Evidence map›Paper›PMID 12362271›Full record

ReviewOncogene2002

Chromosome instability in human lung cancers: possible underlying mechanisms and potential consequences in the pathogenesis.

Akira Masuda, Takashi Takahashi

Abstract readReview
PubMed Publisher
In one paragraph

Review in Oncogene, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
2.9field-weighted citation impact, top 10% 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

50 citing papers in PubMed, 131 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Clinical Utility of Chromosomal Aneusomy in Individuals at High Risk of Lung Cancer.Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer · 2017
    Article
  13. Shorter telomeres and high telomerase activity correlate with a highly aggressive phenotype in breast cancer cell lines.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Ionizing radiation-induced γ-H2AX activity in whole blood culture and the risk of lung cancer.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2013
    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 at 1 institution in 1 country.

Akira MasudaDivision of Molecular Oncology, Aichi Cancer Center Research Institute, 1-1 Kanokoden, Chikusa-ku, Nagoya 464-8681, Japan.
Takashi Takahashi
Aichi Cancer Center · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chromosomal abnormality is one of the hallmarks of neoplastic cells, and the persistent presence of chromosome instability (CIN) has been demonstrated in human cancers, including lung cancer. Recent progress in molecular and cellular biology as well as cytogenetics has shed light on the underlying mechanisms and the biological and clinical significance of chromosome abnormalities and the CIN phenotype. Chromosome abnormalities can be classified broadly into numerical (i.e., aneuploidy) and structural alterations (e.g., deletion, translocation, homogenously staining region (HSR), double minutes (DMs)). However, both alterations usually occur in the same cells, suggesting some overlap in their underlying mechanisms. Missegregation of chromosomes may result from various causes, including defects of mitotic spindle checkpoint, abnormal centrosome formation and failure of cytokinesis, while structural alterations of chromosomes may be caused especially by failure in the repair of DNA double-strand breaks (DSBs) due to the impairment of DNA damage checkpoints and/or DSB repair systems. Recent studies also suggest that telomere erosion may be involved. The consequential acquisition of the CIN phenotype would give lung cancer cells an excellent opportunity to efficiently alter their characteristics so as to be more malignant and suitable to their microenvironment, thereby gaining a selective growth advantage.

Indexed as

Chromosome AberrationsAnimalsHumansLung NeoplasmsMice

Identifiers

PMID12362271
OpenAlexW1964729637

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.