Results 91 to 100 of about 553,087 (356)

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

siRNA-mediated silencing of bFGF gene inhibits the proliferation, migration, and invasion of human pituitary adenoma cells

open access: yesTumor Biology, 2017
Human pituitary adenoma is one of the most common intracranial tumors with an incidence as high as 16.7%. Recent evidence has hinted a relationship between growth factors of pituitary or hypothalamic origin and proliferation of human pituitary adenoma ...
Kai Zhou   +6 more
doaj   +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

Seminal plasma and prostaglandin E2 up-regulate fibroblast growth factor 2 expression in endometrial adenocarcinoma cells via E-series prostanoid-2 receptor-mediated transactivation of the epidermal growth factor receptor and extracellular signal-regulated kinase pathway [PDF]

open access: yes, 2006
We report a multiwavelength (X-ray, ultraviolet/optical/infrared, radio) analysis of the relativistic tidal disruption event candidate Sw J2058+05 from 3 months to 3 yr post-discovery in order to study its properties and compare its behavior with that of
Bower, Geoffrey C.   +15 more
core   +2 more sources

Abstract #1595981: Changes in Fibroblast Growth Factor-23 and the Klotho Protein Axis in Diabetic Nephropathy [PDF]

open access: bronze, 2023
Nozimakhon Nazarova   +7 more
openalex   +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

Incorporation of FGF-2 into Pharmaceutical Grade Fucoidan/Chitosan Polyelectrolyte Multilayers

open access: yesMarine Drugs, 2020
Biopolymer polyelectrolyte multilayers are a commonly studied soft matter system for wound healing applications due to the biocompatibility and beneficial properties of naturally occurring polyelectrolytes.
Natalie L. Benbow   +3 more
doaj   +1 more source

Tumor Necrosis Factor - Related Apoptosis-Inducing Ligand (TRAIL) promotes angiogenesis and ischemia- induced neovascularization via NADPH Oxidase 4 (NOX4) and Nitric Oxide - dependent mechanisms [PDF]

open access: yes, 2015
Background — Tumor necrosis factor–related apoptosis-inducing ligand (TRAIL) has the ability to inhibit angiogenesis by inducing endothelial cell death, as well as being able to promote pro- angiogenic activity in vitro.
Azahri, N   +10 more
core   +2 more sources

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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