ReviewBiomarkers in cancer2015
Oncogene Overdose: Too Much of a Bad Thing for Oncogene-Addicted Cancer Cells.
Review in Biomarkers in cancer, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
20 citing papers in PubMed, 27 citations in OpenAlex.
- Variant-Specific Landscape of Mutual Exclusivity Among BRAF, EGFR, and KRAS Oncogenes Reveals Overlap With Functionally Antagonistic Mutant Pairs.International journal of cancer · 2026Article
- Empowering Inference of Epistasis on the Basis of Mutual Exclusivity, Co-Occurrence, Functional Antagonism and Synergy in ERK-Pathway Oncogenes.International journal of cancer · 2026Article
- A Systematic Review of Evidence for the Cost of Therapeutic Resistance in Cancer.bioRxiv : the preprint server for biology · 2025Article
- Article
- Myeloid-Derived Growth Factor-Regulated Oncogenesis in Lung Adenocarcinoma Is Associated with EGFR Status and Cancer Aggressiveness.Journal of proteome research · 2025Article
- Single-cell Resolved Oncogene Co-expression: From Principles to Clinical Impact.Blood cancer discovery · 2025Article
- Exploiting Paradoxical Activation of Oncogenic MAPK Signaling by Targeting Mitochondria to SensitizeInternational journal of molecular sciences · 2025Article
- Mechanisms of KRAS inhibitor resistance in KRAS-mutant colorectal cancer harboring Her2 amplification and aberrant KRAS localization.NPJ precision oncology · 2025Article
- Multi-omic and single-cell profiling of chromothriptic medulloblastoma reveals genomic and transcriptomic consequences of genome instability.Nature communications · 2024Article
- Article
- ERK pathway agonism for cancer therapy: evidence, insights, and a target discovery framework.NPJ precision oncology · 2024Review
- Article
- DUSP4 protects BRAF- and NRAS-mutant melanoma from oncogene overdose through modulation of MITF.Life science alliance · 2022Article
- Temporal and spatial topography of cell proliferation in cancer.Nature cell biology · 2022Article
- SuperDendrix algorithm integrates genetic dependencies and genomic alterations across pathways and cancer types.Cell genomics · 2022Article
- Evolution of MET and NRAS gene amplification as acquired resistance mechanisms in EGFR mutant NSCLC.NPJ precision oncology · 2021Article
- Long-read sequencing unveils IGH-DUX4 translocation into the silenced IGH allele in B-cell acute lymphoblastic leukemia.Nature communications · 2019Article
- What makes oncogenes mutually exclusive?Small GTPases · 2017Review
- The well-accepted notion that gene amplification contributes to increased expression still remains, after all these years, a reasonable but unproven assumption.Journal of carcinogenesis · 2016Review
- Novel drug discovery platform for spinocerebellar ataxia, using fluorescence technology targeting β-III-spectrin.The Journal of biological chemistryArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Acquired resistance to targeted inhibitors remains a major, and inevitable, obstacle in the treatment of oncogene-addicted cancers. Newer-generation inhibitors may help overcome resistance mutations, and inhibitor combinations can target parallel pathways, but durable benefit to patients remains elusive in most clinical scenarios. Now, recent studies suggest a third approach may be available in some cases-exploitation of oncogene overexpression that may arise to promote resistance. Here, we discuss the importance of maintaining oncogenic signaling at "just-right" levels in cells, with too much signaling, or oncogene overdose, being potentially as detrimental as too little. This is highlighted in particular by recent studies of mutant-BRAF in melanoma and the fusion kinase nucleophosmin-anaplastic lymphoma kinase (NPM-ALK) in anaplastic large cell lymphoma. Oncogene overdose may be exploitable to prolong tumor control through intermittent dosing in some cases, and studies of acute lymphoid leukemias suggest that it may be specifically pharmacologically inducible.
Indexed as
Identifiers
What OpenQuestion holds
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.