. We investigated expression of switch/sucrose non-fermentable (SWI/SNF) chromatin remodelling complex components and claudin-4 expression.
Methods And Results: Twenty-two ovarian and three retroperitoneal mucinous tumours were investigated using antibodies against SMARCB1, SMARCA4, SMARCA2, ARID1A and claudin-4.
Want AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!