Evidence map›Paper›PMID 35366325›Full record

ReviewEndocrinology2022

Targeting mTOR in the Context of Diet and Whole-body Metabolism.

Nikos Koundouros, John Blenis

Open access · bronzeAbstract readReview
In one paragraph

Review in Endocrinology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.0field-weighted citation impact, top 26% 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

10 citing papers in PubMed, 15 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
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

2 authors at 1 institution in 1 country.

Nikos KoundourosMeyer Cancer Center, Weill Cornell Medicine, New York, NY 10021,USA.ORCID 0000-0001-8378-9673
John BlenisMeyer Cancer Center, Weill Cornell Medicine, New York, NY 10021,USA.ORCID 0000-0003-3622-2337
Cornell University · US

Funding

SIGNAL TRANSDUCTION TO PP70 S6KR01GM051405 · NIGMS · WEILL MEDICAL COLL OF CORNELL UNIV · PI BLENIS, JOHN · 1995 to 2023
$14.0M
ONCOGENIC REGULATION OF S6 PROTEIN KINASE &CELL GROWTHR01CA046595 · NCI · WEILL MEDICAL COLL OF CORNELL UNIV · PI JOHN BLENIS · 1988 to 2026
$10.6M
NCI NIH HHS R01 CA046595NIGMS NIH HHS R01 GM051405
6 · The paper itself

Abstract

The mechanistic target of the rapamycin (mTOR) signaling pathway is the central regulator of cell growth and proliferation by integrating growth factor and nutrient availability. Under healthy physiological conditions, this process is tightly coordinated and essential to maintain whole-body homeostasis. Not surprisingly, dysregulated mTOR signaling underpins several diseases with increasing incidence worldwide, including obesity, diabetes, and cancer. Consequently, there is significant clinical interest in developing therapeutic strategies that effectively target this pathway. The transition of mTOR inhibitors from the bench to bedside, however, has largely been marked with challenges and shortcomings, such as the development of therapy resistance and adverse side effects in patients. In this review, we discuss the current status of first-, second-, and third-generation mTOR inhibitors as a cancer therapy in both preclinical and clinical settings, with a particular emphasis on the mechanisms of drug resistance. We focus especially on the emerging role of diet as an important environmental determinant of therapy response, and posit a conceptual framework that links nutrient availability and whole-body metabolic states such as obesity with many of the previously defined processes that drive resistance to mTOR-targeted therapies. Given the role of mTOR as a central integrator of cell metabolism and function, we propose that modulating nutrient inputs through dietary interventions may influence the signaling dynamics of this pathway and compensatory nodes. In doing so, new opportunities for exploiting diet/drug synergies are highlighted that may unlock the therapeutic potential of mTOR inhibitors as a cancer treatment.

Indexed as

Signal TransductionTOR Serine-Threonine KinasesDietHumansObesitySirolimusMTOR protein, humanSirolimusTOR Serine-Threonine Kinasesdietdrug resistancemetabolismmTOR

Identifiers

PMID35366325
PMCPMC9391686
OpenAlexW4225688078

What Socratic holds

Textmetadata
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 Socratic graph.