Evidence map›Paper›PMID 32383436›Full record

ReviewTrends in cancer2020

Mechanisms Underlying Recurrent Genomic Amplification in Human Cancers.

Hisashi Tanaka, Takaaki Watanabe

Abstract readReview
In one paragraph

Review in Trends in cancer, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
–field-weighted citation impact
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

44 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Antibiotic resistance mediated by gene amplifications.npj antimicrobials and resistance · 2024
    Review
  13. Mechanical stress during confined migration causes aberrant mitoses and c-MYC amplification.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  14. Basket Trials: Past, Present, and Future.Annual review of cancer biology · 2024
    Article
  15. Review
  16. Article
  17. Review
  18. Computational inference of eIF4F complex function and structure in human cancers.Proceedings of the National Academy of Sciences of the United States of America · 2024
    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

2 authors.

Hisashi TanakaDepartment of Surgery, Cedars-Sinai Medical Center, West Hollywood, CA 90046, USA; Biomedical Sciences, Cedars-Sinai Medical Center, West Hollywood, CA 90046, USA; Samuel Oschin Comprehensive Cancer Institute, Cedars-Sinai Medical Center, West Hollywood, CA 90046, USA. Electronic address: Hisashi.Tanaka@cshs.org.
Takaaki WatanabeDepartment of Surgery, Cedars-Sinai Medical Center, West Hollywood, CA 90046, USA; Molecular Life Science, Tokai University School of Medicine, Kanagawa, Japan.

Funding

Mechanisms of gene amplification in human cancersR01CA149385 · NCI · CLEVELAND CLINIC LERNER COM-CWRU · PI TANAKA, HISASHI · 2010 to 2022
$3.4M
NCI NIH HHS R01 CA149385
6 · The paper itself

Abstract

Focal copy-number increases (genomic amplification) pinpoint oncogenic driver genes and therapeutic targets in cancer genomes. With the advent of genomic technologies, recurrent genomic amplification has been mapped throughout the genome. Recurrent amplification could be solely due to positive selection for the tumor-promoting effects of amplified gene products. Alternatively, recurrence could result from the susceptibility of the loci to amplification. Distinguishing between these possibilities requires a full understanding of the amplification mechanisms. Two mechanisms, the formation of double minute (DM) chromosomes and breakage-fusion-bridge (BFB) cycles, have been repeatedly linked to genomic amplification, and the impact of both mechanisms has been confirmed in cancer genomics data. We review the details of these mechanisms and discuss the mechanisms underlying recurrence.

Indexed as

ChromothripsisGene AmplificationAnimalsCarcinogenesisCell LineDNA BreaksDNA Copy Number VariationsDNA RepairHumansNeoplasmsOncogenesTelomerebreakage-fusion-bridge cyclesdouble minute chromosomesgenomic amplification

Identifiers

PMID32383436
PMCPMC7285850

What OpenQuestion holds

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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.