Results 61 to 70 of about 245,950 (239)

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

YAP1::TFE3 mediates endothelial‐to‐mesenchymal plasticity in epithelioid hemangioendothelioma

open access: yesMolecular Oncology, EarlyView.
The YAP1::TFE3 fusion protein drives endothelial‐to‐mesenchymal transition (EndMT) plasticity, resulting in the loss of endothelial characteristics and gain of mesenchymal‐like properties, including resistance to anoikis, increased migratory capacity, and loss of contact growth inhibition in endothelial cells.
Ant Murphy   +9 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

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

Nitrogen Organic Compounds: Emergent Chemicals in Landfill Leachate

open access: yesChemical Engineering Transactions, 2010
preview not available - see full-text PDF article.
E. Lovatel   +2 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

Liquid biopsy epigenetics: establishing a molecular profile based on cell‐free DNA

open access: yesMolecular Oncology, EarlyView.
Cell‐free DNA (cfDNA) fragments in plasma from cancer patients carry epigenetic signatures reflecting their cells of origin. These epigenetic features include DNA methylation, nucleosome modifications, and variations in fragmentation. This review describes the biological properties of each feature and explores optimal strategies for harnessing cfDNA ...
Christoffer Trier Maansson   +2 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

Serum levels of organochlorine pesticides and polychlorinated biphenyls among inhabitants of Greater Metropolitan Rio de Janeiro, Brazil

open access: yesCadernos de Saúde Pública
Levels of persistent organochlorine pesticides (OCPs) and polychlorinated biphenyls (PCBs) were determined in the blood serum of people living and working in the urban area of greater Rio de Janeiro city.
Isabella Fernandes Delgado   +5 more
doaj  

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