Evidence map›Paper›PMID 19107609›Full record

ReviewMedical molecular morphology2008

The Kras2 oncogene and mouse lung carcinogenesis.

Gang-Hong Lee

Abstract readReview
PubMed Publisher
In one paragraph

Review in Medical molecular morphology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.4field-weighted citation impact, top 36% 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

1 citing paper in PubMed, 8 citations in OpenAlex.

  1. 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

1 author at 1 institution in 1 country.

Gang-Hong LeeDepartment of Pathology, Kochi University School of Medicine, Kohasu, Oko-cho, Nankoku, Kochi, 783-8505, Japan. ghlee@kochi-u.ac.jp
Kōchi University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Activating point mutations of the mouse Kras2 oncogene or its human homologue, KRAS, are critical for lung adenocarcinoma genesis, independent of the species. Significantly, in the mouse, several polymorphic Kras2 alleles have been identified, which cosegregate with genetic susceptibility to chemical induction of lung tumors. Moreover, a major lung tumor susceptibility locus, the Pas1 (Pulmonary adenoma susceptibility 1), was found to colocalize with Kras2 on distal chromosome 6 on linkage analysis. The Kras2 may thus be involved in both cellular transformation and genetic control of tumor susceptibility. In this review, the focus is on current knowledge regarding the relationship between Kras2 and experimental mouse lung carcinogenesis, especially from the aspect of disease predisposition. Because mouse and human lung tumors share considerable similarities, the experimental information should provide clues to personalized medicine in the human setting.

Indexed as

Genetic Predisposition to DiseaseLungAllelesAnimalsAntigens, NeoplasmAntigens, NuclearGenes, Tumor SuppressorHumansLung NeoplasmsMicePhenotypePoint MutationProto-Oncogene Proteins p21(ras)Antigens, NeoplasmAntigens, NuclearHras protein, mousePASD1 protein, humanProto-Oncogene Proteins p21(ras)

Identifiers

PMID19107609
OpenAlexW2089714617

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.