Results 101 to 110 of about 5,188,056 (277)

PARP inhibitors elicit distinct transcriptional programs in homologous recombination competent castration‐resistant prostate cancer

Molecular Oncology, EarlyView.
PARP inhibitors are used to treat a small subset of prostate cancer patients. These studies reveal that PARP1 activity and expression are different between European American and African American prostate cancer tissue samples. Additionally, different PARP inhibitors cause unique and overlapping transcriptional changes, notably, p53 pathway upregulation.
Moriah L. Cunningham, Jasibel Vasquez‐Gonzalez, Samantha M. Barnada, Salome Tchotorlishvili, Latese Jones, Ryan Maguire, Genevieve Lewis, Kinza Rizwan, Jenny Deng, Salma Koachar, Drithi Patel, Hailey Shankle, Tessa Mulders, Namra Ajmal, Charalambos Solomides, Emad S. Alnemri, Teresa F. Alnemri, Ayesha A. Shafi, Leonard G. Gomella, Wm Kevin Kelly, Steven B. McMahon, Matthew J. Schiewer   +21 more
wiley   +1 more source

Investigating the cell of origin and novel molecular targets in Merkel cell carcinoma: a historic misnomer

Molecular Oncology, EarlyView.
This study indicates that Merkel cell carcinoma (MCC) does not originate from Merkel cells, and identifies gene, protein & cellular expression of immune‐linked and neuroendocrine markers in primary and metastatic Merkel cell carcinoma (MCC) tumor samples, linked to Merkel cell polyomavirus (MCPyV) status, with enrichment of B‐cell and other immune cell
Richie Jeremian, Sriraam Sivachandran, Melissa Galati, Brandon Ramchatesingh, Hibo Rijal, Johnny Hanna, Elena Netchiporouk, May Chergui, Margaret Redpath, Samy Abou Setah, Ivan V. Litvinov   +10 more
wiley   +1 more source

Emerging role of ARHGAP29 in melanoma cell phenotype switching

Molecular Oncology, EarlyView.
This study gives first insights into the role of ARHGAP29 in malignant melanoma. ARHGAP29 was revealed to be connected to tumor cell plasticity, promoting a mesenchymal‐like, invasive phenotype and driving tumor progression. Further, it modulates cell spreading by influencing RhoA/ROCK signaling and affects SMAD2 activity. Rho GTPase‐activating protein
Beatrice Charlotte Tröster, Melanie Kappelmann‐Fenzl, Anja Katrin Bosserhoff, Nicole Rachinger   +3 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

Design and development of the quad redundant servoactuator for the space shuttle solid rocket booster thrust vector control [PDF]

, 1980
The design and theory of operation of the servoactuator used for thrust vector control of the space shuttle solid rocket booster is described accompanied by highlights from the development and qualification test programs.
Lominick, J. M.
core   +1 more source

A synthetic benzoxazine dimer derivative targets c‐Myc to inhibit colorectal cancer progression

Molecular Oncology, EarlyView.
Benzoxazine dimer derivatives bind to the bHLH‐LZ region of c‐Myc, disrupting c‐Myc/MAX complexes, which are evaluated from SAR analysis. This increases ubiquitination and reduces cellular c‐Myc. Impairing DNA repair mechanisms is shown through proteomic analysis.
Nicharat Sriratanasak, Bodee Nutho, Worawat Wattanathana, Narumon Phaonakrop, Bunnatut Panasawatwong, Katharina Erlenbach‐Wuensch, Sittiruk Roytrakul, Regine Schneider‐Stock, Pithi Chanvorachote   +8 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

Test of classical nucleation theory on deeply supercooled high-pressure simulated silica

, 2006
We test classical nucleation theory (CNT) in the case of simulations of deeply supercooled, high density liquid silica, as modelled by the BKS potential.
Becker R., Debenedetti P. G., Farkas L., Gibbs J. W., Ivan Saika-Voivod, Peter H. Poole, Richard K. Bowles, Volmer M.   +7 more
core   +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

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