Evidence map›Paper›PMID 21519908›Full record

ReviewFamilial cancer2011

LKB1 signaling in advancing cell differentiation.

Lina Udd, Tomi P Mäkelä

Abstract readReview
PubMed Publisher
In one paragraph

Review in Familial cancer, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

8 citing papers in PubMed, 12 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. MicroRNA-17 promotes normal ovarian cancer cells to cancer stem cells development via suppression of the LKB1-p53-p21/WAF1 pathway.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015
    Article
  5. Article
  6. Lkb1/Stk11 regulation of mTOR signaling controls the transition of chondrocyte fates and suppresses skeletal tumor formation.Proceedings of the National Academy of Sciences of the United States of America · 2013
    Article
  7. Article
  8. Article
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.

Lina UddInstitute of Biotechnology and Genome-Scale Biology Research Program, University of Helsinki, P.O. Box 56 (Biocenter 1), 00014, Helsinki, Finland.
Tomi P Mäkelä
University of Helsinki · FI

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The Peutz-Jeghers syndrome (PJS) culprit kinase LKB1 phosphorylates and activates multiple intracellular kinases regulating cell metabolism and polarity. The relevance of each of these pathways is highly variable depending on the tissue type, but typically represents functions of differentiated cells. These include formation and maintenance of specialized cell compartments in nerve axons, swift refunneling of metabolites and restructuring of cell architecture in response to environmental cues in committed lymphocytes, and ensuring energy-efficient oxygen-based energy expenditure. Such features are often lost or reduced in cancer cells, and indeed LKB1 defects in PJS-associated and sporadic cancers and even the benign PJS polyps lead to differentiation defects, including expansion of partially differentiated epithelial cells in PJS polyps and epithelial-to-mesenchymal transition in carcinomas. This review focuses on the involvement of LKB1 in the differentiation of epithelial, mesenchymal, hematopoietic and germinal lineages.

Indexed as

Cell DifferentiationAMP-Activated Protein Kinase KinasesCell PolarityHumansPeutz-Jeghers SyndromeProtein Serine-Threonine KinasesAMP-Activated Protein Kinase KinasesProtein Serine-Threonine KinasesSTK11 protein, human

Identifiers

PMID21519908
OpenAlexW2112292650

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.