Evidence map›Paper›PMID 1423822›Full record

ReviewCancer metastasis reviews1992

Adhesion molecules and tumor cell interaction with endothelium and subendothelial matrix.

K V Honn, D G Tang

Abstract readReview
PubMed Publisher
In one paragraph

Review in Cancer metastasis reviews, 1992. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed
4.5field-weighted citation impact, top 4% 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

62 citing papers in PubMed, 231 citations in OpenAlex.

  1. Mucin Glycans: A Target for Cancer Therapy.Molecules (Basel, Switzerland) · 2023
    Review
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  19. Novel INTeraction of MUC4 and galectin: potential pathobiological implications for metastasis in lethal pancreatic cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2011
    Article
  20. Physiopathology of spine metastasis.International journal of surgical oncology · 2011
    Article

2 more citing papers are in PubMed but not listed here.

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.

K V HonnDepartment of Radiation Oncology, Wayne State University, Detroit, MI 48202.
D G Tang
Wayne State University · US

Funding

THROMBOXANES: ROLE IN TUMOR GROWTH AND METASTASISR01CA029997 · NCI · WAYNE STATE UNIVERSITY · PI HONN, KENNETH V · 1985 to 2008
$1.7M
TUMOR CELL ADHESIVE GLYCOPROTEINS AND METASTASISR01CA047115 · NCI · WAYNE STATE UNIVERSITY · PI HONN, KENNETH V · 1988 to 2004
$1.0M
NCI NIH HHS CA 29997-10NCI NIH HHS CA 47115-06
6 · The paper itself

Abstract

Cancer metastasis poses the greatest challenge to the eradication of malignancy. The majority of clinical and experimental evidence indicates that metastasis is a non-random, organ-specific process. Tumor cell interaction with endothelium and subendothelial matrix constitutes the most crucial factor in determining the organ preference of metastasis. A plethora of cell surface adhesion molecules, which encompass four major families (i.e., integrins, cadherins, immunoglobulins and selectins) and many other unclassified molecules, mediate tumor-host interactions. Adhesion molecules and adhesion processes are involved in most, if not all, of the intermediate steps of the metastatic cascade. Decreased E-cadherin expression and increased CD44 expression are clearly correlated with the acquisition of the invasive capacity of primary tumor cells. Similarly, altered expression pattern of many other adhesion molecules such as upregulated expression of the laminin receptors and depressed expression of fibronectin receptors (alpha 5 beta 1) appears to be involved in tumor cell invasion into the subendothelial matrix. Tumor cell-endothelium interactions involve several well-defined sequential steps that can be analyzed by the 'Docking and Locking' hypothesis at the molecular level. Tumor cell-matrix interactions are determined by the repertoire of adhesion receptors of tumor cells and the unique composition of organ-specific matrices. Our experimental data, together with others', suggest that the integrin alpha IIb beta 3 is one of the major players in these tumor-host interactions. Tumor-host interaction is a dynamic process which is constantly modulated by a host of factors including various cytokines, growth factors and arachidonate metabolites such as 12(S)-HETE. Delineation of the molecular mechanisms of tumor-host interactions may provide additional means to intervene in the metastatic process.

Indexed as

Neoplastic Cells, CirculatingAnimalsCell AdhesionCell Adhesion MoleculesEndothelium, VascularExtracellular MatrixHumansNeoplasm MetastasisOrgan SpecificityCell Adhesion Molecules

Identifiers

PMID1423822
OpenAlexW2031142145

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.