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FOXF2 expression triggered by endocrine therapy orchestrates therapeutic resistance through reorganization of chromatin architecture in breast cancer.
Cancer Lett
January 2025
Department of Biochemistry and Molecular Biology; Key Laboratory of Breast Cancer Prevention and Treatment of the Ministry of Education, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center of Cancer, Tianjin 300060, China. Electronic address:
Patients with estrogen receptor-positive (ER+) breast cancer require long-term endocrine therapy. However, endocrine resistance remains a critical issue to be addressed. Herein, we show that ERα repressed FOXF2 transcription in ER+ breast cancer through H3K27me3 modification, therefore endocrine therapy triggered FOXF2 transcription via loss of H3K27me3.
View Article and Find Full Text PDFEpigenetics.
Adv Exp Med Biol
June 2024
Departments of Medicine and Cell and Developmental Biology, Institute for Regenerative Medicine, Epigenetics Institute and the Cardiovascular Institute, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, PA, USA.
Epigenetics is the study of heritable changes to the genome and gene expression patterns that are not caused by direct changes to the DNA sequence. Examples of these changes include posttranslational modifications to DNA-bound histone proteins, DNA methylation, and remodeling of nuclear architecture. Collectively, epigenetic changes provide a layer of regulation that affects transcriptional activity of genes while leaving DNA sequences unaltered.
View Article and Find Full Text PDFGastric SMARCA4-deficient undifferentiated tumor (SMARCA4-UT): a clinicopathological analysis of four rare cases.
Orphanet J Rare Dis
June 2024
Department of Pathology, West China Hospital, Sichuan University, No. 37 Guo Xue Xiang, Chengdu, 610041, Sichuan, P.R. China.
Background: SMARCA4, as one of the subunits of the SWI/SNF chromatin remodeling complex, drives SMARCA4-deficient tumors. Gastric SMARCA4-deficient tumors may include gastric SMARCA4-deficient carcinoma and gastric SMARCA4-deficient undifferentiated tumor (SMARCA4-UT). Gastric SMARCA4-UT is rare and challenging to diagnose in clinical practice.
View Article and Find Full Text PDFSMARCA4-deficient undifferentiated gastric carcinoma: a case series and literature review.
Gastric Cancer
September 2024
Department of Pathology, Asan Medical Center, University of Ulsan College of Medicine, 88, Olympic-Ro 43-Gil, Songpa-Gu, Seoul, 05505, Republic of Korea.
Article Synopsis
- - Undifferentiated gastric carcinoma features anaplastic cells without clear differentiation, making it hard to diagnose and treat; recent studies link it to mutations in the SWI/SNF complex, especially in the SMARCA4 subunit.
- - A report of six cases of SMARCA4-deficient undifferentiated gastric carcinoma reveals its rarity and common diagnostic challenges, predominantly affecting males over 50 with non-specific symptoms.
- - Histologically, these tumors show a sheet-like growth pattern and loss of important markers, with conventional chemotherapy proving ineffective, emphasizing the need for surgical removal and new treatment methods.
Thoracic SMARCA4-deficient tumors: a clinicopathological analysis of 52 cases with SMARCA4-deficient non-small cell lung cancer and 20 cases with thoracic SMARCA4-deficient undifferentiated tumor.
PeerJ
February 2024
Department of Pathology, West China Hospital, Sichuan University, Chengdu, Sichuan, China.
Background: Thoracic SMARCA4-deficient undifferentiated tumor (SMARCA4-UT) is a distinct clinicopathological entity with an aggressive clinical course. Additionally, SMARCA4/BRG1 deficiency can be observed in a few patients with non-small cell lung cancer (NSCLC). We aimed to compare the clinicopathological, immunohistochemical and prognostic features of SMARCA4-deficient NSCLC (SMARCA4-dNSCLC) with those of thoracic SMARCA4-UT.
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