ReviewBritish journal of clinical pharmacology2016
AKT in cancer: new molecular insights and advances in drug development.
Review in British journal of clinical pharmacology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 158 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
158 citing papers in PubMed, 264 citations in OpenAlex.
- AKT mutant allele-specific activation dictates pharmacologic sensitivities.Nature communications · 2022Trial
- Phase 2 study of TAS-117, an allosteric akt inhibitor in advanced solid tumors harboring phosphatidylinositol 3-kinase/v-akt murine thymoma viral oncogene homolog gene mutations.Investigational new drugs · 2021Trial
- Effect of Capivasertib in Patients With an AKT1 E17K-Mutated Tumor: NCI-MATCH Subprotocol EAY131-Y Nonrandomized Trial.JAMA oncology · 2021Trial
- Pre-surgical trial of the AKT inhibitor MK-2206 in patients with operable invasive breast cancer: a New York Cancer Consortium trial.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2018Trial
- Enhanced antitumor efficacy of sulfasalazine and mesalazine in colorectal cancer through modulatory action of Lacticaseibacillus rhamnosus GG.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Epstein-Barr virus-encoded microRNAs: central players in nasopharyngeal and gastric carcinoma pathogenesis.Archives of virology · 2026Review
- Afuresertib plus fulvestrant for pretreated HR-positive, HER2-negative, advanced breast cancer: a phase Ib trial.Nature communications · 2026Article
- Anticancer potential ofFrontiers in pharmacology · 2026Article
- The mechanism of the PI3K-AKT-mTOR signaling pathway in renal cell carcinoma: current developments and future prospects.Frontiers in oncology · 2026Review
- Advances in Understanding How RhoB Regulates Akt Inhibition Efficacy in NSCLC.Current cancer drug targets · 2026Article
- Helminth-derived stefin-1 selectively reduces leukemic cell viability and promotes apoptosis in U937 cells.PloS one · 2026Article
- Co-encapsulation of an AKT Inhibitor Enhances the Tumor-cell Selectivity of STING Agonists in Co-delivery Liposomes.Pharmaceutical research · 2025Article
- Resistance to Allosteric Inhibitors.Journal of molecular biology · 2025Review
- Bisabolol as a natural anticancer agent: molecular insights and therapeutic potential in oncology.Medical oncology (Northwood, London, England) · 2025Review
- Integrated pan-cancer and melanoma-specific analysis of angiopoietin-2: prognostic value, immune microenvironment modulation, and ceRNA network regulation.Discover oncology · 2025Article
- Signaling networks and MiRNA crosstalk in ovarian cancer chemoresistance.Journal of ovarian research · 2025Review
- Article
- Correlation between CTMP expression levels and resistance to trastuzumab in HER2 + metastatic breast cancer.Discover oncology · 2025Article
- CaMKK2 as a therapeutic target to combat metastasis in glioblastoma.Molecular biology reports · 2025Review
- Cellular and molecular mechanisms of arenobufagin in cancer therapy: a systematic review.Discover oncology · 2025Review
98 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
4 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The phosphatidylinositol-3 kinase (PI3K)-AKT pathway is one of the most commonly dysregulated pathways in all of cancer, with somatic mutations, copy number alterations, aberrant epigenetic regulation and increased expression in a number of cancers. The carefully maintained homeostatic balance of cell division and growth on one hand, and programmed cell death on the other, is universally disturbed in tumorigenesis, and downstream effectors of the PI3K-AKT pathway play an important role in this disturbance. With a wide array of downstream effectors involved in cell survival and proliferation, the well-characterized direct interactions of AKT make it a highly attractive yet elusive target for cancer therapy. Here, we review the salient features of this pathway, evidence of its role in promoting tumorigenesis and recent progress in the development of therapeutic agents that target AKT.
Indexed as
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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.