ArticleCancer cell2006
Can't kick that oncogene habit.
Article in Cancer cell, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 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
10 citing papers in PubMed, 21 citations in OpenAlex.
- The Position of EGF Deprivation in the Management of Advanced Non-Small Cell Lung Cancer.Frontiers in oncology · 2021Review
- TLR3 engagement induces IRF-3-dependent apoptosis in androgen-sensitive prostate cancer cells and inhibits tumour growth in vivo.Journal of cellular and molecular medicine · 2015Article
- Article
- Selective induction of cell death in melanoma cell lines through targeting of Mcl-1 and A1.PloS one · 2012Article
- c-Myc dependent expression of pro-apoptotic Bim renders HER2-overexpressing breast cancer cells dependent on anti-apoptotic Mcl-1.Molecular cancer · 2011Article
- Proapoptotic signaling induced by RIG-I and MDA-5 results in type I interferon-independent apoptosis in human melanoma cells.The Journal of clinical investigation · 2009Article
- Modelling Myc inhibition as a cancer therapy.Nature · 2008Article
- Oncogene cooperation in tumor maintenance and tumor recurrence in mouse mammary tumors induced by Myc and mutant Kras.Proceedings of the National Academy of Sciences of the United States of America · 2008Article
- Why do cancer cells become "addicted" to oncogenic epidermal growth factor receptor?PLoS medicine · 2007Review
- Overcoming resistance to molecularly targeted anticancer therapies: Rational drug combinations based on EGFR and MAPK inhibition for solid tumours and haematologic malignancies.Drug resistance updates : reviews and commentaries in antimicrobial and anticancer chemotherapy · 2007Review
Corrections and comments
- Comment on
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
One of the most exciting developments in recent cancer treatment has been the move away from crude cytotoxic agents toward drugs that inhibit specific targets in specific cellular pathways. One assumption of this strategy is that maintenance of human cancers is dependent upon a limited cadre of therapeutically tractable oncogenic lesions. In this issue of Cancer Cell, an intriguing paper from Sharma et al. endorses this approach by showing that evolution appears to be working for us. They show that an innate asymmetry in the dynamics of intracellular signaling biases pathway inhibition in favor of cell death. This bias may significantly potentiate targeted cancer therapies.
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.