Results 61 to 70 of about 1,032,590 (316)

Hybrid Storage Systems: A Survey of Architectures and Algorithms

open access: yesIEEE Access, 2018
Data center storage architectures face rapidly increasing demands for data volume and quality of service requirements today. Hybrid storage systems have turned out to be the one of the most popular choices in fulfilling these demands.
Junpeng Niu, Jun Xu, Lihua Xie
doaj   +1 more source

Aggressive prostate cancer is associated with pericyte dysfunction

open access: yesMolecular Oncology, EarlyView.
Tumor‐produced TGF‐β drives pericyte dysfunction in prostate cancer. This dysfunction is characterized by downregulation of some canonical pericyte markers (i.e., DES, CSPG4, and ACTA2) while maintaining the expression of others (i.e., PDGFRB, NOTCH3, and RGS5).
Anabel Martinez‐Romero   +11 more
wiley   +1 more source

The neural crest‐associated gene ERRFI1 is involved in melanoma progression and resistance toward targeted therapy

open access: yesMolecular Oncology, EarlyView.
ERRFI1, a neural crest (NC)‐associated gene, was upregulated in melanoma and negatively correlated with the expression of melanocytic differentiation markers and the susceptibility of melanoma cells toward BRAF inhibitors (BRAFi). Knocking down ERRFI1 significantly increased the sensitivity of melanoma cells to BRAFi.
Nina Wang   +8 more
wiley   +1 more source

Glycosylated LGALS3BP is highly secreted by bladder cancer cells and represents a novel urinary disease biomarker

open access: yesMolecular Oncology, EarlyView.
Urinary LGALS3BP is elevated in bladder cancer patients compared to healthy controls as detected by the 1959 antibody–based ELISA. The antibody shows enhanced reactivity to the high‐mannose glycosylated variant secreted by cancer cells treated with kifunensine (KIF).
Asia Pece   +18 more
wiley   +1 more source

Survivin and Aurora Kinase A control cell fate decisions during mitosis

open access: yesMolecular Oncology, EarlyView.
Aurora A interacts with survivin during mitosis and regulates its centromeric role. Loss of Aurora A activity mislocalises survivin, the CPC and BubR1, leading to disruption of the spindle checkpoint and triggering premature mitotic exit, which we refer to as ‘mitotic slippage’.
Hana Abdelkabir   +2 more
wiley   +1 more source

CDK11 inhibition induces cytoplasmic p21WAF1 splice variant by p53 stabilisation and SF3B1 inactivation

open access: yesMolecular Oncology, EarlyView.
CDK11 inhibition stabilises the tumour suppressor p53 and triggers the production of an alternative p21WAF1 splice variant p21L, through the inactivation of the spliceosomal protein SF3B1. Unlike the canonical p21WAF1 protein, p21L is localised in the cytoplasm and has reduced cell cycle‐blocking activity.
Radovan Krejcir   +12 more
wiley   +1 more source

Reduced vascular leakage correlates with breast carcinoma T regulatory cell infiltration but not with metastatic propensity

open access: yesMolecular Oncology, EarlyView.
A mouse model for vascular normalization and a human breast cancer cohort were studied to understand the relationship between vascular leakage and tumor immune suppression. For this, endothelial and immune cell RNAseq, staining for vascular function, and immune cell profiling were employed.
Liqun He   +8 more
wiley   +1 more source

Improving PARP inhibitor efficacy in bladder cancer without genetic BRCAness by combination with PLX51107

open access: yesMolecular Oncology, EarlyView.
Clinical trials on PARP inhibitors in urothelial carcinoma (UC) showed limited efficacy and a lack of predictive biomarkers. We propose SLFN5, SLFN11, and OAS1 as UC‐specific response predictors. We suggest Talazoparib as the better PARP inhibitor for UC than Olaparib.
Jutta Schmitz   +15 more
wiley   +1 more source

Class IIa HDACs forced degradation allows resensitization of oxaliplatin‐resistant FBXW7‐mutated colorectal cancer

open access: yesMolecular Oncology, EarlyView.
HDAC4 is degraded by the E3 ligase FBXW7. In colorectal cancer, FBXW7 mutations prevent HDAC4 degradation, leading to oxaliplatin resistance. Forced degradation of HDAC4 using a PROTAC compound restores drug sensitivity by resetting the super‐enhancer landscape, reprogramming the epigenetic state of FBXW7‐mutated cells to resemble oxaliplatin ...
Vanessa Tolotto   +13 more
wiley   +1 more source

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