Evidence map›Paper›PMID 11480565›Full record

ArticleLeukemia2001

Cell adhesion-mediated drug resistance (CAM-DR) protects the K562 chronic myelogenous leukemia cell line from apoptosis induced by BCR/ABL inhibition, cytotoxic drugs, and gamma-irradiation.

J S Damiano, L A Hazlehurst, W S Dalton

Abstract read
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In one paragraph

Article in Leukemia, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers.

0numbers the graph read from it
0cells of the map it votes in
73citing papers in PubMed
3.3field-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

73 citing papers in PubMed, 186 citations in OpenAlex.

  1. Trial
  2. Review
  3. Beyond DNA damage: 3D tumor models and the integrin mechanobiology of radioresistance.Journal of experimental & clinical cancer research : CR · 2026
    Review
  4. Review
  5. Article
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  7. Article
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  15. Effect of mechanical forces on cellular response to radiation.Radiotherapy and oncology : journal of the European Society for Therapeutic Radiology and Oncology · 2022
    Review
  16. Article
  17. Article
  18. Experimental and therapeutic medicine · 2022
    Article
  19. Article
  20. Article

13 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

3 authors at 2 institutions in 1 country.

J S DamianoDepartment of Interdisciplinary Oncology, H Lee Moffitt Cancer Center and Research Institute, University of South Florida Tampa 33612, USA.
L A Hazlehurst
W S Dalton
Moffitt Cancer Center · USUniversity of South Florida · US

Funding

STAT SIGNALING IN TUMOR PROGRESSIONP01CA082533 · NCI · UNIVERSITY OF SOUTH FLORIDA · PI JOVE, RICHARD · 2000 to 2004
$5.8M
DRUG RESISTANCE IN MULTIPLE MYELOMAR01CA077859 · NCI · UNIVERSITY OF SOUTH FLORIDA · PI DALTON, WILLIAM STEVEN · 1998 to 2011
$3.5M
NCI NIH HHS CA77859NCI NIH HHS CA82533
6 · The paper itself

Abstract

Integrin-mediated cellular adhesion to extracellular matrix (ECM) components is an important determinant of chemotherapeutic response of human myeloma cells. Here, we demonstrate that when K562 chronic myelogenous leukemia (CML) cells are adhered to fibronectin (FN), they become resistant to apoptosis induced by the BCR/ABL inhibitors AG957 and STI-571, as well as DNA damaging agents and gamma-irradiation. This phenomenon, termed cell adhesion-mediated drug resistance (CAM-DR), was induced by adhesion through the alpha5beta1 (VLA-5) integrin. Phosphotyrosine analysis demonstrates that anti-apoptotic signaling through integrins in K562 cells is independent of the tyrosine kinases activated by BCR/ABL, with the possible exception of an unknown 80 kDa protein. Cytoprotection of FN-adhered CML cells indicates that tumor-ECM interactions may be critical for the emergence of drug-resistant tumor populations and treatment failure in this disease. Antagonists of beta1 integrin-mediated adhesion or corresponding signal transduction elements may sensitize CML cells to chemotherapy and prevent resistance to the novel BCR/ABL kinase inhibitors being used for the treatment of this disease.

Indexed as

Antineoplastic AgentsApoptosisCell AdhesionDrug Resistance, NeoplasmGenes, ablHumansK562 CellsLeukemia, Myelogenous, Chronic, BCR-ABL PositiveReceptors, FibronectinSignal TransductionAntineoplastic AgentsReceptors, Fibronectin

Identifiers

PMID11480565
OpenAlexW2326572877

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.