Results 41 to 50 of about 173,282 (309)

Investigating the cell of origin and novel molecular targets in Merkel cell carcinoma: a historic misnomer

open access: yesMolecular Oncology, EarlyView.
This study indicates that Merkel cell carcinoma (MCC) does not originate from Merkel cells, and identifies gene, protein & cellular expression of immune‐linked and neuroendocrine markers in primary and metastatic Merkel cell carcinoma (MCC) tumor samples, linked to Merkel cell polyomavirus (MCPyV) status, with enrichment of B‐cell and other immune cell
Richie Jeremian   +10 more
wiley   +1 more source

Adaptaquin is selectively toxic to glioma stem cells through disruption of iron and cholesterol metabolism

open access: yesMolecular Oncology, EarlyView.
Adaptaquin selectively kills glioma stem cells while sparing differentiated brain cells. Transcriptomic and proteomic analyses show Adaptaquin disrupts iron and cholesterol homeostasis, with iron chelation amplifying cytotoxicity via cholesterol depletion, mitochondrial dysfunction, and elevated reactive oxygen species.
Adrien M. Vaquié   +16 more
wiley   +1 more source

Patient‐specific pharmacogenomics demonstrates xCT as predictive therapeutic target in colon cancer with possible implications in tumor connectivity

open access: yesMolecular Oncology, EarlyView.
This study integrates transcriptomic profiling of matched tumor and healthy tissues from 32 colorectal cancer patients with functional validation in patient‐derived organoids, revealing dysregulated metabolic programs driven by overexpressed xCT (SLC7A11) and SLC3A2, identifying an oncogenic cystine/glutamate transporter signature linked to ...
Marco Strecker   +16 more
wiley   +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

Multibody-Based Input and State Observers Using Adaptive Extended Kalman Filter

open access: yesSensors, 2021
The aim of this work is to explore the suitability of adaptive methods for state estimators based on multibody dynamics, which present severe non-linearities.
Antonio J. Rodríguez   +3 more
doaj   +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

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

An Integrated Adaptive Kalman Filter for High-Speed UAVs

open access: yesApplied Sciences, 2019
In order to solve the problems of filtering divergence and low accuracy in Kalman filter (KF) applications in a high-speed unmanned aerial vehicle (UAV), this paper proposed a new method of integrated robust adaptive Kalman filter: strong adaptive Kalman
Tiantian Huang   +4 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

Home - About - Disclaimer - Privacy