Results 41 to 50 of about 47,919 (269)
Epigenetic reprogramming of lineage switching in cancer
Cancer cells rarely commit to a single identity. Epigenetic mechanisms and tumor microenvironment cues push epithelial cells toward flexible, hybrid states that can shift into mesenchymal, neuroendocrine, or stem‐like fates, driving metastasis, drug resistance, and tumor heterogeneity. Targeting the epigenetic regulators behind these transitions, using
Ezgi Boyvatlı +4 more
wiley +1 more source
This article presents an extended backstepping control method to reduce the grid-side current harmonics caused by grid voltage distortion. A dynamic model considering the grid voltage as an external disturbance is derived in the stationary reference ...
Hang Yin +3 more
doaj +1 more source
The role of miR‐335‐5p in the redifferentiation of BRAF p.V600E thyroid cancers
The BRAF p.V600E mutation promotes thyroid cancer dedifferentiation and radioiodine resistance. Using a network approach, we identified miR‐335‐5p as a key regulator of BRAF‐mutated thyroid tumors. Restoring miR‐335‐5p increased thyroid‐specific gene expression and iodine uptake in cells and organoids.
Valeria Pecce +11 more
wiley +1 more source
Exploring the driving factors and their mitigation potential in global energy-related CO2 emission
In order to quantify the contribution of the mitigation strategies, an extended Kaya identity has been proposed in this paper for decomposing the various factors that influence the CO2 emission.
Zhiyuan Ma +6 more
doaj +1 more source
Processor Interconnection Strategies [PDF]
In this paper, we describe four families of topologies for interconnecting many identical processors into a computer network. Each family extends to arbitrarily many processors while keeping the number of neighbors of any one processor fixed. These families are investigated with respect to bus load, routing algorithms, and the relation between the ...
Raphael A. Finkel, Marvin H. Solomon
openaire +1 more source
This study shows that lung adenocarcinomas exploit developmental branching morphogenesis to acquire a therapy resistant basal‐like tumour cell state. This process was found to be regulated by combined TP53 loss‐of‐function and type‐I interferon signalling, identifying a novel axis for biomarker and therapeutic target discovery.
Kamila J Bienkowska +13 more
wiley +1 more source
The novel styrylquinazolinone‐based molecule W1B effectively suppresses glioblastoma by inhibiting IGF1R and EGFR. In high‐glucose microenvironments driving tumor resistance, W1B acts synergistically with the EGFR inhibitor dacomitinib. This combination safely blocks compensatory survival signaling in zebrafish xenograft models. Showcasing promising in
Patryk Rurka +9 more
wiley +1 more source
Epidemics on interconnected networks [PDF]
13 pages, 7 ...
Mark Dickison +2 more
openaire +3 more sources
Single‐cell multi‐omics reveals epigenetic heterogeneity across therapy‐adaptive tumor states, including quiescent/dormant, drug‐tolerant persister, and EMT‐like phenotypes. By linking regulatory features with state‐associated biomarkers, these approaches inform biomarker‐guided therapeutic strategies for evolving tumors.
Hee Jung Kim +3 more
wiley +1 more source
Translating whole‐genome doubling into precision medicine in cancer
Whole‐genome doubling creates a WGD‐positive tumor state characterized by persistent chromosomal instability, karyotypic diversification, and cellular stress. These same biological pressures drive aggressive tumor evolution while exposing therapeutic vulnerabilities, providing a rationale for WGD‐informed precision medicine. Whole‐genome doubling (WGD)
Sejung Lee, Junghyeok Lim, Jinhyuk Bhin
wiley +1 more source

