ALK-Rearranged Renal Cell Carcinomas in Children.
Omaha, United States. In Genes Chromosomes Cancer, Feb 2016
In our review of 168 pediatric RCC prospectively registered on Children's Oncology Group AREN03B2 protocol, we identified six RCC (3.5%) that demonstrated a unique epithelioid morphology and a peculiar immunophenotypic profile that includes expression of ALK, TFE3 and retention of INI1.
SMARCB1/INI1 Genetic Alterations in Renal Medullary Carcinomas.
Córdoba, Spain. In Eur Urol, Feb 2016
UNASSIGNED: Inactivation of the tumor suppressor gene SMARCB1 (also known as INI1) by interchromosomal balanced translocations is a molecular mechanism that characterizes renal medullary carcinoma and might be relevant for the development of more effective therapeutic strategies.
Adult Atypical Teratoid/Rhabdoid Tumors.
Boston, United States. In World Neurosurg, Jan 2016
Due to the complex histology of AT/RTs, the differential diagnosis of these tumors is quite challenging and increasingly relies on demonstration of characteristic SMARCB1/INI1 inactivation in tumor cells.
Recently described neoplasms of the sinonasal tract.
Baltimore, United States. In Semin Diagn Pathol, Jan 2016
This manuscript will review the clinicopathologic features of some of the recently described sinonasal tumor types: NUT midline carcinoma, HPV-related carcinoma with adenoid cystic-like features, SMARCB1 (INI-1) deficient sinonasal carcinoma, biphenotypic sinonasal sarcoma, and adamantinoma-like Ewing family tumor.
SWI/SNF chromatin remodeling and human malignancies.
In Annu Rev Pathol, 2014
The first evidence of the involvement of these complexes in carcinogenesis was provided by the identification of biallelic, truncating mutations of the SMARCB1 gene in malignant rhabdoid tumors, a highly aggressive childhood cancer.
Biology and Treatment of Rhabdoid Tumor.
Los Angeles, United States. In Crit Rev Oncog, 2014
SMARCB1 is a member of the SWI/SNF chromatin-remodeling complex and functions as a tumor suppressor in the vast majority of rhabdoid tumors.
Linking the SWI/SNF complex to prostate cancer.
Boston, United States. In Nat Genet, 2013
Although mutations in SWI/SNF genes are uncommon in prostate cancer, a new study shows that SChLAP1, a long noncoding RNA frequently expressed in aggressive prostate tumors, drives cancer by directly disrupting SNF5, a core subunit of the SWI/SNF complex.