ReviewBritish journal of cancer2014
Targeting molecular addictions in cancer.
Review in British journal of cancer, 2014. 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, 37 citations in OpenAlex.
- Suppression of AKT Activation Through LZK Inhibition Limits Tumor Growth in Esophageal and Head and Neck Cancers.Molecular cancer therapeutics · 2026Article
- The construction and analysis of tricarboxylic acid cycle related prognostic model for cervical cancer.Frontiers in genetics · 2023Article
- A CGA/EGFR/GATA2 positive feedback circuit confers chemoresistance in gastric cancer.The Journal of clinical investigation · 2022Article
- Article
- TGFβ2-mediated epithelial-mesenchymal transition and NF-κB pathway activation contribute to osimertinib resistance.Acta pharmacologica Sinica · 2021Article
- A cytoskeleton regulator AVIL drives tumorigenesis in glioblastoma.Nature communications · 2020Article
- Maintaining protein stability of ∆Np63 via USP28 is required by squamous cancer cells.EMBO molecular medicine · 2020Article
- Increased 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase-3 activity in response to EGFR signaling contributes to non-small cell lung cancer cell survival.The Journal of biological chemistry · 2019Article
- Article
- Ezh2 inhibition in Kras-driven lung cancer amplifies inflammation and associated vulnerabilities.The Journal of experimental medicine · 2018Article
- ETS-targeted therapy: can it substitute for MEK inhibitors?Clinical and translational medicine · 2017Review
- Coordinated Activities of Multiple Myc-dependent and Myc-independent Biosynthetic Pathways in Hepatoblastoma.The Journal of biological chemistry · 2016Article
- MAP3K11/GDF15 axis is a critical driver of cancer cachexia.Journal of cachexia, sarcopenia and muscle · 2016Article
- Placental origins of adverse pregnancy outcomes: potential molecular targets: an Executive Workshop Summary of the Eunice Kennedy Shriver National Institute of Child Health and Human Development.American journal of obstetrics and gynecology · 2016Article
- Rapid, Multiplexed Phosphoprotein Profiling Using Silicon Photonic Sensor Arrays.ACS central science · 2015Article
- FOXP4 modulates tumor growth and independently associates with miR-138 in non-small cell lung cancer cells.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015Article
- Protecting the normal in order to better kill the cancer.Cancer medicine · 2015Review
- Analysis of exosome release as a cellular response to MAPK pathway inhibition.Langmuir : the ACS journal of surfaces and colloids · 2015Article
- Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cancer cells depend on a finite number of critical signals for their survival. Oncogene addiction, that is, the acquired dependence of a cancer cell on the activity of a single oncogenic gene product, has been the basis for the targeted therapy paradigm, and operationally defines such signals. Additionally, cancer cells have altered metabolic requirements that create addictions to specific nutrients such as glucose and glutamine. In this review, I will discuss the therapeutic opportunities that these two types of molecular addictions offer, focusing on lessons learned from targeting members of the epidermal growth factor receptor family of kinases, and components of MAPK pathway. I will also discuss the challenges in simultaneously harnessing two types of molecular addictions for therapeutic benefit, and the importance of understanding not only the effects of oncogenic signal transduction on metabolism, but also the impact of metabolic states on signal transduction.
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.