Survival analysis indicated that methylation of the CSR1 promoter, and to a lesser extent down-regulation of CSR1 protein expression, was associated with a high rate of prostate cancer metastasis.
Survival analysis indicated that methylation of the CSR1 promoter, and to a lesser extent down-regulation of CSR1 protein expression, was associated with a high rate of prostate cancer metastasis.
Expression of CSR1 in PC3 cell xenografts produced a dramatic reduction (>8-fold) in tumor size, rate of invasion (0 versus 31%), and mortality (13 versus 100%).
They therefore suggest that dysregulation of APC activity, possibly through downregulation of APC7, may be associated with tumorigenesis in breast cancer.
Background The contribution of the lung or the plant gain ( PG ; ie, change in blood gases per unit change in ventilation) to Cheyne-Stokes respiration ( CSR ) in heart failure has only been hypothesized by mathematical models, but never been directly evaluated.
The mean relative expression levels in severe HFMD and control HFMD patients were 10.1-fold and 5.0-fold, respectively, P value <.001.We found that SCARA3 is associated with severity of HFMD, and it may be a potential prognostic marker to predict the HFMD progression in EV71 infected patients.
In this phase I clinical study, we evaluated the safety and bioactivity of CSR-T cell therapy in 14 patients with recurrent glioblastoma who were unresponsive to surgical resection and standard radiotherapy.
In this phase I clinical study, we evaluated the safety and bioactivity of CSR-T cell therapy in 14 patients with recurrent glioblastoma who were unresponsive to surgical resection and standard radiotherapy.
Patients with myocarditis showed significantly reduced LA passive strain (LA ε<sub>e</sub>: 26.3 ± 14.5 vs. 33.5 ± 10.1%, p = .007), LA peak early negative strain rate (LA SRe: -1.94 ± 0.59 1/s vs. -1.46 ± 0.62 1/s, p < .001), LV global longitudinal strain (LV GLS: -17.2 ± 4.9% vs. -13.3 ± 6.2%, p < .001), LV midventricular circumferential strain (LV mid CS: -25.9 ± 4.7% vs. -22.0 ± 6.5%, p < .001), and an increased RV basal circumferential SR (RV basal CSR: -0.70 ± 028 vs. -0.58 ± 0.34 1/s, p = .096) compared to healthy controls.
In 22 childhood cancer survivors (median age: 14.8, range 6.4-21.6 years), mean GLS (- 13.83 ± 0.74% to - 15.94 ± 0.74%, p = 0.002), GCS (- 18.79 ± 1.21% to - 20.74 ± 0.84%, p = 0.027), LSR (- 0.78 ± 0.04 to - 0.88 ± 0.04 s<sup>-1</sup>, p = 0.022), and CSR (- 1.08 ± 0.07 to - 1.21 ± 0.06 s<sup>-1</sup>, p = 0.027) improved on therapy.
Knowledge of this abnormal FC might lead to a better understanding of the mechanism underlying CNSP-CSR, especially the descending pain modulation system involved in chronic pain.
Here, we describe a patient whose features we would suggest represent a new FGFR2-related syndrome, craniosynostosis with XY male-to-female sex reversal or CSR.
SCARA3 levels in effusions and primary carcinomas were unrelated to patient age, tumor grade, FIGO stage, residual tumor volume after surgery, response to chemotherapy, or survival (P > .05 for all).
Scavenger receptor class A, member 3 (SCARA3) was previously found to be overexpressed in ovarian/primary peritoneal carcinoma (OC/PPC) compared with breast carcinoma effusions by global gene expression analysis.
Within the CSR gene set, a group of 42 v-Src inducible genes was associated with reduced disease- and metastasis-free survival in several independent patient cohorts with breast or lung cancer.
Within the CSR gene set, a group of 42 v-Src inducible genes was associated with reduced disease- and metastasis-free survival in several independent patient cohorts with breast or lung cancer.
Within the CSR gene set, a group of 42 v-Src inducible genes was associated with reduced disease- and metastasis-free survival in several independent patient cohorts with breast or lung cancer.
Four Ig-CSRdeficiency phenotypes have been so far reported: the description of the activation-induced cytidine deaminase (AID) deficiency (Ig-CSR deficiency 1), caused by recessive mutations of AICDA gene, characterized by a defect in CSR and SHM, clearly established the role of AID in the induction of the Ig gene rearrangements underlying CSR and SHM.