Evidence map›Paper›PMID 10854236›Full record

ArticleThe American journal of pathology2000

Perturbation of hyaluronan interactions by soluble CD44 inhibits growth of murine mammary carcinoma cells in ascites.

R M Peterson, Q Yu, I Stamenkovic, B P Toole

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

31 citing papers in PubMed, 111 citations in OpenAlex.

  1. Review
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  13. Review
  14. Inhibition of Functional Hyaluronan-CD44 Interactions in CD133-positive Primary Human Ovarian Carcinoma Cells by Small Hyaluronan Oligosaccharides.Clinical cancer research : an official journal of the American Association for Cancer Research · 2009
    Article
  15. Protumorigenic role of HAPLN1 and its IgV domain in malignant pleural mesothelioma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2009
    Article
  16. Review
  17. Hyaluronan, CD44 and Emmprin: partners in cancer cell chemoresistance.Drug resistance updates : reviews and commentaries in antimicrobial and anticancer chemotherapy · 2008
    Review
  18. Article
  19. Article
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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

4 authors at 2 institutions in 1 country.

R M PetersonDepartment of Anatomy and Cellular Biology, Tufts University School of Medicine, Massachusetts General Hospital, Boston, MA 02111, USA.
Q Yu
I Stamenkovic
B P Toole
Massachusetts General Hospital · USTufts University · US

Funding

Inhibition of Tumor Progression by Hyaluronan OligomersR01CA073839 · NCI · TUFTS UNIVERSITY BOSTON · PI TOOLE, BRYAN P · 1997 to 2008
$1.8M
BIOLOGY AND FUNCTION OF LYMPHOCYTE ADHESION MOLECULESR01GM048614 · NIGMS · MASSACHUSETTS GENERAL HOSPITAL · PI STAMENKOVIC, IVAN · 1994 to 2001
$533k
BIOLOGY AND FUNCTION OF CD44 ISOFORMSR01CA055735 · NCI · MASSACHUSETTS GENERAL HOSPITAL · PI STAMENKOVIC, IVAN · 1992 to 2001
$495k
NCI NIH HHS CA55735NCI NIH HHS CA73839NCI NIH HHS R01 CA073839NIGMS NIH HHS GM48614
6 · The paper itself

Abstract

Hyaluronan accumulates in ascites during intraperitoneal proliferation of TA3/St murine mammary carcinoma cells and at sites of their invasion of the peritoneal wall. To determine whether hyaluronan is functionally involved in these events, ascites tumor formation was compared in mice injected intraperitoneally with stable transfectants of TA3/St cells that overexpress soluble CD44, a hyaluronan-binding protein, versus in mice injected with transfectants expressing mutated soluble CD44 that does not bind hyaluronan. The soluble CD44 transfectants temporarily grew at a reduced rate within the peritoneal cavity, then went into G(1) arrest and were subsequently cleared from the peritoneum. However, transfectants overexpressing mutant soluble CD44 that does not bind hyaluronan exhibited similar ascites accumulation, growth rates, and cell-cycle profiles in vivo to wild-type and vector-transfected TA3/St cells, all of which continued to grow until the tumors became fatal. The soluble CD44-transfected TA3/St cells also failed to attach to and form tumors in the peritoneal wall. When grown in vitro in soft agar, the soluble CD44 transfectants exhibited a dramatic reduction in colony formation compared to wild-type, vector-transfected, and mutant soluble CD44-transfected TA3/St cells. Thus, perturbation of hyaluronan interactions by soluble CD44 has a direct effect on the growth characteristics of these tumor cells, leading to inhibition of anchorage-independent growth in vitro and ascites growth in vivo.

Indexed as

AnimalsAscitesCarcinomaCell DivisionDrug InteractionsFemaleG1 PhaseHyaluronan ReceptorsHyaluronic AcidMammary Neoplasms, ExperimentalMiceNeoplasm InvasivenessPeritoneumSolubilityTransfectionTumor Cells, CulturedHyaluronan ReceptorsHyaluronic Acid

Identifiers

PMID10854236
PMCPMC1850079
OpenAlexW2064818784

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.