Evidence map›Paper›PMID 32127696›Full record

ReviewNature reviews. Endocrinology2020

Insulin-PI3K signalling: an evolutionarily insulated metabolic driver of cancer.

Benjamin D Hopkins, Marcus D Goncalves, Lewis C Cantley

Registry-linked trialOpen access · greenAbstract readReview
In one paragraph

Review in Nature reviews. Endocrinology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT06611501 (Glycemic Regulation as Endometriosis Adjunct Treatment), which is not on this map. Cited by 178 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
178citing papers in PubMed, 1 pooled it
13.6field-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.

NCT06611501 phase2active not recruitingnot on this mapstarted 2025, after this paper: background citation

Glycemic Regulation as Endometriosis Adjunct Treatment

TypeinterventionalSponsorBoston Children's HospitalRan2025 to 2027Enrolled14ConditionsPelvic Pain, EndometriosisArmsMetformin Hydrochloride, Placebo
3 · Its place in the literature

Who cites it

178 citing papers in PubMed, 1 synthesis or guideline pooled it, 271 citations in OpenAlex.

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118 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 2 institutions in 1 country.

Benjamin D HopkinsDepartment of Genetics and Genomic Sciences, Icahn School of Medicine at Mount Sinai, New York, NY, USA. Benjamin.Hopkins@mssm.edu.ORCID http://orcid.org/0000-0002-7970-6430
Marcus D GoncalvesMeyer Cancer Center, Department of Medicine, Weill Cornell Medicine, New York, NY, USA.ORCID http://orcid.org/0000-0002-0784-9248
Lewis C CantleyMeyer Cancer Center, Department of Medicine, Weill Cornell Medicine, New York, NY, USA.ORCID http://orcid.org/0000-0002-1298-7653
Cornell University · USIcahn School of Medicine at Mount Sinai · US

Funding

Role of Phosphoinositides and Protein Kinases in the control of Cancer MetabolismR35CA197588 · NCI · WEILL MEDICAL COLL OF CORNELL UNIV · PI LEWIS C. CANTLEY · 2016 to 2026
$10.2M
Utilizing Precision Medicine to elucidate the mechanisms underpinning treatment efficacyR00CA230384 · NCI · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI HOPKINS, BENJAMIN D. · 2019 to 2021
$718k
The Role of Hypoketonemia in the Cancer Anorexia-Cachexia SyndromeK08CA230318 · NCI · WEILL MEDICAL COLL OF CORNELL UNIV · PI GONCALVES, MARCUS DASILVA · 2018 to 2021
$599k
NCI NIH HHS K08 CA230318NCI NIH HHS R00 CA230384NCI NIH HHS R35 CA197588
6 · The paper itself

Abstract

Cancer is driven by incremental changes that accumulate, eventually leading to oncogenic transformation. Although genetic alterations dominate the way cancer biologists think about oncogenesis, growing evidence suggests that systemic factors (for example, insulin, oestrogen and inflammatory cytokines) and their intracellular pathways activate oncogenic signals and contribute to targetable phenotypes. Systemic factors can have a critical role in both tumour initiation and therapeutic responses as increasingly targeted and personalized therapeutic regimens are used to treat patients with cancer. The endocrine system controls cell growth and metabolism by providing extracellular cues that integrate systemic nutrient status with cellular activities such as proliferation and survival via the production of metabolites and hormones such as insulin. When insulin binds to its receptor, it initiates a sequence of phosphorylation events that lead to activation of the catalytic activity of phosphoinositide 3-kinase (PI3K), a lipid kinase that coordinates the intake and utilization of glucose, and mTOR, a kinase downstream of PI3K that stimulates transcription and translation. When chronically activated, the PI3K pathway can drive malignant transformation. Here, we discuss the insulin-PI3K signalling cascade and emphasize its roles in normal cells (including coordinating cell metabolism and growth), highlighting the features of this network that make it ideal for co-option by cancer cells. Furthermore, we discuss how this signalling network can affect therapeutic responses and how novel metabolic-based strategies might enhance treatment efficacy for cancer.

Indexed as

AnimalsBiological EvolutionEndocrine SystemHumansInsulinNeoplasmsPhosphatidylinositol 3-KinasesSignal TransductionInsulinPhosphatidylinositol 3-Kinases

Identifiers

PMID32127696
PMCPMC7286536
OpenAlexW3009258273

What OpenQuestion holds

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Read underepoch 390

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.