ReviewNature reviews. Cancer2015
Directly targeting transcriptional dysregulation in cancer.
Review in Nature reviews. Cancer, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
68 citing papers in PubMed.
- Self-sufficient killing of malignant tumors by an engineered cancer-selective gene circuit.Cell reports. Medicine · 2026Article
- PDK1 elevation was induced by epigenetic modifications of KDM3A and METTL16 to mediate TKI resistance and cancer development.Genes & diseases · 2026Article
- Article
- Integrative analysis identifies the atypical repressor E2F8 as a targetable transcriptional activator driving lethal prostate cancer.Oncogene · 2025Article
- Functional analysis of cancer-associated germline risk variants.Nature genetics · 2025Article
- Single-cell transcriptomics reveals the multidimensional dynamic heterogeneity from primary to metastatic gastric cancer.iScience · 2025Article
- A large-scale cancer-specific protein-DNA interaction network.Life science alliance · 2024Article
- KDM5B promotes SMAD4 loss-driven drug resistance through activating DLG1/YAP to induce lipid accumulation in pancreatic ductal adenocarcinoma.Cell death discovery · 2024Article
- Activation of Bivalent Gene POU4F1 Promotes and Maintains Basal-like Breast Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Functional Classification of Fusion Proteins in Sarcoma.Cancers · 2024Review
- EGR1 suppresses HCC growth and aerobic glycolysis by transcriptionally downregulating PFKL.Journal of experimental & clinical cancer research : CR · 2024Article
- A large-scale cancer-specific protein-DNA interaction network.bioRxiv : the preprint server for biology · 2024Article
- Therapeutic targeting of CPSF3-dependent transcriptional termination in ovarian cancer.Science advances · 2023Article
- Tumor Cell-Intrinsic c-Myb Upregulation Stimulates Antitumor Immunity in a Murine Colorectal Cancer Model.Cancer immunology research · 2023Article
- Review
- MLL4 Regulates the Progression of Non-Small-Cell Lung Cancer by Regulating the PI3K/AKT/SOX2 Axis.Cancer research and treatment · 2023Article
- Identification and verification of the temozolomide resistance feature gene DACH1 in gliomas.Frontiers in oncology · 2023Article
- A network medicine approach for identifying diagnostic and prognostic biomarkers and exploring drug repurposing in human cancer.Computational and structural biotechnology journal · 2023Article
- Role of ZNF143 and Its Association with Gene Expression Patterns, Noncoding Mutations, and the Immune System in Human Breast Cancer.Life (Basel, Switzerland) · 2022Article
- NF-kB in Signaling Patterns and Its Temporal Dynamics Encode/Decode Human Diseases.Life (Basel, Switzerland) · 2022Review
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
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Drugs that target intracellular signalling pathways have markedly improved progression-free survival of patients with cancers who were previously regarded as untreatable. However, the rapid emergence of therapeutic resistance, as a result of bypass signalling or downstream mutation within kinase-mediated signalling cascades, has curtailed the benefit gained from these therapies. Such resistance mechanisms are facilitated by the linearity and redundancy of kinase signalling pathways. We argue that, in each cancer, the dysregulation of key transcriptional regulators not only defines the cancer phenotype but is essential for its development and maintenance. Furthermore, we propose that, as therapeutic targets, these transcriptional regulators are less prone to bypass by alternative mutational events or clonal heterogeneity, and therefore we must rekindle our efforts to directly target transcriptional regulation across a broad range of cancers.
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Registered trials
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.