Results 71 to 80 of about 818,208 (218)

PRC2 represses transcribed genes on the imprinted inactive X chromosome in mice

open access: yesGenome Biology, 2017
Background Polycomb repressive complex 2 (PRC2) catalyzes histone H3K27me3, which marks many transcriptionally silent genes throughout the mammalian genome.
Emily Maclary   +5 more
doaj   +1 more source

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

open access: yesMolecular 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   +9 more
wiley   +1 more source

Hijacking emergency granulopoiesis: Neutrophil ontogeny and reprogramming in cancer

open access: yesMolecular Oncology, EarlyView.
Neutrophils are highly plastic innate immune cells; their functions in cancer extend beyond the tumour microenvironment. This Review summarises current understanding of neutrophil maturation and heterogeneity and highlights tumour‐induced granulopoiesis as a systemic programme that expands immature, immunosuppressive neutrophils via tumour‐derived ...
Gabriela Marinescu, Yi Feng
wiley   +1 more source

Stimulator of interferon genes agonist augmented antitumor immunity of osimertinib in Egfr‐mutated lung cancer

open access: yesMolecular Oncology, EarlyView.
Combining osimertinib with the STING agonist ADU‐S100 activates innate and adaptive immunity to overcome the non‐inflamed microenvironment of Egfr‐mutant lung cancer. This combination increases NK and CD8+ T‐cell infiltration, associated with activation of the STING‐IRF3 pathway and local immunogenic cell death.
Jun Nishimura   +19 more
wiley   +1 more source

A whole-organism landscape of X-inactivation in humans

open access: yeseLife
As females are mosaic for X-inactivation, direct determination of X-linked allelic expression in bulk tissues is typically unfeasible. Using females that are non-mosaic (completely skewed) for X-inactivation (nmXCI) has proven a powerful and natural ...
Bjorn Gylemo   +2 more
doaj   +1 more source

Loss of IGF‐1R impairs DNA‐PKcs recruitment to chromatin leading to defective end‐joining

open access: yesMolecular Oncology, EarlyView.
IGF‐1R promotes radioresistance by facilitating DNA‐PKcs recruitment to chromatin, enabling non‐homologous end‐joining (NHEJ) repair of double‐strand breaks. Inhibition or loss of IGF‐1R disrupts this recruitment to damage sites, driving compensatory reliance on microhomology‐mediated end‐joining (MMEJ) repair.
Matthew O. Ellis   +3 more
wiley   +1 more source

Oncogenes and tumor suppressor genes: functions and roles in cancers

open access: yesMedComm
Cancer, being the most formidable ailment, has had a profound impact on the human health. The disease is primarily associated with genetic mutations that impact oncogenes and tumor suppressor genes (TSGs).
Tikam Chand Dakal   +12 more
doaj   +1 more source

USP29‐regulated noncanonical stabilization of the hypoxia‐inducible factor‐α in aggressive prostate cancer

open access: yesMolecular Oncology, EarlyView.
We identify USP29 as the only DUB mirroring CA9 expression, a marker of hypoxia and HIF pathway activation associated with PCA aggressiveness. USP29 stabilizes HIF‐1α and HIF‐2α via a noncanonical mechanism that is independent of PHD/pVHL activity yet relies on proteasomal regulation, establishing USP29 as a previously unrecognized regulator of hypoxic
Amelie S Schober   +16 more
wiley   +1 more source

YY1 binding is a gene-intrinsic barrier to Xist-mediated gene silencing

open access: yesEMBO Reports
X chromosome inactivation (XCI) in mammals is mediated by Xist RNA which functions in cis to silence genes on a single X chromosome in XX female cells, thereby equalising levels of X-linked gene expression relative to XY males.
Joseph S Bowness   +3 more
doaj   +1 more source

Finding novel vulnerabilities of hypomorphic BRCA1 alleles

open access: yesMolecular Oncology, EarlyView.
Synthetic lethality screens performed to identify novel vulnerabilities often model complete gene loss, thereby overlooking patient‐derived hypomorphic mutations. In this study, we have performed genome‐wide CRISPR screens on BRCA1 hypomorphic mutations, showing BRCA1I26A behaves like wild‐type, while BRCA1R1699Q mimics deficiency. Furthermore, we have
Anne Schreuder   +10 more
wiley   +1 more source

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