Evidence map›Paper›PMID 15016317›Full record

ReviewCancer science2004

Molecular footprints of human lung cancer progression.

Jun Yokota, Takashi Kohno

Open access · bronzeAbstract readReview
In one paragraph

Review in Cancer science, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed, 2 pooled it
4.0field-weighted citation impact, top 6% 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

48 citing papers in PubMed, 2 syntheses or guidelines pooled it, 140 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Homozygous deletion mapping in myeloma samples identifies genes and an expression signature relevant to pathogenesis and outcome.Clinical cancer research : an official journal of the American Association for Cancer Research · 2010
    Trial
  4. Review
  5. Article
  6. Review
  7. Article
  8. Drugging KRAS: current perspectives and state-of-art review.Journal of hematology & oncology · 2022
    Review
  9. Article
  10. KRAS mutation in pancreatic cancer.Seminars in oncology · 2021
    Review
  11. Article
  12. Article
  13. Effect of Cetuximab andYonago acta medica · 2019
    Article
  14. Article
  15. Nuclear Morphometry of Lung Squamous Cell Carcinomas in Cytologic Study.Annals of thoracic and cardiovascular surgery : official journal of the Association of Thoracic and Cardiovascular Surgeons of Asia · 2018
    Article
  16. Article
  17. Review
  18. miR-33a inhibits cell proliferation and invasion by targeting CAND1 in lung cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2018
    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 at 1 institution in 1 country.

Jun YokotaBiology Division, National Cancer Center Research Institute, 5-1-1 Tsukiji, Chuo-ku, Tokyo 104-0045, Japan. jyokota@gan2.ncc.go.jp
Takashi Kohno
National Cancer Research Institute · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lung cancer is the leading cause of cancer-related death in the world. To understand the molecular processes and pathways of, and contributing factors to lung cancer progression, genetic alterations in various progression stages of lung cancer cells have been studied, since these alterations can be regarded as molecular footprints representing the individual processes of multistage lung carcinogenesis. The results indicate that defects in both the p53 and RB/p16 pathways are essential for the malignant transformation of lung epithelial cells. Several other genes, such as K-ras, PTEN and MYO18B, are genetically altered less frequently than p53 and RB/p16 in lung cancer cells, suggesting that alterations in these genes are associated with further malignant progression or unique phenotypes in a subset of lung cancer cells. However, it is still unclear what genes control the metastatic potential of lung cancer cells. Further analyses of molecular footprints in lung cancer cells, in particular in the cells of metastatic sites, will give us valuable information to fully understand the process of lung cancer progression, and to find novel ways of controlling it. Molecular footprints at the sites of p53 mutations and p16 deletions further indicate that DNA repair activities for G:C to T:A transversion and non-homologous end-joining of DNA double-strand breaks play important roles in the accumulation of genetic alterations in lung cancer cells. Thus, identification of environmental as well as genetic factors inducing or suppressing the occurrence of such alterations would be a clue to find novel ways of lung cancer prevention.

Indexed as

Disease ProgressionGene Expression Regulation, NeoplasticGenes, Tumor SuppressorLung NeoplasmsModels, Genetic

Identifiers

PMID15016317
PMCPMC11159118
OpenAlexW2055103019

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.