ReviewEMBO reports2016
Drugging the addict: non-oncogene addiction as a target for cancer therapy.
Review in EMBO reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 99 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
99 citing papers in PubMed.
- COPZ1 depletion induces cell death through different mechanisms in in vitro murine models of thyroid cancer.European thyroid journal · 2026Article
- Combination AURKA and WEE1 Inhibition Exhibits Efficacy in EGFR or Pan-ERBB Inhibitor-Resistant Head and Neck Squamous Cell Carcinoma.Cancer research communications · 2026Article
- TONSL Promotes Hepatocellular Carcinoma Progression by Inhibiting Apoptosis Through Homologous Recombination Repair.Cancer science · 2026Article
- Novel therapeutic targets at the crossroad between epigenetics and signal transduction pathways in B-cell lymphomas.Clinical and experimental medicine · 2026Review
- Integrative multi-omics defines melanoma drug response networks and ARID1A-dependent resistance mechanisms.Molecular systems biology · 2026Article
- Human DEAH-box helicase 8 regulates HSF1-mediated stress response and cancer-associated pre-mRNA splicing in tumour cells.NAR cancer · 2026Article
- Targeting the Endoplasmic Reticulum Oxidoreductin-1 Alpha-Protein Disulfide Isomerase Redox Interface as a Therapeutic Strategy in Cancer.Biomedicines · 2026Review
- Dominant-negative TP53 mutations potentiated by the HSF1-regulated proteostasis network.Molecular cell · 2026Article
- Genome agnostic, multi-level non-oncogene addiction-based systems pharmacology for rescuing metastatic relapsed/refractory neoplasias.Frontiers in pharmacology · 2026Review
- Thiazole-driven heterocyclic hybrids as EGFR inhibitors: progress in synthesis and anticancer applications.RSC advances · 2025Review
- Transcriptional regulation of protein synthesis by mediator kinase represents a therapeutic vulnerability in MYC-driven medulloblastoma.Nature communications · 2025Article
- Defining the Antitumor Mechanism of Action of a Clinical-stage Compound as a Selective Degrader of the Nuclear Pore Complex.Cancer discovery · 2025Article
- De novo pyrimidine synthesis is a collateral metabolic vulnerability in NF2-deficient mesothelioma.EMBO molecular medicine · 2025Article
- Molecular roles of microRNA-21 and exosomal miR-21 in gastrointestinal cancers: diagnostic, therapeutic, and drug resistance insights.Frontiers in molecular biosciences · 2025Review
- Advances in Synthetic Lethality in Potential Oncology Therapeutic Approaches.Current topics in medicinal chemistry · 2025Review
- Chemotherapeutic agents and leucine deprivation induce codon-biased aberrant protein production in cancer.Nucleic acids research · 2024Article
- Predicting DNA damage response in non-small cell lung cancer organoids via simultaneous label-free autofluorescence multiharmonic microscopy.Redox biology · 2024Article
- Targeting immunogenic cell stress and death for cancer therapy.Nature reviews. Drug discovery · 2024Review
- PML restrains p53 activity and cellular senescence in clear cell renal cell carcinoma.EMBO molecular medicine · 2024Article
- C/EBPβ-induced lymphoid-to-myeloid transdifferentiation emulates granulocyte-monocyte progenitor biology.Stem cell reports · 2024Article
39 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
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Historically, cancers have been treated with chemotherapeutics aimed to have profound effects on tumor cells with only limited effects on normal tissue. This approach was followed by the development of small-molecule inhibitors that can target oncogenic pathways critical for the survival of tumor cells. The clinical targeting of these so-called oncogene addictions, however, is in many instances hampered by the outgrowth of resistant clones. More recently, the proper functioning of non-mutated genes has been shown to enhance the survival of many cancers, a phenomenon called non-oncogene addiction. In the current review, we will focus on the distinct non-oncogenic addictions found in cancer cells, including synthetic lethal interactions, the underlying stress phenotypes, and arising therapeutic opportunities.
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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.