Results 121 to 130 of about 316,694 (219)

CD47 promotes mitogen‐activated protein kinase and epithelial‐to‐mesenchymal transition molecular programs to drive prometastatic phenotypes in non‐small cell lung cancer

Molecular Oncology, EarlyView.
Beyond its role in immune evasion, this study identified that CD47 drives tumor‐intrinsic signaling in non‐small cell lung cancer (NSCLC). Transcriptomic profiling and functional studies revealed that CD47 regulates cell adhesion, migration, and metastasis through an ERK–EMT signaling axis.
Asa P.Y. Lau, Lilian G. Zhai, Ryunosuke Hoshi, Zackary Rousseau, Abraam Zakhary, Yin Fang Wu, Rola M. Saleeb, Heyu Ni, Kelsie L. Thu   +8 more
wiley   +1 more source

KDM7A and KDM1A inhibition suppresses tumour promoting pathways in prostate cancer

Molecular Oncology, EarlyView.
Treatment resistance is a major challenge for patients with advanced prostate cancer. This study examined an alternative approach to target the major prostate cancer‐promoting pathway by targeting epigenetic factors, whose levels are higher in tumours.
Jennie N Jeyapalan, Veronika M Metzler, Simone de Brot, Corinne L Woodcock, Anna E Harris, Jennifer Lothion‐Roy, Emeli M Nilsson, Atara Ntekim, Michael S Toss, Jenny L Persson, Francesca Khani, Brian D Robinson, Lorraine J Gudas, Emad Rakha, David M Heery, Catrin S Rutland, Nigel P Mongan   +16 more
wiley   +1 more source

Heterozygous loss‐of‐function alleles associate the conserved 3′‐5′ exoribonuclease EXOSC10 with hypersensitivity to the anticancer drug 5‐fluorouracil

Molecular Oncology, EarlyView.
EXOSC10, an essential nuclear RNA exosome‐associated 3′‐5′ exoribonuclease, is inhibited by the anticancer drug 5‐fluorouracil (5‐FU), and EXOSC10 depletion increases 5‐FU sensitivity. The colon‐cancer variant EXOSC10S402T, located in a proteolysis motif, is stable and nuclear but nonfunctional in vivo.
Radhika Sain, Yann Le Page, Frédéric Percevault, Emmanuelle Becker, Luc Negroni, Almudena Fernandez, Marta Cantero, Diego Muñoz‐Santos, Lluís Montoliu, Cyrille Garnier, Michael Primig   +10 more
wiley   +1 more source

Cell‐cycle‐specific lesion evolution rather than inhibition of double‐strand‐break repair underpins cisplatin radiosensitization

Molecular Oncology, EarlyView.
We analyze cisplatin–DNA adducts (CDAs) and double‐strand breaks (DSBs) in a cell‐cycle‐dependent manner. We find that CDAs form similarly across all cell cycle phases. DSBs arise only in S‐phase. CDAs might not directly impair DSB repair, but S‐phase DSB lesions evolve in the presence of CDAs and disrupt repair in G2, also causing radiosensitization ...
Ye Qiu, Xixi Lin, Emil Mladenov, Veronika Mladenova, Jürgen Thomale, Ali Sak, Yao Wang, Yunxuan Deng, Eleni Gkika, Martin Stuschke, George Iliakis   +10 more
wiley   +1 more source

Radiation-induced esophagitis in lung cancer

Lung Cancer: Targets and Therapy, 2016
Sarah Baker, Alysa Fairchild Department of Radiation Oncology, Cross Cancer Institute, University of Alberta, Edmonton, AB, Canada Abstract: Radiation-induced esophagitis is the most common local acute toxicity of radiotherapy (RT) delivered for the
Baker S, Fairchild A
doaj  

Hijacking emergency granulopoiesis: Neutrophil ontogeny and reprogramming in cancer

Molecular Oncology, EarlyView.
Neutrophils are highly plastic innate immune cells; their functions in cancer extend beyond the tumour microenvironment. This Review summarises current understanding of neutrophil maturation and heterogeneity and highlights tumour‐induced granulopoiesis as a systemic programme that expands immature, immunosuppressive neutrophils via tumour‐derived ...
Gabriela Marinescu, Yi Feng
wiley   +1 more source

Interaction of HS1BP3 with cortactin modulates TKS5 localisation, cell secretion and cancer malignancy

Molecular Oncology, EarlyView.
Here, we demonstrate that HS1BP3 interacts with Cortactin through a proline‐rich region (PRR3.1) and show that this interaction, and HS1BP3 itself, promote cancer cell proliferation and invasion. Inhibition of this interaction leads to build‐up of TKS5 in multivesicular endosomes and altered secretion of CD63 and CD9, providing an explanation for the ...
Arja Arnesen Løchen, Kristiane Søreng, Chiara Veroni, Laura Trachsel‐Moncho, Nagham Asp, Robin Gaupset, Lars Gustav Lyckander, Helene Knævelsrud, Lars Eftang, Anne Simonsen   +9 more
wiley   +1 more source

Editorial: Novel and emerging therapies in heart failure

Frontiers in Cardiovascular Medicine, 2023
Grigorios Giamouzis, Grigorios Giamouzis, Andrew Xanthopoulos, Konstantinos Dean Boudoulas, Georgios Karagiannis, John Skoularigis, John Skoularigis, Filippos Triposkiadis, Filippos Triposkiadis   +8 more
doaj   +1 more source

Proteasome inhibitor, ixazomib prevents topoisomerase‐I degradation and reverses irinotecan resistance in colorectal cancer

Molecular Oncology, EarlyView.
Ixazomib inhibits proteasome‐mediated degradation of topoisomerase I induced by irinotecan, thereby restoring drug sensitivity and promoting tumor cell death in colorectal cancer. Irinotecan, a topoisomerase I (topoI) inhibitor, is widely used for colorectal cancer, but resistance remains a major clinical challenge.
Yuho Ebata, Koji Ando, Hirofumi Hasuda, Koshi Mimori, Elizabeth C. Unan, Siddhartha Pulukuri, Aahana Tiku, Allison Berger, Eiji Oki, Ajit Bharti, Tomoharu Yoshizumi   +10 more
wiley   +1 more source

Circulating tumor cell viability during and after radiotherapy mirrors treatment response in cancer patients

Molecular Oncology, EarlyView.
Radiotherapy (RT) response depends on the DNA repair capacity of tumor and host cells. We show that circulating tumor cell (CTC) counts and apoptosis rates before and after RT predict treatment response and outcome, which can be accessed via easily accessible liquid biopsy approaches. Created in BioRender. Wikman, H.
Yvonne Goy, Jana Löptien, Cornelia Coith, Afroditi Nanou, Katharina Hintelmann, Pinnschmidt Hans, Cordula Petersen, Klaus Pantel, Sabine Riethdorf, Kerstin Borgmann, Harriet Wikman   +10 more
wiley   +1 more source