Evidence map›Paper›PMID 9109439›Full record

ArticleThe Journal of clinical investigation1997

Gene rearrangement: a novel mechanism for MDR-1 gene activation.

L A Mickley, B A Spengler, T A Knutsen, J L Biedler, T Fojo

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.6field-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

24 citing papers in PubMed, 98 citations in OpenAlex.

  1. Multidrug Resistance: Are We Still Afraid of the Big Bad Wolf.Pharmaceuticals (Basel, Switzerland) · 2025
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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

5 authors at 1 institution in 1 country.

L A MickleyMedicine Branch, DCS, NCI, Bethesda, Maryland 20892, USA.
B A Spengler
T A Knutsen
J L Biedler
T Fojo
Memorial Sloan Kettering Cancer Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Drug resistance, a major obstacle to cancer chemotherapy, can be mediated by MDR-1/P-glycoprotein. Deletion of the first 68 residues of MDR-1 in an adriamycin-selected cell line after a 4;7 translocation, t(4q;7q), resulted in a hybrid mRNA containing sequences from both MDR-1 and a novel chromosome 4 gene. Further selection resulted in amplification of a hybrid gene. Expression of the hybrid mRNA was controlled by the chromosome 4 gene, providing a model for overexpression of MDR-1. Additional hybrid mRNAs in other drug-selected cell lines and in patients with refractory leukemia, with MDR-1 juxtaposed 3' to an active gene, establishes random chromosomal rearrangements with overexpression of hybrid MDR-1 mRNAs as a mechanism of acquired drug resistance.

Indexed as

Gene RearrangementGenes, MDRAmino Acid SequenceAntibiotics, AntineoplasticBase SequenceChromosomes, Human, Pair 4Chromosomes, Human, Pair 7DNA, NeoplasmDNA PrimersDoxorubicinDrug Resistance, MultipleGene Expression Regulation, NeoplasticHumansHybridization, GeneticIn Situ Hybridization, FluorescenceMolecular Sequence DataAntibiotics, AntineoplasticDNA, NeoplasmDNA PrimersDoxorubicinRNA, MessengerRNA, Neoplasm

Identifiers

PMID9109439
PMCPMC508019
OpenAlexW2046112186

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.