Results 171 to 180 of about 389,974 (269)

Deciphering transcriptional plasticity in pancreatic ductal adenocarcinoma reveals alterations in sensory neuron innervation

Molecular Oncology, EarlyView.
Pancreatic sensory neurons innervating healthy and PDAC tissue were retrogradely labeled and profiled by single‐cell RNA sequencing. Tumor‐associated innervation showed a dominant neurofilament‐positive subtype, altered mitochondrial gene signatures, and reduced non‐peptidergic neurons.
Elena Genova, Michele Montrone, Uday Rangaswamy, Francesco Diversi, Irene Schiavo, Denise Ferrarini, Roberta Di Florio, Irene Longo, Michele Coscia, Nicola Zamboni, Giorgia Demontis, Lisa Veghini, Vincenzo Corbo, Remo Sanges, Paul Heppenstall   +14 more
wiley   +1 more source

Differential expression of cancer‐related genes supports prediction of poor response to first‐line treatments in T‐ALL pediatric patients with high minimal residual disease

Molecular Oncology, EarlyView.
In the present work, we have identified a transcriptional signature based on the differential expression of six genes (BCL2&MAST4, HSH2D&LAT2, METRN&PITPNM2) that would facilitate the early detection of T‐cell acute lymphoblastic leukemia (T‐ALL) patients prone to a poor treatment response and could be implemented at diagnosis, along with other risk ...
Antonio Lahera, Laura Vela‐Martín, Pablo Fernández‐Navarro, José Luis López‐Lorenzo, Javier Cornago, Pilar Llamas, Eduardo Pérez‐Gómez, José Luis Marín‐Rubio, Manuel Fresno, Javier Santos, José Fernández‐Piqueras, María Villa‐Morales   +11 more
wiley   +1 more source

E2A selectively regulates TGF‐β–induced apoptosis in KRAS‐mutant non‐small cell lung cancer

Molecular Oncology, EarlyView.
Ability to induce apoptosis by TGF‐β is frequently lost in advanced lung adenocarcinoma despite intact TGF‐β signaling. We identify E2A as a mutant KRAS–dependent mediator of resistance to TGF‐β–induced apoptosis. TGF‐β induces E2A via SMAD3 in mutant KRAS cells, and E2A silencing restores apoptosis and enhances radiation response in cell lines ...
Sergei Chuikov, Shiva Krishna Katkam, Zhefan Wang, Venkateshwar G. Keshamouni   +3 more
wiley   +1 more source

Foreign aid and development in Nepal : proceedings of a seminar (Oct. 4-5, 1983)

, 1983
Integrated Development Systems
core  

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

Integrated Information Systems [PDF]

Yearbook of Medical Informatics, 2000
openaire   +2 more sources

Seminar on Financial Resource Mobilization for the Sixth Plan of Nepal, May 26, 1980

, 1980
Integrated Development Systems
core  

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

Adaptor protein CIN85 potentiates the motility of osteosarcoma cells via the Akt/mTOR and MMP2‐COL3A1 axis

Molecular Oncology, EarlyView.
CIN85 is highly expressed in osteosarcoma, particularly in metastatic lesions. Its overexpression increases cell migration and Matrigel invasion, while silencing CIN85 suppresses these behaviors. Transcriptome analysis shows that CIN85 regulates MMP2, COL3A1, and Akt/mTOR signaling. Targeting these pathways reverses CIN85‐induced motility, highlighting
Iryna Horak, Iva Staniczková Zambo, Matěj Přikryl, Peter Múdry, Danica Zapletalová, Jarmila Navrátilová, Jiří Navrátil, Jan Šmarda, Liudmyla Drobot, Petr Beneš, Lucia Knopfová   +10 more
wiley   +1 more source