Evidence map›Paper›PMID 31817676›Full record

ReviewCells2019

Targeting mTOR and Metabolism in Cancer: Lessons and Innovations.

Cedric Magaway, Eugene Kim, Estela Jacinto

Open access · goldAbstract readReview
In one paragraph

Review in Cells, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 129 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
129citing papers in PubMed, 2 pooled it
9.5field-weighted citation impact, top 1% of its field
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

129 citing papers in PubMed, 2 syntheses or guidelines pooled it, 216 citations in OpenAlex.

  1. Life Course Trajectories of Body Mass Index and Risk of Cancer in Adulthood: Systematic Review and Meta-Analysis.Obesity reviews : an official journal of the International Association for the Study of Obesity · 2026
    Pooled it
  2. Pooled it
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  5. The Sirtuin Network: Linking NADDiabetes/metabolism research and reviews · 2026
    Review
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  15. Energy metabolism in health and diseases.Signal transduction and targeted therapy · 2025
    Review
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69 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Cedric MagawayDepartment of Biochemistry and Molecular Biology, Rutgers-Robert Wood Johnson Medical School, Piscataway, NJ 08854, USA.
Eugene KimDepartment of Biochemistry and Molecular Biology, Rutgers-Robert Wood Johnson Medical School, Piscataway, NJ 08854, USA.
Estela JacintoDepartment of Biochemistry and Molecular Biology, Rutgers-Robert Wood Johnson Medical School, Piscataway, NJ 08854, USA.ORCID 0000-0001-7118-1759
Rutgers, The State University of New Jersey · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cancer cells support their growth and proliferation by reprogramming their metabolism in order to gain access to nutrients. Despite the heterogeneity in genetic mutations that lead to tumorigenesis, a common alteration in tumors occurs in pathways that upregulate nutrient acquisition. A central signaling pathway that controls metabolic processes is the mTOR pathway. The elucidation of the regulation and functions of mTOR can be traced to the discovery of the natural compound, rapamycin. Studies using rapamycin have unraveled the role of mTOR in the control of cell growth and metabolism. By sensing the intracellular nutrient status, mTOR orchestrates metabolic reprogramming by controlling nutrient uptake and flux through various metabolic pathways. The central role of mTOR in metabolic rewiring makes it a promising target for cancer therapy. Numerous clinical trials are ongoing to evaluate the efficacy of mTOR inhibition for cancer treatment. Rapamycin analogs have been approved to treat specific types of cancer. Since rapamycin does not fully inhibit mTOR activity, new compounds have been engineered to inhibit the catalytic activity of mTOR to more potently block its functions. Despite highly promising pre-clinical studies, early clinical trial results of these second generation mTOR inhibitors revealed increased toxicity and modest antitumor activity. The plasticity of metabolic processes and seemingly enormous capacity of malignant cells to salvage nutrients through various mechanisms make cancer therapy extremely challenging. Therefore, identifying metabolic vulnerabilities in different types of tumors would present opportunities for rational therapeutic strategies. Understanding how the different sources of nutrients are metabolized not just by the growing tumor but also by other cells from the microenvironment, in particular, immune cells, will also facilitate the design of more sophisticated and effective therapeutic regimen. In this review, we discuss the functions of mTOR in cancer metabolism that have been illuminated from pre-clinical studies. We then review key findings from clinical trials that target mTOR and the lessons we have learned from both pre-clinical and clinical studies that could provide insights on innovative therapeutic strategies, including immunotherapy to target mTOR signaling and the metabolic network in cancer.

Indexed as

Energy MetabolismAntineoplastic AgentsHumansMolecular Targeted TherapyNeoplasmsPhosphatidylinositol 3-KinasesProtein Kinase InhibitorsSignal TransductionTOR Serine-Threonine KinasesAntineoplastic AgentsMTOR protein, humanPhosphatidylinositol 3-KinasesProtein Kinase InhibitorsTOR Serine-Threonine Kinasescancer metabolismkinase inhibitorsmetabolismmTORC1mTORC2mTOR inhibitorsmTOR in immunotherapymTOR signalingnutrient metabolismrapalogs

Identifiers

PMID31817676
PMCPMC6952948
OpenAlexW2991727328

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.