Results 81 to 90 of about 268,026 (223)

Emerging role of ARHGAP29 in melanoma cell phenotype switching

Molecular Oncology, EarlyView.
This study gives first insights into the role of ARHGAP29 in malignant melanoma. ARHGAP29 was revealed to be connected to tumor cell plasticity, promoting a mesenchymal‐like, invasive phenotype and driving tumor progression. Further, it modulates cell spreading by influencing RhoA/ROCK signaling and affects SMAD2 activity. Rho GTPase‐activating protein
Beatrice Charlotte Tröster, Melanie Kappelmann‐Fenzl, Anja Katrin Bosserhoff, Nicole Rachinger   +3 more
wiley   +1 more source

In vitro properties of patient serum predict clinical outcome after high dose rate brachytherapy of hepatocellular carcinoma

Molecular Oncology, EarlyView.
Following high dose rate brachytherapy (HDR‐BT) for hepatocellular carcinoma (HCC), patients were classified as responders and nonresponders. Post‐therapy serum induced increased BrdU incorporation and Cyclin E expression of Huh7 and HepG2 cells in nonresponders, but decreased levels in responders.
Lukas Salvermoser, Jan Niklas Schäfer, Shraga Nahum Goldberg, Philipp Maximilian Kazmierczak, Moritz Nikolaus Gröper, Philipp Franz Linden, Elif Öcal, Tanja Burkard, Stefanie Corradini, Najib Ben Khaled, Moritz Wildgruber, Max Seidensticker, Jens Ricke, Matthias Stechele, Marianna Alunni‐Fabbroni   +14 more
wiley   +1 more source

A synthetic benzoxazine dimer derivative targets c‐Myc to inhibit colorectal cancer progression

Molecular Oncology, EarlyView.
Benzoxazine dimer derivatives bind to the bHLH‐LZ region of c‐Myc, disrupting c‐Myc/MAX complexes, which are evaluated from SAR analysis. This increases ubiquitination and reduces cellular c‐Myc. Impairing DNA repair mechanisms is shown through proteomic analysis.
Nicharat Sriratanasak, Bodee Nutho, Worawat Wattanathana, Narumon Phaonakrop, Bunnatut Panasawatwong, Katharina Erlenbach‐Wuensch, Sittiruk Roytrakul, Regine Schneider‐Stock, Pithi Chanvorachote   +8 more
wiley   +1 more source

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

Molecular 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, Davod R. Shah, Eliane E. S. Brechbühl, Michael McNicholas, Zhaoyang Xu, John H. Stockley, Laura Morcom, Diana Gold Diaz, Gemma C. Girdler, Rachel V. Seear, Gabriel Balmus, Rajiv R. Ratan, Harry Bulstrode, James A. Nathan, Manav Pathania, Kevin M. Brindle, David H. Rowitch   +16 more
wiley   +1 more source

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

Molecular 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, Keren Zohar, Martin Böttcher, Thomas Wartmann, Henry Freudenstein, Maximilian Doelling, Mihailo Andric, Wenjie Shi, Or Kakhlon, Katrin Hippe, Beatrix Jahnke, Dimitrios Mougiakakos, Franziska Baenke, Daniel Stange, Roland S. Croner, Michal Linial, Ulf D. Kahlert   +16 more
wiley   +1 more source

Aggressive prostate cancer is associated with pericyte dysfunction

Molecular 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, Ane Martinez‐Larrinaga, Joaquim Grego‐Bessa, Saioa Garcia‐Longarte, Hielke van Splunder, Ianire Astobiza, Amaia Ercilla, Laura Bozal‐Basterra, Isabel Mendizabal, Pilar Villacampa, Arkaitz Carracedo, Mariona Graupera   +11 more
wiley   +1 more source

Glycosylated LGALS3BP is highly secreted by bladder cancer cells and represents a novel urinary disease biomarker

Molecular 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, Giulio Lovato, Ilaria Cela, Arianna Mercatelli, Benedetta Ferro, Jussi Nikkola, Sara Pagotto, Tommaso Grottola, Vincenzo De Laurenzi, Rossella Cicchetti, Antonio Marchetti, Luigi Schips, Rossano Lattanzio, Stefano Iacobelli, Emily Capone, Peter Black, Mads Daugaard, Michele Marchioni, Gianluca Sala   +18 more
wiley   +1 more source

Generating Random Elements of Finite Distributive Lattices

, 1997
This survey article describes a method for choosing uniformly at random from any finite set whose objects can be viewed as constituting a distributive lattice. The method is based on ideas of the author and David Wilson for using ``coupling from the past'
Propp, James
core   +4 more sources

Survivin and Aurora Kinase A control cell fate decisions during mitosis

Molecular 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, Shalitha Wickrama Arachchige, Sally P. Wheatley   +2 more
wiley   +1 more source

CDK11 inhibition induces cytoplasmic p21WAF1 splice variant by p53 stabilisation and SF3B1 inactivation

Molecular 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, Lukasz Arcimowicz, Lucia Martinkova, Vaclav Hrabal, Filip Zavadil Kokas, Tomas Henek, Martina Kucerikova, Ondrej Bonczek, Pavlina Zatloukalova, Lenka Hernychova, Philip J. Coates, Borivoj Vojtesek, David P. Lane   +12 more
wiley   +1 more source