Evidence map›Paper›PMID 21819957›Full record

ArticleThe American journal of pathology2011

Phosphatase and tensin homolog on chromosome 10 is phosphorylated in primary effusion lymphoma and Kaposi's sarcoma.

Debasmita Roy, Dirk P Dittmer

Open access · greenAbstract read
In one paragraph

Article in The American journal of pathology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.7field-weighted citation impact, top 15% 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

21 citing papers in PubMed, 27 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Precise Immunodetection of PTEN Protein in Human Neoplasia.Cold Spring Harbor perspectives in medicine · 2019
    Review
  6. Article
  7. Article
  8. PTEN proteoforms in biology and disease.Cellular and molecular life sciences : CMLS · 2017
    Review
  9. Article
  10. Article
  11. The expression profiles of microRNAs in Kaposi's sarcoma.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015
    Article
  12. Review
  13. Article
  14. Modulation of B-cell exosome proteins by gamma herpesvirus infection.Proceedings of the National Academy of Sciences of the United States of America · 2013
    Article
  15. Article
  16. Dysregulation of fatty acid synthesis and glycolysis in non-Hodgkin lymphoma.Proceedings of the National Academy of Sciences of the United States of America · 2012
    Article
  17. Article
  18. Rapalogs in viral cancers.Expert opinion on investigational drugs · 2012
    Article
  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

2 authors at 1 institution in 1 country.

Debasmita RoyCurriculum in Genetics and Molecular Biology, Lineberger Comprehensive Cancer Center, Center for AIDS Research, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599-7290, USA.
Dirk P Dittmer
University of North Carolina at Chapel Hill · US

Funding

West Coast AIDS and Cancer Specimen Resource (ACSR)U01CA066529 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI MCGRATH, MICHAEL SHANNON · 1994 to 2012
$16.1M
ART Modulation of Viral Pathogenesis in Oral EpitheliaR01DE018304 · NIDCR · UNIV OF NORTH CAROLINA CHAPEL HILL · PI DITTMER, DIRK P · 2007 to 2025
$6.9M
Targeted Therapies for HIV-Associated Kaposi Sarcoma and LymphomaR01CA163217 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI BLOSSOM A DAMANIA, Dirk P Dittmer · 2011 to 2026
$5.5M
NCI NIH HHS CA066529NCI NIH HHS CA163217NCI NIH HHS R01 CA163217NCI NIH HHS U01 CA066529NIDCR NIH HHS DE018304NIDCR NIH HHS R01 DE018304
6 · The paper itself

Abstract

Primary effusion lymphoma (PEL) is a non-Hodgkin's B-cell lymphoma driven by Kaposi's sarcoma-associated herpesvirus. It is uniquely sensitive to mTOR, PI3K, and Akt inhibitors; however, the basis of this requirement for the mTOR pathway remains to be elucidated. The phosphatase and tensin homolog gene (PTEN) on chromosome 10 controls the first step in the phosphatidylinositol 3 kinase (PI3K)-Akt-mammalian target of rapamycin (mTOR) pathway and is genetically inactivated in many solid tumors. We find an absence of PTEN deletions, mutations, or protein mislocalization in PEL. However, we find consistent hyperphosphorylation at serine 380 of PTEN, which is an inactivating modification, in PEL cell lines and in tumor xenografts. We also evaluated a large tissue microarray of Kaposi's sarcoma biopsies and observed concordant high levels of phospho-PTEN, phospho-Akt, and phospho-S6 ribosomal protein. Reintroduction of PTEN into PEL inhibited colony formation in soft agar, verifying the functional dependence of PEL on PI3K signaling. This was also true for PEL cell lines that carried mutant p53 and for KS-like cell lines. Activating PTEN in these cancers may yield a new treatment strategy for PEL, KS, and similar PTEN wild-type lymphomas.

Indexed as

AnimalsBiopsyCell Line, TumorCell ProliferationDisease Models, AnimalEnzyme ActivationHumansImmunohistochemistryLymphoma, Primary EffusionMicePhosphatidylinositol 3-KinasesPhosphorylationPhosphoserineProto-Oncogene Proteins c-aktPTEN PhosphohydrolaseRibosomal Protein S6Phosphatidylinositol 3-KinasesPhosphoserineProto-Oncogene Proteins c-aktPTEN PhosphohydrolasePTEN protein, humanRibosomal Protein S6

Identifiers

PMID21819957
PMCPMC3181371
OpenAlexW2071146908

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.