Evidence map›Paper›PMID 19931269›Full record

ArticleCancer letters2010

Fhit loss in lung preneoplasia: relation to DNA damage response checkpoint activation.

Roberto Cirombella, Giuseppe Montrone, Antonella Stoppacciaro, Simona Giglio, Stefano Volinia, Paolo Graziano, Kay Huebner, Andrea Vecchione

RetractedErratum issuedOpen access · greenAbstract read
In one paragraph

Article in Cancer letters, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.8field-weighted citation impact, top 24% 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

5 citing papers in PubMed, 8 citations in OpenAlex.

  1. FHIT, a Novel Modifier Gene in Pulmonary Arterial Hypertension.American journal of respiratory and critical care medicine · 2019
    Article
  2. Sensing Bacterial-Induced DNA Damaging EffectsFrontiers in immunology · 2018
    Review
  3. Article
  4. microRNA-based cancer cell reprogramming technology.Experimental and therapeutic medicine · 2012
    Article
  5. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 2 institutions in 1 country.

Roberto CirombellaDivision of Pathology, II University of Rome La Sapienza, Ospedale Santo Andrea, Rome, Italy.
Giuseppe Montrone
Antonella Stoppacciaro
Simona Giglio
Stefano Volinia
Paolo Graziano
Kay Huebner
Andrea Vecchione
Azienda Ospedaliera Sant'Andrea · ITOspedale generale di zona San Camillo Treviso · IT

Funding

ROLE OF THE FHIT LOCUS IN ENVIRONMENTAL CARCINOGENESISP01CA077738 · NCI · THOMAS JEFFERSON UNIVERSITY · PI HUEBNER, KAY · 2000 to 2004
$5.6M
Fhit modulation of cell cycle progression and DNA damage responseR01CA132453 · NCI · OHIO STATE UNIVERSITY · PI HUEBNER, KAY · 2007 to 2010
$1.3M
FHIT Gene Therapy in Cancer Prevention and TreatmentR01CA115965 · NCI · OHIO STATE UNIVERSITY · PI CROCE, CARLO M · 2007 to 2011
$1.1M
NCI NIH HHS CA115965NCI NIH HHS CA132453NCI NIH HHS P01 CA077738NCI NIH HHS R01 CA115965NCI NIH HHS R01 CA132453
6 · The paper itself

Abstract

Loss of heterozygosity at the FHIT locus is coincident with activation of DNA damage response checkpoint proteins; thus damage at fragile loci may trigger checkpoint activation. We examined preneoplastic lesions adjacent to non-small cell lung carcinomas for alterations to expression of Fhit and activated checkpoint proteins. Expression scores were analyzed for pair-wise associations and correlations among proteins and type of lesion. Hyperplastic and dysplastic lesions were positive for nuclear gammaH2AX expression; 12/20 dysplastic lesions were negative for Fhit expression. Fhit positive lesions showed expression of most checkpoint proteins examined, while Fhit negative lesions showed absence of expression of Chk1 and phosphoChk1. The results show that loss of expression of Fhit is significantly directly correlated with absence of activated Chk1 in dysplasia, and suggest a connection between loss of Fhit and modulation of checkpoint activity.

Indexed as

Acid Anhydride HydrolasesBis(5'-adenosyl)triphosphataseCheckpoint Kinase 1Chromosome Fragile SitesDNA DamageDNA, NeoplasmGene Expression Regulation, NeoplasticHeterozygoteHumansHyperplasiaImmunohistochemistryIn Situ Hybridization, FluorescenceLung NeoplasmsNeoplasm ProteinsPrecancerous ConditionsProtein KinasesAcid Anhydride HydrolasesBis(5'-adenosyl)triphosphataseCheckpoint Kinase 1CHEK1 protein, humanDNA, NeoplasmNeoplasm ProteinsProtein Kinases

Identifiers

PMID19931269
PMCPMC2849884
OpenAlexW2048712200

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.