ArticleGenome biology2006
Deciphering cellular states of innate tumor drug responses.
Article in Genome biology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers, 2 of them syntheses that pooled it.
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Who cites it
68 citing papers in PubMed, 2 syntheses or guidelines pooled it, 124 citations in OpenAlex.
- Disrupting Mechanisms that Regulate Genomic Repeat Elements to Combat Cancer and Drug Resistance.Frontiers in cell and developmental biology · 2022Pooled it
- Meta-analysis of multiple microarray datasets reveals a common gene signature of metastasis in solid tumors.BMC medical genomics · 2011Pooled it
- Epigenetic Activation of the KDM6B-DKK1 Axis Promotes Colorectal Cancer Peritoneal Metastasis Through Wnt/β-Catenin-Associated EMT.Journal of cellular and molecular medicine · 2026Article
- PharmaFormer predicts clinical drug responses through transfer learning guided by patient derived organoid.NPJ precision oncology · 2025Article
- Identification and Validation of Biomarkers to Predict Early Diagnosis of Inflammatory Bowel Disease and Its Progression to Colorectal Cancer.Biochemical genetics · 2025Article
- The clinical relevance and prediction efficacy from therapy of tumor microenvironment related signature score in colorectal cancer.Frontiers in oncology · 2023Article
- Single-cell and bulk transcriptome sequencing identifies two epithelial tumor cell states and refines the consensus molecular classification of colorectal cancer.Nature genetics · 2022Article
- Emerging roles of cystathionine β-synthase in various forms of cancer.Redox biology · 2022Review
- The expression and prognostic value of Src homology 2 domain-containing transforming protein C3 (SHC3) and its potential role in colorectal cancer.Translational cancer research · 2021Article
- Identification of Hub Genes in Different Stages of Colorectal Cancer through an Integrated Bioinformatics Approach.International journal of environmental research and public health · 2021Article
- Article
- A tumor microenvironment-specific gene expression signature predicts chemotherapy resistance in colorectal cancer patients.NPJ precision oncology · 2021Article
- INHBA is a novel mediator regulating cellular senescence and immune evasion in colorectal cancer.Journal of Cancer · 2021Article
- m6A methyltransferase METTL3 maintains colon cancer tumorigenicity by suppressing SOCS2 to promote cell proliferation.Oncology reports · 2020Observational
- A stroma-related lncRNA panel for predicting recurrence and adjuvant chemotherapy benefit in patients with early-stage colon cancer.Journal of cellular and molecular medicine · 2020Article
- Biglycan as a potential diagnostic and prognostic biomarker in multiple human cancers.Oncology letters · 2020Article
- KIF20A Predicts Poor Survival of Patients and Promotes Colorectal Cancer Tumor Progression through the JAK/STAT3 Signaling Pathway.Disease markers · 2020Article
- High expression of eukaryotic initiation factor 3M predicts poor prognosis in colon adenocarcinoma patients.Oncology letters · 2020Article
- Development of an Experimental Model for Analyzing Drug Resistance in Colorectal Cancer.Cancers · 2018Review
- TRIP13 promotes tumor growth and is associated with poor prognosis in colorectal cancer.Cell death & disease · 2018Article
8 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe molecular mechanisms underlying innate tumor drug resistance, a major obstacle to successful cancer therapy, remain poorly understood. In colorectal cancer (CRC), molecular studies have focused on drug-selected tumor cell lines or individual candidate genes using samples derived from patients already treated with drugs, so that very little data are available prior to drug treatment.
resultsTranscriptional profiles of clinical samples collected from CRC patients prior to their exposure to a combined chemotherapy of folinic acid, 5-fluorouracil and irinotecan were established using microarrays. Vigilant experimental design, power simulations and robust statistics were used to restrain the rates of false negative and false positive hybridizations, allowing successful discrimination between drug resistance and sensitivity states with restricted sampling. A list of 679 genes was established that intrinsically differentiates, for the first time prior to drug exposure, subsequently diagnosed chemo-sensitive and resistant patients. Independent biological validation performed through quantitative PCR confirmed the expression pattern on two additional patients. Careful annotation of interconnected functional networks provided a unique representation of the cellular states underlying drug responses.
conclusionMolecular interaction networks are described that provide a solid foundation on which to anchor working hypotheses about mechanisms underlying in vivo innate tumor drug responses. These broad-spectrum cellular signatures represent a starting point from which by-pass chemotherapy schemes, targeting simultaneously several of the molecular mechanisms involved, may be developed for critical therapeutic intervention in CRC patients. The demonstrated power of this research strategy makes it generally applicable to other physiological and pathological situations.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.