Results 211 to 220 of about 19,516,845 (337)

p190A/ARHGAP35 and p190B/ARHGAP5 proteins in endometrial cancer: a novel cancer‐relevant paralog interplay

Molecular Oncology, EarlyView.
This study identifies ARHGAP5, in addition to the frequently mutated ARHGAP35, as significantly mutated in endometrial cancer. Mutations in both genes co‐occur and are associated with their correlated downregulation. Functional CRISPR studies show that both paralogs regulate similar pathways, including actin cytoskeleton organization.
Mathilde Pinault, Capucine Heraud, Mélissa Correia de Oliveira, Véronique Neaud, Valérie Valesco, Valérie Prouzet‐Mauleon, Béatrice Turcq, Jean‐William Dupuy, Anne‐Aurélie Raymond, Sabrina Croce, Frédéric Saltel, Valérie Lagrée, Violaine Moreau   +12 more
wiley   +1 more source

<i>StrokeTime</i>: A comprehensive longitudinal scRNA-seq atlas of the ischemic mouse brain. [PDF]

iScience
Anrather J, Garcia-Bonilla L.
europepmc   +1 more source

Letter to George, from Gene, Burnett, Wisconsin, January 26, 1862

An item in the George Woodard and Gene Smith letters ...
Woodard, George T., -1864, Smith, Gene E.   +1 more
core  

Bridging the gap: a genetically validated avian chorioallantoic membrane platform for investigation of spontaneous circulating tumor cells

Molecular Oncology, EarlyView.
We established the avian chorioallantoic membrane (CAM) assay as a scalable in vivo model for studying circulating tumor cells (CTCs). Human gastrointestinal tumors spontaneously released genetically validated CTCs that were detected across multiple platforms, demonstrating that the CAM model provides an accessible tool for investigating early cancer ...
Dennis Roth, Rui P. L. Neves, Julia Geheb, Christian Ballmeyer, Nathalie Gaßmann, Kiki C. Andree, Monica Sudarsanam, Christiane Driemel, Celine Örencik, Andrè Franken, Eslam Elmaghraby, Sven H. Loosen, Roderburg Christoph, Sebastian Schoelch, Hans Neubauer, Wolfram T. Knoefel, Nikolas H. Stoecklein, Georg Fluegen   +17 more
wiley   +1 more source

Recovering CDR3 sequences from RNA-seq data: a critical assessment of computational and experimental strategies. [PDF]

Genomics Inform
AmeliMojarad M, AmeliMojarad M.
europepmc   +1 more source

Extracellular matrix remodeling and immune reprogramming drive residual tumor progression of liver cancer after incomplete microwave ablation

Molecular Oncology, EarlyView.
Incomplete microwave ablation (iMWA) of liver cancer triggers a biphasic progression in residual tumors. At Day 3, the microenvironment is characterized by acute inflammatory responses and extracellular matrix (ECM) remodeling. By Day 14, a profound shift occurs toward oncogenic signal transduction and immunosuppression, marked by macrophage ...
Yu Liu, Yubei He, Nikolaus Berndt, Michael Mülleder, Kathrin Textoris‐Taube, Jing Guo, Matthias Stechele, Justus Ramtke, Shraga Nahum Goldberg, Lynn Jeanette Savic   +9 more
wiley   +1 more source

Microcapillary-assisted acoustoelectric platform for selective single-cell isolation and in situ transfection. [PDF]

Microsyst Nanoeng
Xu X, Zhou Z, Li G, Liang J, Wu J, Lu J, Shen F, Wu S, Ruan Z, Dong S, Luo J, Cao Z.   +11 more
europepmc   +1 more source

Unique circulating miRNAome signatures captured with distinct molecular states in Lynch syndrome and sporadic colorectal cancer

Molecular Oncology, EarlyView.
Circulating microRNA profiles distinguish nonmalignant Lynch syndrome from cancer‐associated Lynch syndrome, sporadic colorectal cancer, and healthy controls. Age‐stratified analysis reveals disease‐specific regulatory states, and a six‐miRNA panel shows concordant separation in an independent colorectal tissue cohort.
Ramadhani Salum Chambuso, Md Shohel Ul Islam, Rosa M Xicola, Raj Ramesar, Xavier Llor, Sinclair Steele   +5 more
wiley   +1 more source

The Distribution of Gene Frequencies in Populations of Polyploids [PDF]

Proceedings of the National Academy of Sciences, 1938
openaire   +2 more sources

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