Results 161 to 170 of about 3,959,615 (299)

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

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

Mortalidade por causas externas em crianças e adolescentes: tendências de 1979 a 1995

open access: yesRevista de Saúde Pública
OBJETIVO: Analisar a magnitude e a tendência da mortalidade por grupos específicos de causas externas em crianças e adolescentes residentes no Recife, no período de 1979 a 1995.
Maria Dilma de A Barros   +2 more
doaj  

Cytoplasmic p21 promotes stemness of colon cancer cells via activation of the NFκB pathway

open access: yesMolecular Oncology, EarlyView.
Cytoplasmic p21 promotes colorectal cancer stem cell (CSC) features by destabilizing the NFκB–IκB complex, activating NFκB signaling, and upregulating BCL‐xL and COX2. In contrast to nuclear p21, cytoplasmic p21 enhances spheroid formation and stemness transcription factor CD133.
Arnatchai Maiuthed   +10 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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