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This archived document is maintained by the Oregon State Library as part of the Oregon Documents Depository Program. It is for informational purposes and may not be suitable for legal purposes.v. 1, no. 2 (May 2008)-v. 2, no. 1 (Feb. 2009)Mode of access:
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"Why should anyone want to make things better for me particularly?" : A qualitative exploration of Care Opinion and NHS care improvements Patient Experience Journal [PDF]
Our thanks go to our stakeholder group and CareOpinion for their support.Peer ...
Campbell, Marion K. +4 more
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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
"June 1958."; "Mission: To provide special emergency welfare services to individuals and families."A plan on serving the immediate needs of people in an enemy attack on the United ...
Kansas. Survival Plan Project.
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ATP‐Binding Cassette (ABC) transporters play a key role in drug resistance and cancer progression. We analyzed the correlation between ABC transporter gene alterations and patient survival in breast and prostate cancers using large‐scale genomic datasets.
Abdulaziz H. Alanazi +2 more
doaj +1 more source
We retrospectively studied antibody immunity in 92 candidemia patients, using sera taken at candidemia diagnosis. All patients showed the presence of IgG antibodies against all tested Candida antigens, namely Als3, Mp65, Hyr1 and Eno1, at levels ...
Carla Bromuro +9 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
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
A cancer survival model that takes sociodemographic variations in 'normal' mortality into account: comparison with other models [PDF]
Study objectives - Sociodemographic differentials in cancer survival have occasionally been studied by using a relative-survival approach, where all-cause mortality among persons with a cancer diagnosis is compared with that among similar persons without
Kravdal, Øystein
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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

