Evidence map›Paper›PMID 20855625›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2010

Polymorphic genetic control of tumor invasion in a mouse model of pancreatic neuroendocrine carcinogenesis.

Matthew G H Chun, Jian-Hua Mao, Christopher W Chiu, Allan Balmain, Douglas Hanahan

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.1field-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

15 citing papers in PubMed, 21 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. The dark side of synaptic proteins in tumours.British journal of cancer · 2022
    Review
  5. Article
  6. Article
  7. A set of microRNAs coordinately controls tumorigenesis, invasion, and metastasis.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. 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

5 authors at 3 institutions in 3 countries.

Matthew G H ChunDepartment of Biochemistry and Biophysics, Diabetes Center, and Helen Diller Family Comprehensive Cancer Center, University of California, San Francisco, CA 94143, USA.
Jian-Hua Mao
Christopher W Chiu
Allan Balmain
Douglas Hanahan
UCSF Helen Diller Family Comprehensive Cancer Center · USUniversity of California, San Francisco · USDiabetes Australia · AU

Funding

Identification of epithelial tumor susceptiility genesU01CA084244 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI BALMAIN, ALLAN · 1999 to 2013
$13.3M
Genetic Analysis of Developmental MutationsU01HD043430 · NICHD · BRIGHAM AND WOMEN'S HOSPITAL · PI BEIER, DAVID R. · 2002 to 2007
$5.5M
TARGETED ONCOGENESIS AND DIABETES IN TRANSGENIC MICER01CA045234 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI HANAHAN, DOUGLAS · 1987 to 2009
$2.5M
NCI NIH HHS 5R01CA45234-24NCI NIH HHS R01 CA045234NCI NIH HHS U01 CA084244NCI NIH HHS U01-CA84244NICHD NIH HHS U01 HD043430NICHD NIH HHS U01-HD43430
6 · The paper itself

Abstract

Cancer is a disease subject to both genetic and environmental influences. In this study, we used the RIP1-Tag2 (RT2) mouse model of islet cell carcinogenesis to identify a genetic locus that influences tumor progression to an invasive growth state. RT2 mice inbred into the C57BL/6 (B6) background develop both noninvasive pancreatic neuroendocrine tumors (PNET) and invasive carcinomas with varying degrees of aggressiveness. In contrast, RT2 mice inbred into the C3HeB/Fe (C3H) background are comparatively resistant to the development of invasive tumors, as are RT2 C3HB6(F1) hybrid mice. Using linkage analysis, we identified a 13-Mb locus on mouse chromosome 17 with significant linkage to the development of highly invasive PNETs. A gene residing in this locus, the anaplastic lymphoma kinase (Alk), was expressed at significantly lower levels in PNETs from invasion-resistant C3H mice compared with invasion-susceptible B6 mice, and pharmacological inhibition of Alk led to reduced tumor invasiveness in RT2 B6 mice. Collectively, our results demonstrate that tumor invasion is subject to polymorphic genetic control and identify Alk as a genetic modifier of invasive tumor growth.

Indexed as

Polymorphism, GeneticAdenoma, Islet CellAnaplastic Lymphoma KinaseAnimalsCell Transformation, NeoplasticChromosomes, MammalianGenetic LinkageGenetic LociMiceMice, Inbred C3HMice, Inbred C57BLPancreatic NeoplasmsProtein-Tyrosine KinasesPyrimidinesReceptor Protein-Tyrosine KinasesAlk protein, mouseAnaplastic Lymphoma KinaseNVP-TAE684Protein-Tyrosine KinasesPyrimidinesReceptor Protein-Tyrosine Kinases

Identifiers

PMID20855625
PMCPMC2951397
OpenAlexW2046784076

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.