Results 191 to 200 of about 9,686,810 (338)

Multidimensional OMICs reveal ARID1A orchestrated control of DNA damage, splicing, and cell cycle in normal‐like and malignant urothelial cells

open access: yesMolecular Oncology, EarlyView.
Loss of the frequently mutated chromatin remodeler ARID1A, a subunit of the SWI/SNF cBAF complex, results in less open chromatin, alternative splicing, and the failure to stop cells from progressing through the cell cycle after DNA damage in bladder (cancer) cells. Created in BioRender. Epigenetic regulators, such as the SWI/SNF complex, with important
Rebecca M. Schlösser   +11 more
wiley   +1 more source

Core outcome domain sets for clinical trials in epidermolysis bullosa - a COSEB protocol to achieve consensus on "what" to measure. [PDF]

open access: yesTrials
Korte EWH   +11 more
europepmc   +1 more source

Outcome studies [PDF]

open access: yesDevelopmental Medicine & Child Neurology, 1999
openaire   +2 more sources

Multi‐omic characterization of consensus molecular subtype 1 (CMS1) colorectal cancer with dampened immune response improves precision medicine

open access: yesMolecular Oncology, EarlyView.
This study highlights the importance of multi‐omic analyses in characterizing colorectal cancers. Indeed, our analysis revealed a rare CMS1 exhibiting dampened immune activation, including reduced PD‐1 expression, moderate CD8+ T‐cell infiltration, and suppressed JAK/STAT pathway.
Livia Concetti   +10 more
wiley   +1 more source

Chemoresistome mapping in individual breast cancer patients unravels diversity in dynamic transcriptional adaptation

open access: yesMolecular Oncology, EarlyView.
This study used longitudinal transcriptomics and gene‐pattern classification to uncover patient‐specific mechanisms of chemotherapy resistance in breast cancer. Findings reveal preexisting drug‐tolerant states in primary tumors and diverse gene rewiring patterns across patients, converging on a few dysregulated functional modules. Despite receiving the
Maya Dadiani   +14 more
wiley   +1 more source

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