Evidence map›Paper›PMID 19887614›Full record

ArticleCancer research2009

Retinoblastoma family proteins have distinct functions in pulmonary epithelial cells in vivo critical for suppressing cell growth and tumorigenesis.

David S Simpson, Nicole A Mason-Richie, Caitlin A Gettler, Kathryn A Wikenheiser-Brokamp

Open access · bronzeAbstract read
In one paragraph

Article in Cancer research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
4.7field-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

32 citing papers in PubMed, 41 citations in OpenAlex.

  1. The Tumor Suppressor p53 Downregulates p107 (International journal of molecular sciences · 2025
    Article
  2. Article
  3. Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. CRISPR-mediated modeling and functional validation of candidate tumor suppressor genes in small cell lung cancer.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. 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

4 authors at 2 institutions in 1 country.

David S SimpsonPathology and Laboratory Medicine, Cincinnati Children's Hospital Medical Center and University of Cincinnati College of Medicine, Cincinnati, Ohio 45229-3039, USA.
Nicole A Mason-Richie
Caitlin A Gettler
Kathryn A Wikenheiser-Brokamp
Cincinnati Children's Hospital Medical Center · USUniversity of Cincinnati · US

Funding

Role of Rb Family in Lung Epithelial Response to InjuryR01HL079193 · NHLBI · UNIVERSITY OF CINCINNATI · PI WIKENHEISER-BROKAMP, KATHRYN ANN · 2005 to 2013
$3.4M
NHLBI NIH HHS R01 HL079193
6 · The paper itself

Abstract

Lung cancer is the leading cause of cancer deaths, accounting for more deaths than breast, colon, and prostate cancer combined. The retinoblastoma (Rb)/p16 tumor suppressive pathway is deregulated in most cancers. Loss of p16 occurs more frequently than Rb loss, suggesting that p16 suppresses cancer by regulating Rb as well as the related proteins p107 and p130. However, direct evidence demonstrating that p130 or p107 cooperate with Rb to suppress epithelial cancers associated with p16 loss is currently lacking. Moreover, the roles of p130 and p107 in lung cancer are not clear. In the present studies, Rb ablation was targeted to the lung epithelium in wild-type, p107, or p130 null mice to determine unique and overlapping Rb family functions critical in tumor suppression. Rb ablation during development resulted in marked epithelial abnormalities despite p107 upregulation. In contrast, p130 and p107 were not required during development but had distinct functions in the Rb-deficient epithelium: p107 was required to suppress proliferation, whereas a novel proapoptotic function was identified for p130. Adult Rb-ablated lungs lacked the epithelial phenotype seen at birth and showed compensatory p107 upregulation and p16 induction in epithelial cell lineages that share phenotypic characteristics with human non-small cell lung cancers (NSCLC) that frequently show p16 loss. Importantly, Rb/p107-deficient, but not Rb/p130-deficient, lungs developed tumors resembling NSCLC. Taken together, these studies identify distinct Rb family functions critical in controlling epithelial cell growth, and provide direct evidence that p107 cooperates with Rb to protect against a common adult cancer.

Indexed as

AnimalsApoptosisBlotting, WesternCell ProliferationCyclin-Dependent Kinase Inhibitor p16ImmunohistochemistryIn Situ Nick-End LabelingLung NeoplasmsMiceMice, KnockoutRespiratory MucosaRetinoblastoma-Like Protein p107Retinoblastoma-Like Protein p130Retinoblastoma ProteinReverse Transcriptase Polymerase Chain ReactionCyclin-Dependent Kinase Inhibitor p16Rbl1 protein, mouseRbl2 protein, mouseRetinoblastoma-Like Protein p107Retinoblastoma-Like Protein p130Retinoblastoma Protein

Identifiers

PMID19887614
PMCPMC2778863
OpenAlexW2010631202

What OpenQuestion holds

Textmetadata
LicenceTDM
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.