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In relation to the opinion of a court, decided.

The holding in a particular case is the ultimate decision of a court of a Justiciable controversy.

West's Encyclopedia of American Law, edition 2. Copyright 2008 The Gale Group, Inc. All rights reserved.


v. decided or ruled, as "the court held that the contract was valid."

(See: decision, ruling, judgment)

Copyright © 1981-2005 by Gerald N. Hill and Kathleen T. Hill. All Right reserved.
References in periodicals archive ?
The research, led by Johns Hopkins Kimmel Cancer Center researchers, could advance efforts to treat many human cancers with loss of ARID1A that are resistant to current standard treatments, the study team suggests.
Based on the previous research, we hypothesized that FRBI impacts the expression levels and production of ARID1A, PTEN, and FSHR, which are associated with carcinogenesis and progression of ovarian cancer.
However, a statistically significant correlation existed between loss of ARID1A expression and ER (p=0.047), or PR- negativities (p=0.027).
The expression of ARID1A, ING5, and CBX7 genes was significantly lower in the GC group than in the control group (fold change<0.5 and fold regulation<-2).
(17,18) The ARID1A gene is a tumor suppressor gene, and an associated mutation or inactivation is reported in many cancers.
al-Agha et al., "ARID1A mutations in endometriosis-associated ovarian carcinomas," The New England Journal of Medicine, vol.
Kanchwala et al., "Suppression of the SWI/SNF component Arid1a promotes mammalian regeneration," Cell Stem Cell, vol.
For example, significant differences have been noted in the frequencies of mutations among the ARID1A, PTEN, PIK3CA, PPP2R1A (protein phosphatase 2, regulatory subunit A, alpha), TP53, and CTNNB1 genes in low-grade endometrioid endometrial carcinoma, high-grade endometrioid endometrial carcinoma, serous endometrial carcinoma, and endometrial carcinosarcomas, and the pattern of mutations in this 6-gene set has facilitated the histologic reclassification of some endometrial tumors (58).
Apart from the morphologic and clinical features separating type 1 from type 2 ECs, they are further distinguished by specific genetic alterations [14]; EECs are characterized by microsatellite instability (MSI), somatic alterations within the PI3K pathway and the MAPK pathway, and mutations of CTNNB1 ([beta]-catenin) and ARID1A (BAF250a) genes.
Most endometrioid tumors had few SCNA or P53 mutations but frequent mutations in PTEN, CTNNB1, PIK3CA, ARID1A, and KRAS genes.
The most commonly mutated genes included PIK3CA, TP53 and ARID1A.