Results 121 to 130 of about 1,216,010 (296)

Widening the spectrum of players affected by genetic changes in Wilms tumor relapse

iScience
Summary: Few studies investigated the genetics of relapsed Wilms tumor (WT), suggesting the SIX1 gene, the microRNA processing genes, and the MYCN network as possibly involved in a relevant percentage of relapses. We investigated 28 relapsing WT patients
Sara Ciceri, Alessia Bertolotti, Annalisa Serra, Giovanna Gattuso, Luna Boschetti, Maria Capasso, Cecilia Cecchi, Stefania Sorrentino, Paola Quarello, Chiara Maura Ciniselli, Paolo Verderio, Loris De Cecco, Giacomo Manenti, Francesca Diomedi Camassei, Paola Collini, Filippo Spreafico, Daniela Perotti   +16 more
doaj   +1 more source

ABC of Clinical Genetics. Clinical genetic services. [PDF]

BMJ, 1989
openaire   +2 more sources

Exploiting metabolic adaptations to overcome dabrafenib treatment resistance in melanoma cells

Molecular Oncology, EarlyView.
We show that dabrafenib‐resistant melanoma cells undergo mitochondrial remodeling, leading to elevated respiration and ROS production balanced by stronger antioxidant defenses. This altered redox state promotes survival despite mitochondrial damage but renders resistant cells highly vulnerable to ROS‐inducing compounds such as PEITC, highlighting redox
Silvia Eller, Susanne Ebner, Carmen Haselrieder, Julia K. Günther, Astrid Drasche, Sophie Strich, Chiara Volani, Andrea Medici, Aleksandar Nikolajevic, Alex Deltedesco, Johannes E. Sigmund, Michael J. Blumer, Martin Hermann, Johanna Vanacker, Gerald Brandacher, Eduard Stefan, Omar Torres‐Quesada, Jakob Troppmair   +17 more
wiley   +1 more source

Whither social media and clinical genetics? [PDF]

Am J Med Genet A, 2023
Gunter C, Solomon BD.
europepmc   +1 more source

Cell surface interactome analysis identifies TSPAN4 as a negative regulator of PD‐L1 in melanoma

Molecular Oncology, EarlyView.
Using cell surface proximity biotinylation, we identified tetraspanin TSPAN4 within the PD‐L1 interactome of melanoma cells. TSPAN4 negatively regulates PD‐L1 expression and lateral mobility by limiting its interaction with CMTM6 and promoting PD‐L1 degradation.
Guus A. Franken, Andrea Abel Gutierrez, Imke van Rossum, Cornelia G. Spruijt, Michiel Vermeulen, Guido van Mierlo, Blanca Scheijen, Annemiek B. van Spriel   +7 more
wiley   +1 more source

Association studies of up to 1.2 million individuals yield new insights into the genetic etiology of tobacco and alcohol use. [PDF]

, 2019
Tobacco and alcohol use are leading causes of mortality that influence risk for many complex diseases and disorders1. They are heritable2,3 and etiologically related4,5 behaviors that have been resistant to gene discovery efforts6-11.
23andMe Research Team, Bjornsdottir, Gyda, Boardman, Jason D, Boehnke, Michael, Boomsma, Dorret I, Brazel, David M, Chen, Chu, Chen, Fang, Choquet, Hélène, Cucca, Francesco, Datta, Gargi, Davies, Gareth E, Davila-Velderrain, Jose, Docherty, Anna R, Eaton, Charles B, Ehringer, Marissa A, Esko, Tõnu, Faul, Jessica D, Fiorillo, Edoardo, Foerster, Johanna R, Fritsche, Lars G, Gabrielsen, Maiken Elvestad, Gillespie, Nathan A, Gordon, Scott D, Gudbjartsson, Daniel F, Haessler, Jeffrey, Haller, Toomas, Harris, Kathleen Mullan, Heath, Andrew C, Hewitt, John K, Hickie, Ian B, Hokanson, John E, Hopfer, Christian J, Hottenga, Jouke-Jan, Huang, Hongyan, HUNT All-In Psychiatry, Hunter, David J, Iacono, William G, Jang, Seon-Kyeong, Jansen, Philip R, Jiang, Yu, Johnson, Eric O, Kamatani, Yoichiro, Kardia, Sharon LR, Keller, Matthew C, Kellis, Manolis, Kooperberg, Charles, Kraft, Peter, Krauter, Kenneth S, Laakso, Markku, Li, Yue, Lind, Penelope A, Ling, Yueh, Liu, Mengzhen, Loukola, Anu, Lutz, Sharon M, Madden, Pamela AF, Martin, Nicholas G, Matoba, Nana, McGue, Matt, McGuire, Daniel, McMahon, George, McQueen, Matthew B, Medland, Sarah E, Metspalu, Andres, Mohlke, Karen L, Mulas, Antonella, Mägi, Reedik, Nielsen, Jonas B, Okada, Yukinori, Orrù, Valeria, Palviainen, Teemu, Pandit, Anita, Peters, Ulrike, Polderman, Tinca JC, Posthuma, Danielle, Reginsson, Gunnar W, Reiner, Alexander P, Rice, John P, Rimm, Eric, Rose, Richard J, Runarsdottir, Valgerdur, Skogholt, Anne Heidi, Smith, Jennifer A, Stallings, Michael C, Stančáková, Alena, Stefansson, Hreinn, Taylor, Amy E, Thai, Khanh K, Tian, Chao, Tindle, Hilary A, Turman, Constance, Wedow, Robbee, Willemsen, Gonneke, Young, Hannah, Young, Kendra A, Zajac, Gregory JM, Zhan, Xiaowei, Zhao, Wei, Zhou, Wei   +99 more
core  

