Results 121 to 130 of about 2,042,265 (257)
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
Base-excision repair pathway shapes 5-methylcytosine deamination signatures in pan-cancer genomes
Transition of cytosine to thymine in CpG dinucleotides is the most frequent type of mutation in cancer. This increased mutability is commonly attributed to the spontaneous deamination of 5-methylcytosine (5mC), which is normally repaired by the base ...
André Bortolini Silveira +15 more
doaj +1 more source
Loss of IGF‐1R impairs DNA‐PKcs recruitment to chromatin leading to defective end‐joining
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
DNA alteration and repair is undoubtedly as essential stage in the mechanism of chemical carcinogenesis. Present knowledge has in fact shown, and in a rather convincing manner, that the majority of known chemical carcinogens, in addition to radiations and viruses, are also mutagens in the widest sense of the word and usually induce alteration of the ...
L, Santi +4 more
openaire +2 more sources
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
Finding novel vulnerabilities of hypomorphic BRCA1 alleles
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
MITF maintains genome stability in nonmelanocyte lineages
MITF is essential for melanocyte survival and acts as an oncogene in 10%–20% of melanomas. We show that MITF depletion causes genome instability in nonmelanocytic cells, leading to LATS2‐mediated P53 activation, cell cycle arrest, and apoptosis. This study highlights the role of MITF as a genome maintenance factor beyond the melanocyte lineage. Created
Drifa H. Gudmundsdottir +13 more
wiley +1 more source
Breast cancer is a prevalent and significant cause of mortality in women, and manifests as six molecular subtypes. Its further histologic classification into non-invasive ductal or lobular carcinoma (DCIS) and invasive carcinoma (ILC or IDC) underscores ...
Vasiliki Pantazi +8 more
doaj +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
Genetic Background Predicts Uveal Melanoma Patients’ Outcomes
Objective: Single nucleotide polymorphisms (SNPs) in IRF4 and HERC2 are associated with risk for disomy or monosomy of chromosome 3 (D3 or M3) uveal melanoma (UM), respectively.
Thibault Verrier, PhD +17 more
doaj +1 more source

