Evidence map›Paper›PMID 8529099›Full record

ArticleMolecular medicine (Cambridge, Mass.)1995

Expression cloning of cDNAs that render cancer cells resistant to Pseudomonas and diphtheria toxin and immunotoxins.

U Brinkmann, E Brinkmann, I Pastan

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in Molecular medicine (Cambridge, Mass.), 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

13 citing papers in PubMed, 42 citations in OpenAlex.

  1. Article
  2. Role of CSE1L expression in determining recurrence and survival of laryngeal tumors.European archives of oto-rhino-laryngology : official journal of the European Federation of Oto-Rhino-Laryngological Societies (EUFOS) : affiliated with the German Society for Oto-Rhino-Laryngology - Head and Neck Surgery · 2022
    Article
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  5. CAS (CSE1L) signaling pathway in tumor progression and its potential as a biomarker and target for targeted therapy.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
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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

3 authors at 3 institutions in 4 countries.

U BrinkmannLaboratory of Molecular Biology, Division of Cancer Biology, Diagnosis, and Centers, Bethesda, Maryland, USA.
E Brinkmann
I Pastan
Eunice Kennedy Shriver National Institute of Child Health and Human Development · USNational Cancer Institute · USNational Institutes of Health · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundSeveral immunotoxins in which antibodies are coupled to plant or bacterial toxins are now in clinical trials for the treatment of cancer. One of these is B3-LysPE38 in which MAb B3 which reacts with many human cancers, is coupled with a genetically modified form of Pseudomonas exotoxin (PE). MATERIALS AND

methodsTo investigate how cells can become resistant to PE-derived immunotoxins, we constructed an immunotoxin-sensitive MCF-7 breast cancer cell line that contains SV40 T antigen and allows episomal replication of SV40 origin containing plasmids. We transfected a pCDM8/HeLa cDNA expression library into these cells, thereby causing over-expression of the plasmid-encoded genes. The transfected cells were treated with immunotoxin to select for resistance-mediating plasmids, which were reisolated from these cells and amplified in Escherichia coli. The resulting plasmid pool was transfected into cells for two further rounds of selection and plasmid reisolation.

resultsSeveral plasmids that caused immunotoxin resistance were enriched by this selection procedure. Four plasmids were stably transfected into MCF-7 cells and found to increase their resistance to PE-derived immunotoxins by 5- to 20-fold. These plasmids also confer resistance to native PE and to diphtheria toxin but not to ricin or cycloheximide. Thus, they appear to specifically interfere with the action of ADP-ribosylating toxins.

conclusionCancer cells can become resistant to immunotoxins by deregulated expression of normal genes. The clinical significance of this type of resistance will be evaluated in clinical trials.

Indexed as

ADP Ribose TransferasesBacterial ToxinsVirulence FactorsAntigens, Polyomavirus TransformingBreast NeoplasmsCell LineCell SurvivalCloning, MolecularDiphtheria ToxinDNA, ComplementaryDNA ReplicationDose-Response Relationship, DrugDrug Resistance, NeoplasmExotoxinsFemaleHeLa CellsADP Ribose TransferasesAntigens, Polyomavirus TransformingBacterial ToxinsDiphtheria ToxinDNA, ComplementaryExotoxinsImmunotoxinsPseudomonas aeruginosa Exotoxin AVirulence Factors

Identifiers

PMID8529099
PMCPMC2229949
OpenAlexW120152197

What OpenQuestion holds

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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.