Results 131 to 140 of about 7,761,768 (249)

Extracellular vesicle lipidomics liquid biopsy reveals systemic and tumor microenvironment metabolic reprogramming in ovarian cancer

Molecular Oncology, EarlyView.
Extracellular vesicle (EV) lipidomic profiling of plasma and ascites from patients with high‐grade serous ovarian cancer and of ovarian cancer cell lines reveals enrichment of triglycerides (TGs), diacylglycerols (DGs), phosphatidylcholine (PCs), sphingomyelins (SMs), reflecting tumor metabolic reprogramming.
Shikha Rani, Dominic Guanzon, Andrew Lai, Katherin Scholz‐Romero, Sarah Reed, Edita Ritmejeryte, Rohan Lourie, Naven Chetty, Kaltin Ferguson, Carlos Salomon   +9 more
wiley   +1 more source

Population-Based Assessment of Phenoconversion Potential in Switzerland: A Claims Data Study of Key Drug-Metabolizing Enzymes and Transporters

Pharmacogenomics and Personalized Medicine
Marietta M Roth,1,2,* Aline Bencastro,1,2,* Christoph R Meier,1,2 Carola A Huber,3 Henriette E Meyer zu Schwabedissen,4 Samuel S Allemann,5,* Cornelia Schneider1,2,* 1Basel Pharmacoepidemiology Unit, Division of Clinical ...
Roth MM, Bencastro A, Meier CR, Huber CA, Meyer zu Schwabedissen HE, Allemann SS, Schneider C   +6 more
doaj  

A role for eIF5A in translational control of stress‐inducible proteins in multiple myeloma cell lines

Molecular Oncology, EarlyView.
Loss of eIF5A rewires thapsigargin‐mediated endoplasmic reticulum stress responses in multiple myeloma cells by selective translation of mRNA transcripts, consequently dampening thapsigargin‐induced unfolded protein response (UPR) activation and shifting the balance from induction of apoptosis toward cell survival and proliferation.
Demi Both, Ingrid A. M. Derks, Raphaël Vanleyssem, Marine Leclercq, Najla El Hachem, Pierre Close, Eric Eldering, Marco Vincent Haselager   +7 more
wiley   +1 more source

Regulation of the lncRNA NEAT1 by p53‐ΔNp63 crosstalk modulates the DNA damage response and therapeutic efficacy in HNSCC

Molecular Oncology, EarlyView.
In head and neck squamous cell carcinoma (HNSCC) p53 and p63 exert opposite roles on the transcription regulation of the lncRNA NEAT1. Under basal conditions, p53 levels are low and p63 represses NEAT1 expression. Upon genotoxic stress, p53 is rapidly induced, displacing p63 from the NEAT1 promoter leading to NEAT1 transcriptional activation and ...
Sara De Domenico, Veronica La Banca, Silvia D'Amico, Stefano Scalera, Sara Nicolai, Angelo Peschiaroli   +5 more
wiley   +1 more source

SPHINX31 acts as a SRPK1 inhibitor targeting the ATR/DNA‐PKcs/CHK1 replicative checkpoint to inhibit cell growth in non‐small cell lung cancer

Molecular Oncology, EarlyView.
The kinase SRPK1 directly interacts with the protein TOPBP1 and regulates the pre‐mRNA splicing of WIZ thereby contributing to the activation of the ATR/CHK1 replicative checkpoint in response to replicative stress. This allows cancer cells' genomic stability and survival.
Amani Shreim, Aurelie Genoux, Nadiia Zubchuk, Haoyang Zheng, Perla Salameh, Theo Ziegelmeyer, Fabien Dalonneau, Margot Rouchette, Christiane Oddou, Simona Miron, Helene Polveche, Adiilah Mamode Cassim, Carmen Garrido, Eleni Nikolakaki, Didier Auboeuf, Tao Jia, Sophie Zinn‐Justin, Beatrice Eymin   +17 more
wiley   +1 more source

CASynergy: A causal attention model for interpretable prediction of cancer drug synergy.

PLoS Computational Biology
Cancer drug combination therapies offer a promising strategy to overcome resistance and improve treatment efficacy, but identifying synergistic drug pairs is challenging due to complex biological interactions and tumor heterogeneity.
Haitao Li, Long Zheng, Lei Li, Yiwei Chen, Junjie Li, Chunhou Zheng, Yansen Su   +6 more
doaj   +1 more source

Mutant p53R273H disrupts PDPK1 homodimerization and contributes to PDPK1 activation

Molecular Oncology, EarlyView.
How mutant p53R273H drives AKT signaling is unclear. We show that p53R273H, but not wild‐type, directly binds PDPK1 via a mutation‐dependent conformational change. This interaction disrupts inhibitory PDPK1 homodimerization and enhances AKT phosphorylation.
Mei Chee Lim, Alvin Kunyao Guo, Yoko Itahana, Srinivasaraghavan Kannan, Valerie Goh, Mingmin Ong, Terina Yan Wen Tay, Weiying Ye, Sabhashina Radha Krishnan, Jun Nishiyama, Chandra S Verma, Koji Itahana   +11 more
wiley   +1 more source

Drug-drug interactions : from knowledge base to clinical impact

, 2014
Drug usage has increased steadily, and the more drugs used, the higher the risk for adverse effects or loss of effect due to drug-drug interactions. For drug prescribers it is difficult to know what drugs a patient is taking and whether they interact ...
Marine Andersson (18690100)
core   +1 more source

Carriage of CYP2C19 gene alleles and possible drug-drug interactions in patients with coronary artery disease

Рациональная фармакотерапия в кардиологии
Aim. To analyse the frequencies of the CYP2C19 gene alleles and genotypes associated with the metabolism of antiplatelet agents in patients with coronary artery disease (CAD), considering potential drug-drug interactions in real clinical practice in ...
N. A. Vorobyeva, D. D. Komissarova, A. S. Vorontsova, P. A. Vetoshkina   +3 more
doaj   +1 more source

Targeting the EpCAM‐AXL axis to overcome drug resistance in lung cancer

Molecular Oncology, EarlyView.
Lung cancer cells often evade therapy by hijacking signaling pathways. We reveal that cleaved EpCAM (sEpCAM) stabilizes the oncogenic protein AXL, driving NF‐κB and STAT3‐mediated chemoresistance. This EpCAM‐AXL axis identifies a high‐risk patient subset with poor prognosis.
Alexa Guerrero‐Alba, Mark Shacker, Timothy P. Fleming, Michael A. Smith, Ross M. Bremner, Narendra V. Sankpal   +5 more
wiley   +1 more source