Results 151 to 160 of about 1,305,585 (286)

PYCR1 inhibition in bone marrow stromal cells enhances bortezomib sensitivity in multiple myeloma cells by altering their metabolism

Molecular Oncology, EarlyView.
This study investigated how PYCR1 inhibition in bone marrow stromal cells (BMSCs) indirectly affects multiple myeloma (MM) cell metabolism and viability. Culturing MM cells in conditioned medium from PYCR1‐silenced BMSCs impaired oxidative phosphorylation and increased sensitivity to bortezomib.
Inge Oudaert, Lauren van den Broecke, Osman Aksoy, Judith Lind, Sonia Vallet, Arne Van der Vreken, Gamze Ates, Ann Massie, Ken Maes, Kim De Veirman, Elke De Bruyne, Karin Vanderkerken, Klaus Podar, Eline Menu   +13 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

Inhibition of CDK9 enhances AML cell death induced by combined venetoclax and azacitidine

Molecular Oncology, EarlyView.
The CDK9 inhibitor AZD4573 downregulates c‐MYC and MCL‐1 to induce death of cytarabine (AraC)‐resistant AML cells. This enhances VEN + AZA‐induced cell death significantly more than any combination of two of the three drugs in AraC‐resistant AML cells.
Shuangshuang Wu, Jianlei Zhao, Aaban Asfar Azmi, Avanti Gupte, Jenna Thibodeau, Shuang Liu, Jinli Yang, Guan Wang, Holly Edwards, Lisa A. Polin, Juiwanna Kushner, Sijana H. Dzinic, Kathryn White, Julie Boerner, Maik Hüttemann, Jay Yang, Yue Wang, Jeffrey W. Taub, Yubin Ge   +18 more
wiley   +1 more source

Insulin reduces endoplasmic reticulum stress‐induced apoptosis by decreasing mitochondrial hyperpolarization and caspase‐12 in INS‐1 pancreatic β‐cells

Physiological Reports
Pancreatic β‐cell mass is a critical determinant of insulin secretion. Severe endoplasmic reticulum (ER) stress causes β‐cell apoptosis; however, the mechanisms of progression and suppression are not yet fully understood.
Nanako Murata, Kana Nishimura, Naoki Harada, Tomoya Kitakaze, Eiji Yoshihara, Hiroshi Inui, Ryoichi Yamaji   +6 more
doaj   +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

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

Reduced vascular leakage correlates with breast carcinoma T regulatory cell infiltration but not with metastatic propensity

Molecular Oncology, EarlyView.
A mouse model for vascular normalization and a human breast cancer cohort were studied to understand the relationship between vascular leakage and tumor immune suppression. For this, endothelial and immune cell RNAseq, staining for vascular function, and immune cell profiling were employed.
Liqun He, Chiara Testini, Neda Hekmati, Altea Bonello, Aglaia Schiza, Emmanuel Nwadozi, Mia Phillipson, Carina Strell, Michael Welsh   +8 more
wiley   +1 more source

Improving PARP inhibitor efficacy in bladder cancer without genetic BRCAness by combination with PLX51107

Molecular Oncology, EarlyView.
Clinical trials on PARP inhibitors in urothelial carcinoma (UC) showed limited efficacy and a lack of predictive biomarkers. We propose SLFN5, SLFN11, and OAS1 as UC‐specific response predictors. We suggest Talazoparib as the better PARP inhibitor for UC than Olaparib.
Jutta Schmitz, Anna L. Bartkowiak, Michael Rose, Nora Kolks, Patrick Petzsch, Vandana Solanki, Anne Stoffel, Bianca Faßbender, Leandra Lepping, Julka Volkamer, Karl Köhrer, Marc Seifert, Tokameh Mahmoudi, Tahlita C. M. Zuiverloon, Günter Niegisch, Michèle J. Hoffmann   +15 more
wiley   +1 more source

Class IIa HDACs forced degradation allows resensitization of oxaliplatin‐resistant FBXW7‐mutated colorectal cancer

Molecular Oncology, EarlyView.
HDAC4 is degraded by the E3 ligase FBXW7. In colorectal cancer, FBXW7 mutations prevent HDAC4 degradation, leading to oxaliplatin resistance. Forced degradation of HDAC4 using a PROTAC compound restores drug sensitivity by resetting the super‐enhancer landscape, reprogramming the epigenetic state of FBXW7‐mutated cells to resemble oxaliplatin ...
Vanessa Tolotto, Nicolò Gualandi, Ylenia Cortolezzis, Raffaella Picco, Monica Colitti, Francesca D'Este, Mariachiara Gani, Wayne W. Hancock, Giovanni Terrosu, Cristina Degrassi, Francesca Agostini, Claudio Brancolini, Luigi E. Xodo, Eros Di Giorgio   +13 more
wiley   +1 more source