Evidence map›Paper›PMID 21258412›Full record

ReviewOncogene2011

The long and winding road to rational treatment of cancer associated with LKB1/AMPK/TSC/mTORC1 signaling.

W van Veelen, S E Korsse, L van de Laar, M P Peppelenbosch

Abstract readReview
PubMed Publisher
In one paragraph

Review in Oncogene, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed
9.9field-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

61 citing papers in PubMed, 127 citations in OpenAlex.

  1. Trial
  2. The Role of Sigmar1 in Autophagy Regulation and Disease Therapy.International journal of molecular sciences · 2026
    Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Review
  16. Review
  17. The Tumor Suppressor Kinase LKB1: Metabolic Nexus.Frontiers in cell and developmental biology · 2022
    Review
  18. LKB1-PTEN axis controls Th1 and Th17 cell differentiation via regulating mTORC1.Journal of molecular medicine (Berlin, Germany) · 2021
    Article
  19. Review
  20. Review

1 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

4 authors at 1 institution in 1 country.

W van VeelenDepartment of Gastroenterology and Hepatology, Erasmus Medical University Center, Rotterdam, The Netherlands.
S E Korsse
L van de Laar
M P Peppelenbosch
Erasmus MC · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The liver kinase B1 (LKB1)/adenosine mono-phosphate-activated protein kinase (AMPK)/tuberous sclerosis complex (TSC)/mammalian target of rapamycin (mTOR) complex (mTORC1) cassette constitutes a canonical signaling pathway that integrates information on the metabolic and nutrient status and translates this into regulation of cell growth. Alterations in this pathway are associated with a wide variety of cancers and hereditary hamartoma syndromes, diseases in which hyperactivation of mTORC1 has been described. Specific mTORC1 inhibitors have been developed for clinical use, and these drugs have been anticipated to provide efficient treatment for these diseases. In the present review, we provide an overview of the metabolic LKB1/AMPK/TSC/mTORC1 pathway, describe how its aberrant signaling associates with cancer development, and indicate the difficulties encountered when biochemical data are extrapolated to provide avenues for rational treatment of disease when targeting this signaling pathway. A careful examination of preclinical and clinical studies performed with rapamycin or derivatives thereof shows that although results are encouraging, we are only half way in the long and winding road to design rationale treatment targeted at the LKB1/AMPK/TSC/mTORC1 pathway. Inherited cancer syndromes associated with this pathway such as the Peutz-Jeghers syndrome and TSC, provide perfect models to study the relationship between genetics and disease phenotype, and to delineate the complexities that underlie translation of biochemical and genetical information to clinical management, and thus provide important clues for devising novel rational medicine for cancerous diseases in general.

Indexed as

Signal TransductionAMP-Activated Protein Kinase KinasesAntibiotics, AntineoplasticHumansMolecular Targeted TherapyNeoplasmsProtein KinasesProtein Serine-Threonine KinasesSirolimusTOR Serine-Threonine KinasesTuberous SclerosisAMP-Activated Protein Kinase KinasesAntibiotics, AntineoplasticMTOR protein, humanProtein KinasesProtein Serine-Threonine KinasesSirolimusSTK11 protein, humanTOR Serine-Threonine Kinases

Identifiers

PMID21258412
OpenAlexW1522420112

What OpenQuestion 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 OpenQuestion graph.