Evidence map›Paper›PMID 12379883›Full record

ReviewOncogene2002

Genetic alterations of multiple tumor suppressors and oncogenes in the carcinogenesis and progression of lung cancer.

Hirotaka Osada, 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 66 papers.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed
5.1field-weighted citation impact, top 4% 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

66 citing papers in PubMed, 219 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. The Tumor SuppressorCancers · 2021
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Article

6 more citing papers are in PubMed but not listed here.

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.

Hirotaka OsadaDivision 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

Lung cancer has become the leading cause of cancer death in many economically well-developed countries. Recent molecular biological studies have revealed that overt lung cancers frequently develop through sequential morphological steps, with the accumulation of multiple genetic and epigenetic alterations affecting both tumor suppressor genes and dominant oncogenes. Cell cycle progression needs to be properly regulated, while cells have built-in complex and minute mechanisms such as cell cycle checkpoints to maintain genomic integrity. Genes in the p16INK4A-RB and p14ARF-p53 pathways appear to be a major target for genetic alterations involved in the pathogenesis of lung cancer. Several oncogenes are also known to be altered in lung cancer, leading to the stimulation of autocrine/paracrine loops and activation of multiple signaling pathways. It is widely acknowledged that carcinogens in cigarette smoke are deeply involved in these multiple genetic alterations, mainly through the formation of DNA adducts. A current understanding of the molecular mechanisms of lung cancer pathogenesis and progression is presented in relation to cigarette smoking, an absolute major risk factor for lung cancer development, by reviewing genetic alterations of various tumor suppressor genes and oncogenes thus far identified in lung cancer, with brief summaries of their functions and regulation.

Indexed as

Genes, Tumor SuppressorOncogenesCell Transformation, NeoplasticDisease ProgressionHumansLung Neoplasms

Identifiers

PMID12379883
OpenAlexW1993423395

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.