Results 61 to 70 of about 1,215,916 (294)

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

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

Sensitization of Tumors for Attack by Virus-Specific CD8+ T-Cells Through Antibody-Mediated Delivery of Immunogenic T-Cell Epitopes

Frontiers in Immunology, 2019
Anti-tumor immunity is limited by a number of factors including the lack of fully activated T-cells, insufficient antigenic stimulation and the immune-suppressive tumor microenvironment.
Julian P. Sefrin, Lars Hillringhaus, Olaf Mundigl, Karin Mann, Doris Ziegler-Landesberger, Heike Seul, Gloria Tabares, Dominic Knoblauch, Andreas Leinenbach, Irene Friligou, Sebastian Dziadek, Rienk Offringa, Rienk Offringa, Valeria Lifke, Alexander Lifke   +14 more
doaj   +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

Predictors of response and rational combinations for the novel MCL‐1 inhibitor MIK665 in acute myeloid leukemia

Molecular Oncology, EarlyView.
This study characterizes the responses of primary acute myeloid leukemia (AML) patient samples to the MCL‐1 inhibitor MIK665. The results revealed that monocytic differentiation is associated with MIK665 sensitivity. Conversely, elevated ABCB1 expression is a potential biomarker of resistance to the treatment, which can be overcome by the combination ...
Joseph Saad, Rhiannon Newman, Elmira Khabusheva, Sofia Aakko, Eric Durand, Mahesh Tambe, Heikki Kuusanmäki, Alun Parsons, Juho J. Miettinen, Komal Kumar Javarappa, Ezgi June Olgac, Nemo Ikonen, Mika Kontro, Kimmo Porkka, Heiko Maacke, Janghee Woo, Ensar Halilovic, Caroline A. Heckman   +17 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

The neural crest‐associated gene ERRFI1 is involved in melanoma progression and resistance toward targeted therapy

Molecular Oncology, EarlyView.
ERRFI1, a neural crest (NC)‐associated gene, was upregulated in melanoma and negatively correlated with the expression of melanocytic differentiation markers and the susceptibility of melanoma cells toward BRAF inhibitors (BRAFi). Knocking down ERRFI1 significantly increased the sensitivity of melanoma cells to BRAFi.
Nina Wang, Qian Sun, Daniel Novak, Lei Zhu, Juliane Poelchen, Tamara Steinfass, Yiman Wang, Viktor Umansky, Jochen Utikal   +8 more
wiley   +1 more source

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

Editorial: New hypervalent iodine reagents for oxidative coupling—volume II

Frontiers in Chemistry, 2022
Toshifumi Dohi, Jian-Wei Han, Ravi Kumar
doaj   +1 more source