CDS-DB, an omnibus for patient-derived gene expression signatures induced by cancer treatment

Nucleic Acids Res. 2024 Jan 5;52(D1):D1163-D1179. doi: 10.1093/nar/gkad888.

Abstract

Patient-derived gene expression signatures induced by cancer treatment, obtained from paired pre- and post-treatment clinical transcriptomes, can help reveal drug mechanisms of action (MOAs) in cancer patients and understand the molecular response mechanism of tumor sensitivity or resistance. Their integration and reuse may bring new insights. Paired pre- and post-treatment clinical transcriptomic data are rapidly accumulating. However, a lack of systematic collection makes data access, integration, and reuse challenging. We therefore present the Cancer Drug-induced gene expression Signature DataBase (CDS-DB). CDS-DB has collected 78 patient-derived, paired pre- and post-treatment transcriptomic source datasets with uniformly reprocessed expression profiles and manually curated metadata such as drug administration dosage, sampling time and location, and intrinsic drug response status. From these source datasets, 2012 patient-level gene perturbation signatures were obtained, covering 85 therapeutic regimens, 39 cancer subtypes and 3628 patient samples. Besides data browsing, download and search, CDS-DB also supports single signature analysis (including differential gene expression, functional enrichment, tumor microenvironment and correlation analyses), signature comparative analysis and signature connectivity analysis. This provides insights into drug MOA and its heterogeneity in patients, drug resistance mechanisms, drug repositioning and drug (combination) discovery, etc. CDS-DB is available at http://cdsdb.ncpsb.org.cn/.

MeSH terms

  • Antineoplastic Agents* / administration & dosage
  • Antineoplastic Agents* / therapeutic use
  • Databases, Genetic*
  • Dose-Response Relationship, Drug
  • Drug Resistance, Neoplasm / genetics
  • Gene Expression Profiling*
  • Humans
  • Neoplasms* / drug therapy
  • Neoplasms* / genetics
  • Transcriptome / genetics
  • Tumor Microenvironment

Substances

  • Antineoplastic Agents