Evidence map›Paper›PMID 23719831›Full record

ArticleCancer discovery2013

Pten-null tumors cohabiting the same lung display differential AKT activation and sensitivity to dietary restriction.

Natasha L Curry, Mari Mino-Kenudson, Trudy G Oliver, Omer H Yilmaz, Vedat O Yilmaz, Jade Y Moon, Tyler Jacks, David M Sabatini, Nada Y Kalaany

Open access · bronzeAbstract read
In one paragraph

Article in Cancer discovery, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 1 pooled it
2.4field-weighted citation impact, top 11% 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

25 citing papers in PubMed, 1 synthesis or guideline pooled it, 39 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Ablation of insulin receptor substrates 1 and 2 suppressesProceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. Article
  20. 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

9 authors at 5 institutions in 1 country.

Natasha L CurryDivision of Endocrinology, Center for Basic and Translational Obesity Research, Boston , MA 02115, USA.
Mari Mino-Kenudson
Trudy G Oliver
Omer H Yilmaz
Vedat O Yilmaz
Jade Y Moon
Tyler Jacks
David M Sabatini
Nada Y Kalaany
Koch Institute for Integrative Cancer Research At MITBroad Institute · USHarvard University · USAllen Institute · USMassachusetts Institute of Technology · US

Funding

VIRUS PRODUCTION COREP30CA014051 · NCI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI Jacqueline A. Lees · 1985 to 2026
$93.9M
Regulation of the mTOR Pathway By NutrientsR01CA103866 · NCI · WHITEHEAD INSTITUTE FOR BIOMEDICAL RES · PI WEISSMAN, JONATHAN S. · 2004 to 2021
$7.0M
Cell Growth Signaling in Cancer DevelopmentR01CA129105 · NCI · WHITEHEAD INSTITUTE FOR BIOMEDICAL RES · PI WEISSMAN, JONATHAN S. · 2008 to 2021
$5.9M
TRANSLATIONAL CONTROL BY RAPAMYCIN-SENSITIVE SIGNALINGR01AI047389 · NIAID · WHITEHEAD INSTITUTE FOR BIOMEDICAL RES · PI WEISSMAN, JONATHAN S. · 2000 to 2021
$4.9M
Regulation of the Intestinal Stem Cell Niche in AgingK99AG045144 · NIA · WHITEHEAD INSTITUTE FOR BIOMEDICAL RES · PI YILMAZ, OMER · 2013 to 2014
$275k
Howard Hughes Medical InstituteNCI NIH HHS 2-P30-CA14051NCI NIH HHS P30 CA014051NCI NIH HHS R01 CA103866NCI NIH HHS R01 CA129105NIAID NIH HHS R01 AI047389NIA NIH HHS K99 AG045144
6 · The paper itself

Abstract

PTEN loss is considered a biomarker for activated phosphoinositide 3-kinase (PI3K)/AKT, a pathway frequently mutated in cancer, and was recently shown to confer resistance to dietary restriction. Here, we show that Pten loss is not sufficient to drive AKT activation and resistance to dietary restriction in tumors with low growth factor receptor levels. We describe a murine Pten-null Kras-driven lung cancer model that harbors both dietary restriction-resistant, higher-grade, bronchiolar tumors with high AKT activity, and dietary restriction-sensitive, lower-grade, alveolar tumors with low AKT activity. We find that this phenotype is cell autonomous and that normal bronchiolar cells express higher levels of insulin-like growth factor-I receptor (IGF-IR) and of ectonucleoside triphosphate diphosphohydrolase 5 (ENTPD5), an endoplasmic reticulum enzyme known to modulate growth factor receptor levels. Suppression of ENTPD5 is sufficient to decrease IGF-IR levels and sensitize bronchiolar tumor cells to serum in vitro and to dietary restriction in vivo. Furthermore, we find that a significant percentage of human non-small cell lung carcinomas (NSCLC) have low AKT activity despite PTEN loss.

Indexed as

Caloric RestrictionAnimalsCarcinoma, Non-Small-Cell LungDisease Models, AnimalHumansLung NeoplasmsMiceOncogene ProteinsPhenotypePhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktProto-Oncogene Proteins p21(ras)PTEN PhosphohydrolasePyrophosphatasesTumor Cells, CulturedENTPD5 protein, humanHras protein, mouseOncogene ProteinsPcph protein, mousePhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktProto-Oncogene Proteins p21(ras)PTEN PhosphohydrolasePten protein, mousePyrophosphatases

Identifiers

PMID23719831
PMCPMC3743121
OpenAlexW2147952720

What OpenQuestion holds

Textmetadata
LicenceTDM
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.