Results 81 to 90 of about 616,215 (256)

Cross-coupling polycondensation via C–O or C–N bond cleavage

Nature Communications, 2018
π-Conjugated polymers are useful commodities as they are used in the fabrication of organic photovoltaic devices, light-emitting diodes and field effect transistors.
Ze-Kun Yang, Ning-Xin Xu, Ryo Takita, Atsuya Muranaka, Chao Wang, Masanobu Uchiyama   +5 more
doaj   +1 more source

Network divergence analysis identifies adaptive gene modules and two orthogonal vulnerability axes in pancreatic cancer

Molecular Oncology, EarlyView.
Tumors contain diverse cellular states whose behavior is shaped by context‐dependent gene coordination. By comparing gene–gene relationships across biological contexts, we identify adaptive transcriptional modules that reorganize into distinct vulnerability axes.
Brian Nelson, Lyanne Delgado‐Coka, Natalia Marchenko, Luisa F. Escobar‐Hoyos, Kenneth R. Shroyer, Alisa Yurovsky, Trey Ideker, Gábor Balázsi, Thomas MacCarthy, Scott Powers   +9 more
wiley   +1 more source

Palladium(0) Deposited on PAMAM Dendrimers as a Catalyst for C–C Cross Coupling Reactions

Molecules, 2011
PAMAM dendrimers of generations G2–G3 as well as a partially substituted derivative of generation G4 and a low-molecular-weight tricyclic ligand 4 were used to bind Pd(0) nanoparticles. The obtained adducts were tested as catalysts for C–C cross-coupling
Tomasz Borkowski, Paweł Subik, Anna M. Trzeciak, Stanisław Wołowiec   +3 more
doaj   +1 more source

EDNRB‐dependent endothelin signaling reduces proliferation and promotes proneural‐to‐mesenchymal transition in gliomas

Molecular Oncology, EarlyView.
Glioma cells mainly express the endothelin receptor EDNRB, while EDNRA is restricted to a perivascular tumor subpopulation. Endothelin signaling reduces glioma cell proliferation while promoting migration and a proneural‐to‐mesenchymal transition associated with poor prognosis. This pathway activates Ca2+, K+, ERK, and STAT3 signalings and is regulated
Donovan Pineau, Leonor Garcia, Hugo Arnold, Antonija Hanžek, Maialen Arrieta, Laurent R Gauthier, Christine Granotier‐Beckers, François D Boussin, Amaury Herbet, Marie Hautière, Valentin Asei‐Ceschino, Clémentin Jacques, Laura Brard, Thomas Harnois, Valérie Coronas, Bruno Constantin, Aurélien Chatelier, Jean Chemin, Serge Urbach, Martial Seveno, Szimonetta Hideg, Chantal Ripoll, Kasandra Aguilar‐Cázarez, Min Zheng, Guo‐Hao Huang, Sheng‐Qing Lv, Lei Zhang, Philippe Rondard, Laurent Prezeau, Jean‐Philippe Pin, Hugues Duffau, Luc Bauchet, Valérie Rigau, Franck Denat, Charles Truillet, Didier Boquet, Jean‐Philippe Hugnot   +36 more
wiley   +1 more source

IMPDH inhibition enhances cytarabine efficacy in SAMHD1‐expressing leukaemia cells via guanine nucleotide depletion

Molecular Oncology, EarlyView.
Cytarabine is a key therapy for acute myeloid leukaemia (AML), but its efficacy is limited by the dNTPase SAMHD1, which hydrolyses its active metabolite. Screening nucleotide biosynthesis inhibitors revealed that IMPDH inhibitors selectively sensitise SAMHD1‐proficient AML cells to cytarabine.
Miriam Yagüe‐Capilla, Christopher Dirks, Caroline Eiden, Sonja K. Fesenmayer, Femke M. Hormann, Yolande Klootsema, Ingrid Lilienthal, Si Min Zhang, Nikolas Herold, Sean G. Rudd   +9 more
wiley   +1 more source

Somatic mutational landscape in von Hippel–Lindau familial hemangioblastoma

Molecular Oncology, EarlyView.
The causes of central nervous system (CNS) hemangioblastoma in Von Hippel–Lindau (vHL) disease are unclear. We used Whole Exome Sequencing (WES) on familial hemangioblastoma to investigate events that underlie tumor development. Our findings suggest that VHL loss creates a permissive environment for tumor formation, while additional alterations ...
Maja Dembic, Anne Nørremølle, Lilian Bomme Ousager, Lars van Brakel Andersen, Marie Louise Mølgaard Binderup, Mads Thomassen   +5 more
wiley   +1 more source

Hippo pathway at the crossroads of stemness and therapeutic resistance in breast cancer

Molecular Oncology, EarlyView.
Dysregulation of the Hippo pathway drives nuclear accumulation of YAP/TAZ, activating stemness‐related transcriptional programs that sustain breast cancer stemness and fuel therapeutic resistance across subtypes, underscoring Hippo signaling as a targetable vulnerability. Figure created and edited with BioRender.com.
Giulia Schiavoni, Antonella Palmese, Stefano Scalera, Laura Cipriani, Davide Mascolo, Patrizia Vici, Teresa Arcuri, Lorena Filomeno, Eriseld Krasniqi, Giovanni Blandino, Giulia Bon, Marcello Maugeri‐Saccà   +11 more
wiley   +1 more source

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

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