Evidence map›Paper›PMID 16141330›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2005

Deletion of XPC leads to lung tumors in mice and is associated with early events in human lung carcinogenesis.

M Christine Hollander, Robyn T Philburn, Andrew D Patterson, Susana Velasco-Miguel, Errol C Friedberg, R Ilona Linnoila, Albert J Fornace

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
69citing papers in PubMed, 3 pooled it
4.2field-weighted citation impact, top 5% 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

69 citing papers in PubMed, 3 syntheses or guidelines pooled it, 134 citations in OpenAlex.

  1. Pooled it
  2. Associations between polymorphisms of the XPC gene and lung cancer susceptibility: a meta-analysis.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014
    Pooled it
  3. Pooled it
  4. Automated detection of genetic abnormalities combined with cytology in sputum is a sensitive predictor of lung cancer.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2008
    Trial
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. GADD45 in Stress Signaling, Cell Cycle Control, and Apoptosis.Advances in experimental medicine and biology · 2022
    Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
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  20. Article

9 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

7 authors at 3 institutions in 1 country.

M Christine HollanderNational Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA. ch96b@nih.gov
Robyn T Philburn
Andrew D Patterson
Susana Velasco-Miguel
Errol C Friedberg
R Ilona Linnoila
Albert J Fornace
The University of Texas Southwestern Medical Center · USNational Cancer Institute · USNational Institutes of Health · US

Funding

Molecular Pathology of Pulmonary CarcinogenesisZIASC000167 · NCI · DIVISION OF CLINICAL SCIENCES - NCI · PI LINNOILA, ILONA · 2009 to 2014
$6.1M
MOLECULAR PATHOLOGY OF PULMONARY CARCINOGENESISZ01SC000167 · SC · DIVISION OF CLINICAL SCIENCES - NCI · PI LINNOILA, ILONA · 1996 to 2008
$2.0M
6 · The paper itself

Abstract

Chromosome 3p and 1p deletions are among the most frequent genetic changes in human lung cancer and although candidate tumor suppressor genes have been identified in these regions, no causative correlations have been drawn between deletion or mutation of these and lung carcinogenesis. We identify XPC and Gadd45a as genes within each of these regions involved in lung tumor initiation and progression, respectively. One hundred percent of XPC-/- mice develop multiple spontaneous lung tumors with a minority progressing to non-small cell lung adenocarcinoma, occasionally with metastasis to adjacent lymph nodes. Deletion of Gadd45a alone does not lead to increased lung tumors in mice, but coupled with an XPC deletion, it results in lung tumor progression. Analysis of published data indicated allelic loss of XPC in most human lung tumors and allelic loss of Gadd45a in some human lung and other cancer types. Because DNA repair capacity is compromised in XPC+/- cells, it is possible that the loss of a single XPC allele in the human lung might confer a mutator phenotype. Coupled with cigarette carcinogens, decreased DNA repair would lead to additional mutations in genes such as p53 that are frequent targets in lung cancer.

Indexed as

Gene DeletionAllelesAnimalsCarcinoma, Non-Small-Cell LungCell Cycle ProteinsChromosome MappingChromosomes, Human, Pair 1Chromosomes, Human, Pair 3DNA-Binding ProteinsDNA DamageFemaleGADD45 ProteinsHumansLung NeoplasmsMaleMiceCell Cycle ProteinsDNA-Binding ProteinsGADD45A protein, humanGadd45a protein, mouseGADD45 ProteinsNuclear ProteinsXPC protein, humanXpc protein, mouse

Identifiers

PMID16141330
PMCPMC1201581
OpenAlexW2159036652

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.