Results 41 to 50 of about 149 (149)

Plasma lipidomic and metabolomic profiles in high‐grade glioma patients before and after 72‐h presurgery water‐only fasting

Molecular Oncology, EarlyView.
Presurgery 72‐h fasting in GB patients leads to adaptations of plasma lipids and polar metabolites. Fasting reduces lysophosphatidylcholines and increases free fatty acids, shifts triglycerides toward long‐chain TGs and increases branched‐chain amino acids, alpha aminobutyric acid, and uric acid.
Iris Divé, Lisa Hahnefeld, Katharina J. Wenger, Donat Kögel, Joachim Steinbach, Gerd Geisslinger, Michael W. Ronellenfitsch, Irmgard Tegeder   +7 more
wiley   +1 more source

The atypical KRASQ22K mutation directs TGF‐β response towards partial epithelial‐to‐mesenchymal transition in patient‐derived colorectal cancer tumoroids

Molecular Oncology, EarlyView.
TGF‐β has a complex role in cancer, exhibiting both tumor‐suppressive and tumor‐promoting properties. Using a series of differentiated tumoroids, derived from different stages and mutational background of colorectal cancer patients, we replicate this duality of TGF‐β in vitro. Notably, the atypical but highly aggressive KRASQ22K mutation rendered early‐
Theresia Mair, Philip König, Milena Mijović, Jessica Kalla, Anil Baskan, Loan Tran, Kristina Draganić, Pedro Morata Saldaña, Carlos Uziel Pérez Malla, Janette Pfneissl, Andreas Tiefenbacher, Julijan Kabiljo, Velina S. Atanasova, Lisa Wozelka‐Oltjan, Leonhard Müllauer, Michael Bergmann, Raheleh Sheibani‐Tezerji, Gerda Egger   +17 more
wiley   +1 more source

Central tolerance: Essential for preventing autoimmune disease? [PDF]

European Journal of Immunology, 2009
AbstractRecessive central tolerance of developing T cells is caused by antigen‐induced deletion of immature cortical double positive and medullary single positive thymocytes in the absence of TCR editing. There are few examples where it can be convincingly shown that recessive tolerance plays an essential role in preventing autoimmune disease.
openaire   +3 more sources

Multidimensional OMICs reveal ARID1A orchestrated control of DNA damage, splicing, and cell cycle in normal‐like and malignant urothelial cells

Molecular Oncology, EarlyView.
Loss of the frequently mutated chromatin remodeler ARID1A, a subunit of the SWI/SNF cBAF complex, results in less open chromatin, alternative splicing, and the failure to stop cells from progressing through the cell cycle after DNA damage in bladder (cancer) cells. Created in BioRender. Epigenetic regulators, such as the SWI/SNF complex, with important
Rebecca M. Schlösser, Florian Krumbach, Eyleen Corrales, Geoffroy Andrieux, Christian Preisinger, Franziska Liss, Alexandra Golzmann, Melanie Boerries, Kerstin Becker, Ruth Knüchel, Stefan Garczyk, Bernhard Lüscher   +11 more
wiley   +1 more source

Escape from TGF‐β‐induced senescence promotes aggressive hallmarks in epithelial hepatocellular carcinoma cells

Molecular Oncology, EarlyView.
Chronic TGF‐β exposure drives epithelial HCC cells from a senescent state to a TGF‐β resistant mesenchymal phenotype. This transition is characterized by the loss of Smad3‐mediated signaling, escape from senescence, enhanced invasiveness and metastatic potential, and upregulation of key resistance modulators such as MARK1 and GRM8, ultimately promoting
Minenur Kalyoncu, Dilara Demirci, Sude Eris, Bengisu Dayanc, Ece Cakiroglu, Merve Basol, Merve Uysal, Gulcin Cakan‐Akdogan, Fang Liu, Mehmet Ozturk, Gökhan Karakülah, Serif Senturk   +11 more
wiley   +1 more source

ShcD adaptor protein drives invasion of triple negative breast cancer cells by aberrant activation of EGFR signaling

Molecular Oncology, EarlyView.
We identified adaptor protein ShcD as upregulated in triple‐negative breast cancer and found its expression to be correlated with reduced patient survival and increased invasion in cell models. Using a proteomic screen, we identified novel ShcD binding partners involved in EGFR signaling pathways.
Hayley R. Lau, Hayley S. Smith, Begüm Alural, Claire E. Martin, Laura A. New, Manali Tilak, Sara L. Banerjee, Hannah N. Robeson, Nicolas Bisson, Anne‐Claude Gingras, Jasmin Lalonde, Nina Jones   +11 more
wiley   +1 more source

Chemoresistome mapping in individual breast cancer patients unravels diversity in dynamic transcriptional adaptation

Molecular Oncology, EarlyView.
This study used longitudinal transcriptomics and gene‐pattern classification to uncover patient‐specific mechanisms of chemotherapy resistance in breast cancer. Findings reveal preexisting drug‐tolerant states in primary tumors and diverse gene rewiring patterns across patients, converging on a few dysregulated functional modules. Despite receiving the
Maya Dadiani, Gilgi Friedlander, Gili Perry, Nora Balint‐Lahat, Shlomit Gilad, Dana Morzaev‐Sulzbach, Anjana Shenoy, Noa Bossel Ben‐Moshe, Anya Pavlovsky, Rinat Bernstein‐Molho, Eytan Domany, Iris Barshack, Tamar Geiger, Bella Kaufman, Einav Nili Gal‐Yam   +14 more
wiley   +1 more source

Determination of ADP/ATP translocase isoform ratios in malignancy and cellular senescence

Molecular Oncology, EarlyView.
The individual functions of three isoforms exchanging ADP and ATP (ADP/ATP translocases; ANTs) on the mitochondrial membrane remain unclear. We developed a method for quantitatively differentiating highly similar human ANT1, ANT2, and ANT3 using parallel reaction monitoring. This method allowed us to assess changes in translocase levels during cellular
Zuzana Liblova, Dominika Maurencova, Barbora Salovska, Marek Kratky, Tomas Mracek, Zuzana Korandova, Alena Pecinova, Pavla Vasicova, David Rysanek, Ladislav Andera, Ivo Fabrik, Rudolf Kupcik, Pavel Kashmel, Pinky Sultana, Vojtech Tambor, Jiri Bartek, Josef Novak, Marie Vajrychova, Zdenek Hodny   +18 more
wiley   +1 more source

Central and peripheral autoantigen presentation in immune tolerance [PDF]

Immunology, 2004
SummaryRecent studies in both humans and experimental rodent models provide new insight into key mechanisms regulating tolerance to self‐molecules. These recent advances are bringing about a paradigm shift in our views about tolerance to self‐molecules with tissue‐restricted expression.
openaire   +3 more sources

Loss of proton‐sensing GPR4 reduces tumor progression in mouse models of colon cancer

Molecular Oncology, EarlyView.
G protein‐coupled receptor 4 (GPR4) is a pH‐sensing receptor activated by acidic pH. GPR4 expression is increased in patients with inflammatory bowel disease who are at high risk of developing colorectal cancer. In mouse models, loss of GPR4 attenuated tumor progression. This correlated with increased IL2 and natural killer cell activity.
Leonie Perren, Moana Busch, Pedro A. Ruiz, Ermanno Malagola, Valeria Baumeler, Federica Foti, Adelina Gross, Tobias Grütter, Hendrik Edel, Cordelia Schuler, Kristina Handler, Glenn De Lange, Isabelle C. Arnold, Cheryl de Vallière, Klaus Seuwen, Martin Hausmann, Gerhard Rogler   +16 more
wiley   +1 more source