Evidence map›Paper›PMID 15215163›Full record

ArticleThe American journal of pathology2004

Overexpression of PDZK1 within the 1q12-q22 amplicon is likely to be associated with drug-resistance phenotype in multiple myeloma.

Jun Inoue, Takemi Otsuki, Akira Hirasawa, Issei Imoto, Yoshinobu Matsuo, Shiroh Shimizu, Masafumi Taniwaki, Johji Inazawa

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in The American journal of pathology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
3.5field-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

45 citing papers in PubMed, 95 citations in OpenAlex.

  1. Trial
  2. Review
  3. Review
  4. The numerous facets of 1q21Oncology letters · 2024
    Review
  5. Article
  6. Multiomic Mapping of Acquired Chromosome 1 Copy-Number and Structural Variants to Identify Therapeutic Vulnerabilities in Multiple Myeloma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2023
    Article
  7. Interaction of Human OATP1B1 with PDZK1 Is Required for Its Trafficking to the Hepatocyte Plasma Membrane.Drug metabolism and disposition: the biological fate of chemicals · 2023
    Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. PDZK1 induces resistance to apoptosis in esophageal adenocarcinoma cells.Esophagus : official journal of the Japan Esophageal Society · 2021
    Article
  16. Review
  17. Review
  18. Article
  19. Article
  20. Article
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

8 authors at 5 institutions in 3 countries.

Jun InoueDepartment of Molecular Cytogenetics, Medical Research Institute and Graduate School of Biomedical Science, Tokyo Medical and Dental University, 1-5-45 Yushima, Bunkyo-ku, Tokyo 113-8510, Japan.
Takemi Otsuki
Akira Hirasawa
Issei Imoto
Yoshinobu Matsuo
Shiroh Shimizu
Masafumi Taniwaki
Johji Inazawa
Tokyo Medical and Dental University · JPHayashibara (Japan) · JPKawasaki Medical School · JPKyoto Prefectural University of Medicine · JPShimane Prefectural Central Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We investigated DNA copy number aberrations in 37 cell lines derived from multiple myelomas (MMs) using comparative genomic hybridization, and 11 (29.7%) showed high-level gain indicative of gene amplification at 1q12-q22. A corresponding transcriptional mapping using oligonucleotide arrays extracted three up-regulated genes (IRTA2, PDZK1, and S100A6) within the smallest region of overlapping in amplifications. Among them PDZK1 showed amplification and consequent overexpression in the MM cell lines. Amplification of PDZK1 was observed in primary cases of MM as well. MM cell lines with amplification of PDZK1 exhibited the resistance to melphalan-, cis-platin-, and vincristin-induced cell death compared with MM cell lines without its amplifications. Furthermore, down-regulation of PDZK1 with an anti-sense oligonucleotide sensitized a cell line KMS-11 to melphalan, cis-platin, and vincristin. Taken together, our results indicate that PDZK1 is likely to be one of targets for 1q12-q22 amplification in MM and may be associated with the malignant phenotype, including drug resistance, in this type of tumor.

Indexed as

Chromosomes, Human, Pair 1Drug Resistance, MultipleAntineoplastic AgentsAntineoplastic Agents, AlkylatingAntineoplastic Agents, PhytogenicApoptosisCarrier ProteinsCell Line, TumorChromosome MappingCisplatinCytoskeletal ProteinsDown-RegulationGene AmplificationGene DosageGene Expression ProfilingGene Expression Regulation, NeoplasticAntineoplastic AgentsAntineoplastic Agents, AlkylatingAntineoplastic Agents, PhytogenicCarrier ProteinsCisplatinCytoskeletal ProteinsMelphalanMembrane ProteinsPDZK1 protein, humanPdzk1 protein, ratRNA, MessengerVincristine

Identifiers

PMID15215163
PMCPMC1618545
OpenAlexW2141550675

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.