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Accession: PRJNA523724 ID: 523724

Loss of CHD1 promotes chromatin dysregulation leading to heterogeneous mechanisms of resistance to hormone therapy in prostate cancer

This SuperSeries is composed of the SubSeries listed below. Overall design: Refer to individual Series
AccessionPRJNA523724; GEO: GSE126918
TypeUmbrella project
PublicationsZhang Z et al., "Loss of CHD1 Promotes Heterogeneous Mechanisms of Resistance to AR-Targeted Therapy via Chromatin Dysregulation.", Cancer Cell, 2020 Apr 13;37(4):584-598.e11
SubmissionRegistration date: 22-Feb-2019
Charles L. Sawyers Lab, Human Oncology and Pathogenesis, Memorial Sloan Kettering Cancer Center
RelevanceSuperseries
Project Data:
Resource NameNumber
of Links
Sequence data
SRA Experiments453
Publications
PubMed1
PMC1
Other datasets
BioSample453
GEO DataSets4
GEO Data Details
ParameterValue
Data volume, Supplementary Mbytes1974
SRA Data Details
ParameterValue
Data volume, Gbases199
Data volume, Mbytes90392
Loss of CHD1 promotes chromatin dysregulation leading to heterogeneous mechanisms of resistance to hormone therapy in prostate cancer encompasses the following 3 sub-projects:
Project TypeNumber of Projects
Epigenomics1
BioProject
accession
OrganismTitle
PRJNA524393Homo sapiensLoss of CHD1 promotes chromatin dysregulation leading to heterogeneous mechanisms of resistance to hormone therapy in prostate cancer [ATAC-seq] (Charles L. Sawyers Lab, Human...)
Other1
BioProject
accession
NameTitle
PRJNA525865Loss of CHD1 promotes chromatin dysregulation leading to heterogeneous mechanisms of resistance to hormone therapy in prostate cancer [shRNA screen]Loss of CHD1 promotes chromatin dysregulation leading to heterogeneous mechanisms of resistance to hormone therapy in prostate cancer [shRNA screen] (Charles L. Sawyers Lab, Human...)
Transcriptome or Gene expression1
BioProject
accession
OrganismTitle
PRJNA523728Homo sapiensLoss of CHD1 promotes chromatin dysregulation leading to heterogeneous mechanisms of resistance to hormone therapy in prostate cancer [RNA-seq] (Charles L. Sawyers Lab, Human...)

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