ReviewClinical cancer research : an official journal of the American Association for Cancer Research2013
Navigating the therapeutic complexity of PI3K pathway inhibition in melanoma.
Review in Clinical cancer research : an official journal of the American Association for Cancer Research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers, 1 of them a synthesis that pooled it.
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
59 citing papers in PubMed, 1 synthesis or guideline pooled it.
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- Phase II Study of Copanlisib in Patients With PTEN Loss: Results From NCI-MATCH ECOG-ACRIN Trial (EAY131) Subprotocols Z1G and Z1H.JCO precision oncology · 2025Trial
- Simvastatin reprograms lipid metabolism in B16.F10 melanoma cells to favor an early resistant phenotype.Scientific reports · 2026Article
- Experimentally calibrated multiscale model predicts schedule dependent drug combination effects.NPJ systems biology and applications · 2026Article
- mTORC1/2 inhibition induces tumor regression in CDK4/6 inhibitor-insensitive acral melanoma.Cancer gene therapy · 2026Article
- Epigenetic Modulators and Immunotherapy in Malignant Melanoma.Oncology research · 2026Review
- Chelidonine inhibits melanoma cell malignancy by inactivating TLR4/NF-κB and PI3K/AKT signaling pathways.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2025Article
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- Metabolism of tumor infiltrating T cells.Frontiers in immunology · 2025Review
- A recent update on the connection between dietary phytochemicals and skin cancer: emerging understanding of the molecular mechanism.Annals of medicine and surgery (2012) · 2024Review
- A combined opposite targeting of p110δ PI3K and RhoA abrogates skin cancer.Communications biology · 2024Article
- Transforming Growth Factor-β/Smad Signaling Inhibits Melanoma Cancer Stem Cell Self-Renewal, Tumor Formation and Metastasis.Cancers · 2024Article
- A Paradoxical AKT: Exploring the Promise and Challenges of PI3K/AKT/mTOR Targeted Therapies.Journal of cancer immunology · 2024Article
- Article
- Exosome application in tumorigenesis: diagnosis and treatment of melanoma.Medical oncology (Northwood, London, England) · 2022Review
- Multiple primary malignant neoplasm: Case report and comprehensive literature review.Frontiers in oncology · 2022Article
- The role of PI3'-lipid signalling in melanoma initiation, progression and maintenance.Experimental dermatology · 2022Review
- Targeted therapy strategies for melanoma brain metastasis.Neuro-oncology advances · 2021Article
- Unraveling the Wide Spectrum of Melanoma Biomarkers.Diagnostics (Basel, Switzerland) · 2021Review
- 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
2 authors.
Funding
Abstract
Melanoma is entering into an era of combinatorial approaches to build upon recent clinical breakthroughs achieved by novel single-agent therapies. One of the leading targets to emerge from the growing understanding of the molecular pathogenesis, heterogeneity, and resistance mechanisms of melanomas is the phosphoinositide 3-kinase (PI3K)-AKT pathway. Multiple genetic and epigenetic aberrations that activate this pathway have been identified in melanomas de novo and in acquired resistance models. These developments have been paralleled by the establishment of models for preclinical testing and the availability of compounds that target various effectors in the pathway. Thus, in addition to having a strong rationale for targeting, the PI3K-AKT pathway presents an immediate clinical opportunity. However, the development of effective strategies against this pathway must overcome several key challenges, including optimizing patient selection, overcoming feedback loops, and pathway cross-talk that can mediate resistance. This review discusses the current understanding and ongoing research about the PI3K-AKT pathway in melanoma and emerging strategies to achieve clinical benefit in patients by targeting it.
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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.