PARP inhibition and pharmacological ascorbate demonstrate synergy in castration‐resistant prostate cancer

Molecular Oncology, EarlyView.
Pharmacologic ascorbate (vitamin C) increases ROS, disrupts cellular metabolism, and induces DNA damage in CRPC cells. These effects sensitize tumors to PARP inhibition, producing synergistic growth suppression with olaparib in vitro and significantly delayed tumor progression in vivo. Pyruvate rescue confirms ROS‐dependent activity.
Nicolas Gordon, Peter T. Gallagher, Orly I. Richter, Neermala Poudel Neupane, Amy C. Mandigo, Jennifer J. McCann, Emanuela Dylgjeri, Irina Vasilevskaya, Christopher McNair, Channing J. Paller, Wm. Kevin Kelly, Karen E. Knudsen, Matthew J. Schiewer, Ayesha A. Shafi   +13 more
wiley   +1 more source

LDAcoop: Integrating non‐linear population dynamics into the analysis of clonogenic growth in vitro

Molecular Oncology, EarlyView.
Limiting dilution assays (LDAs) quantify clonogenic growth by seeding serial dilutions of cells and scoring wells for colony formation. The fraction of negative wells is plotted against cells seeded and analyzed using the non‐linear modeling of LDAcoop.
Nikko Brix, Daniel Samaga, Katharina Gehr, Benedek Dankó, Mohamed Schumann, Guido Drexler, Ahmed Alnatsha, Georg Beyer, Ujjwal Mahajan, Martin Selmansberger, Julia Mayerle, Claus Belka, Horst Zitzelsberger, Kirsten Lauber   +13 more
wiley   +1 more source

Blueprint for building a patient-centered hereditary cancer program based on stakeholder perspectives

Gynecologic Oncology Reports
Objectives: As the need for clinical cancer genetics services continues to rise, health systems must strategize on how best to deliver this specialized care.
Tamar Nicole Soussana, Michelle Primiano, Muhammad Danyal Ahsan, Carolyn Baron, Lauren Mitchell, Ravi N. Sharaf, Melissa K. Frey   +6 more
doaj   +1 more source

Plecstatin inhibits hepatocellular carcinoma tumorigenesis and invasion through cytolinker plectin

Molecular Oncology, EarlyView.
The ruthenium‐based metallodrug plecstatin exerts its anticancer effect in hepatocellular carcinoma (HCC) primarily through selective targeting of plectin. By disrupting plectin‐mediated cytoskeletal organization, plecstatin inhibits anchorage‐dependent growth, cell polarization, and tumor cell dissemination.
Zuzana Outla, Jan Kosla, Magdalena Prechova, Lukas Frick, Patricia Bortel, Yasmin Borutzki, Andrea Bileck, Christopher Gerner, Samuel M. Meier‐Menches, Selma Osmanagic‐Myers, Martin Gregor   +10 more
wiley   +1 more source