Evidence map›Paper›PMID 9689095›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America1998

In vitro loss of heterozygosity targets the PTEN/MMAC1 gene in melanoma.

G P Robertson, F B Furnari, M E Miele, M J Glendening, D R Welch, J W Fountain, T G Lugo, H J Huang, W K Cavenee

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
3.1field-weighted citation impact, top 7% 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

33 citing papers in PubMed, 97 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Truncating PREX2 mutations activate its GEF activity and alter gene expression regulation in NRAS-mutant melanoma.Proceedings of the National Academy of Sciences of the United States of America · 2016
    Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Melanoma: from mutations to medicine.Genes & development · 2012
    Review
  10. Genetic alterations of PTEN in human melanoma.Cellular and molecular life sciences : CMLS · 2012
    Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Oncogenic mutations of PIK3CA in human cancers.Current topics in microbiology and immunology · 2010
    Review
  17. Review
  18. Genetics and genomics of melanoma.Expert review of dermatology · 2009
    Article
  19. Article
  20. 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

9 authors at 4 institutions in 1 country.

G P RobertsonLudwig Institute for Cancer Research, University of California-San Diego, La Jolla, CA 92093-0660, USA. gprobertson@ucsd.edu
F B Furnari
M E Miele
M J Glendening
D R Welch
J W Fountain
T G Lugo
H J Huang
W K Cavenee
National Cancer Institute · USCancer Research Institute · USLudwig Cancer Research · USUniversity of Southern California · US

Funding

METASTASIS SUPPRESSOR GENES IN HUMAN CUTANEOUS MELANOMAR01CA062168 · NCI · PENNSYLVANIA STATE UNIV HERSHEY MED CTR · PI WELCH, DANNY R · 1994 to 1999
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UNRAVELING THE ROLE OF 9P21 GENE MUTATIONS IN MELANOMAR01CA066021 · NCI · UNIVERSITY OF SOUTHERN CALIFORNIA · PI FOUNTAIN, JANE W. · 1995 to 1997
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INSTRUMENTAL ANALYSISZ01CT000197 · CIT · COMPUTER RESEARCH AND TECHNOLOGY · PI WEISS, G H · 1990 to 1990
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CIT NIH HHS CCT0197NCI NIH HHS CA62168NCI NIH HHS CA66021
6 · The paper itself

Abstract

Gross genetic lesions of chromosome 10 occur in 30-50% of sporadic human melanomas. To test the functional significance of this observation, we have developed an in vitro loss of heterozygosity approach in which a wild-type chromosome 10 was transferred into melanoma cells, where there was selection for its breakage and regional deletion to relieve its growth suppressive effects. The overlap of these events was at band 10q23, the site of the recently isolated PTEN/MMAC1 tumor suppressor gene, suggesting it as a potential target. Although the gene was expressed in the parental cells, both of its chromosomal alleles contained truncating mutations. In vitro loss of heterozygosity resulted in loss of the chromosomally introduced wild-type PTEN/MMAC1, and ectopic expression of the gene caused cell growth suppression. Thus, this approach identified PTEN/MMAC1 as a target in malignant melanoma and may provide an alternative means to localizing tumor suppressor genes.

Indexed as

Loss of HeterozygosityPhosphoric Monoester HydrolasesTumor Suppressor ProteinsBase SequenceDNA PrimersHumansMelanomaProtein Tyrosine PhosphatasesPTEN PhosphohydrolaseTumor Cells, CulturedDNA PrimersPhosphoric Monoester HydrolasesProtein Tyrosine PhosphatasesPTEN PhosphohydrolasePTEN protein, humanTumor Suppressor Proteins

Identifiers

PMID9689095
PMCPMC21353
OpenAlexW2139011197

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.