Results 101 to 110 of about 1,633,229 (254)

Developmental programmes drive cellular plasticity, disease progression and therapy resistance in lung adenocarcinoma

open access: yesMolecular Oncology, EarlyView.
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

Critical notice of published articles in environmental ethics [PDF]

open access: yes, 2020
Critical notice of citations of Rolston's published articles in environmental ...
Rolston, Holmes, 1932-, author
core  

Published journal articles

open access: yes
Here you will find published journal articles from the Climate Resilient Places ...
Tom Gillespie, Thomas K.J. McDermott
core   +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

Number of articles and case reports published per year.

open access: yes, 2013
Number of articles and case reports published per year.
Adam Pawinski (328488)   +2 more
core   +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

Number of (P)SSA articles published per year.

open access: yes, 2019
Number of PSSA articles (black bar) and number of SSA articles (grey bar) published per year and the total number of articles indexed in MEDLINE (black line) per year after the introduction of the method in 1996 (first bar in the graph).
Michael Biehl (390876)   +4 more
core   +1 more source

Access to published article

open access: yesIndian Journal of Pathology and Microbiology, 2021
openaire   +2 more sources

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

Articles published in 2008

open access: yesРоссийский кардиологический журнал, 2008
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Article Aditorial
doaj  

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