ReviewOncotarget2011
Finding cancer's weakest link.
Review in Oncotarget, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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
22 citing papers in PubMed, 42 citations in OpenAlex.
- Targeting SUMOylation in ovarian cancer: Sensitivity, resistance, and the role of MYC.iScience · 2025Article
- The xenobiotic transporterFrontiers in pharmacology · 2024Article
- The Role and Mechanism ofMolecules (Basel, Switzerland) · 2023Review
- Reversible Myc hypomorphism identifies a key Myc-dependency in early cancer evolution.Nature communications · 2022Article
- Review
- Crystal Structures and Nuclear Magnetic Resonance Studies of the Apo Form of the c-MYC:MAX bHLHZip Complex Reveal a Helical Basic Region in the Absence of DNA.Biochemistry · 2019Article
- Dysregulated Transcriptional Control in Prostate Cancer.International journal of molecular sciences · 2019Review
- Insights into the biology and treatment strategies of pancreatic neuroendocrine tumors.Annals of pancreatic cancer · 2019Article
- A selective high affinity MYC-binding compound inhibits MYC:MAX interaction and MYC-dependent tumor cell proliferation.Scientific reports · 2018Article
- Evolution and cancer medicine - transformative insights.Nature reviews. Clinical oncology · 2017Article
- Article
- Directly targeting transcriptional dysregulation in cancer.Nature reviews. Cancer · 2015Review
- Article
- MYC Is a Major Determinant of Mitotic Cell Fate.Cancer cell · 2015Article
- c-Myc and AMPK Control Cellular Energy Levels by Cooperatively Regulating Mitochondrial Structure and Function.PloS one · 2015Article
- Polycomb group proteins and MYC: the cancer connection.Cellular and molecular life sciences : CMLS · 2014Review
- c-MYC-miRNA circuitry: a central regulator of aggressive B-cell malignancies.Cell cycle (Georgetown, Tex.) · 2014Review
- MYC inhibition induces metabolic changes leading to accumulation of lipid droplets in tumor cells.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- A functional yeast survival screen of tumor-derived cDNA libraries designed to identify anti-apoptotic mammalian oncogenes.PloS one · 2013Article
- Origins of Myc proteins--using intrinsic protein disorder to trace distant relatives.PloS one · 2013Article
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 at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The biological programs of vertebrates exhibit a remarkable degree of functional degeneracy, adaptive compensation and robustness, to preserve homeostasis and generate reproducible phenotypic outputs irrespective of variations in signal strength, noise and quality. Cancers are difficult to treat not only because they are so mechanistically diverse but also because they adapt or evolve in response to any pharmacological elective pressure we impose upon them. Hence, an ideal cancer drug target would exert a function both necessary for cancer cell survival and functionally non-redundant, rendering it impossible for tumor cells to compensate for, or evolve independence from, the inhibitory effect of any drug aimed at that target. In this review, we discuss the unique, non-degenerate and highly pleiotropic role played by Myc in coordinating, engaging and maintaining the diverse intracellular and extracellular programs required for cell proliferation in vivo. These properties make Myc a compelling candidate cancer drug target, at least in principle: an assertion recently reinforced by new in vivo genetic data.
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.