Results 71 to 80 of about 1,151,537 (267)

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

Relationship between serum high-sensitivity C-reactive protein and modified TOAST classification as well as OCSP subtypes in patients with acute ischemic stroke

open access: yesChinese Journal of Contemporary Neurology and Neurosurgery, 2014
This paper aims to investigate the relationship between serum high-sensitivity C-reactive protein (hs-CRP) level and modified TOAST classification as well as OCSP subtypes in patients with acute ischemic stroke.
Hua-jun CHANG   +2 more
doaj  

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

Intein‐based modular chimeric antigen receptor platform for specific CD19/CD20 co‐targeting

open access: yesMolecular Oncology, EarlyView.
CARtein is a modular CAR platform that uses split inteins to splice antigen‐recognition modules onto a universal signaling backbone, enabling precise, scarless assembly without re‐engineering signaling domains. Deployed here against CD19 and CD20 in B‐cell malignancies, the design supports flexible multi‐antigen targeting to boost T‐cell activation and
Pablo Gonzalez‐Garcia   +9 more
wiley   +1 more source

MP19-10 PROGNOSTIC SIGNIFICANCE OF C-REACTIVE PROTEIN ON SURVIVAL IN PATIENTS WITH NON-METASTATIC PAPILLARY RENAL CELL CARCINOMA: AN INTERNATIONAL MULTI-RACIAL STUDY [PDF]

open access: bronze, 2019
Masahiro Toide   +14 more
openalex   +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

Within-subject variation of C-reactive protein and high-sensitivity C-reactive protein: A systematic review and meta-analysis.

open access: yesPLoS ONE
BackgroundC-reactive protein (CRP) and high-sensitivity C-reactive protein (hsCRP) are measures of inflammation used in diagnosis, to guide treatment decisions, and in disease prediction.
Alex Gough   +3 more
doaj   +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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