Molecular analysis: microsatellity instability and loss of heterozygosity of tumor suppressor gene in hereditary non-polyposis colorectal cancers (HNPCC).

Vesna Hadziavdić, Nada Pavlović-Calić, Izet Eminović

Open access · hybridAbstract read

In one paragraph

Article in Bosnian journal of basic medical sciences, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it

0cells of the map it votes in

0citing papers in PubMed

–field-weighted citation impact, top 64% 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

0 citing papers in PubMed, 0 citations in OpenAlex.

No citing paper in PubMed yet.

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

3 authors at 3 institutions in 3 countries.

Vesna HadziavdićMedical Centre for Molecular Biology, Institute of Biochemistry, Faculty of Medicine, University of Ljubljana, Vrazov trg 2, 1000 Ljubljana, Slovenia.

Nada Pavlović-Calić

Izet Eminović

University Clinical Centre · PLUniversity of Ljubljana · SIUniversity of Tuzla · BA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

HNPCC (Hereditary non-polyposis colorectal cancers) development is caused by mutation of genes included in system of mismatch repair genes. The mutation exists at 60% of patients in hMSH2 gene, 30% in hMLH1 and 10% both in hPMS1and hPMS2 genes. RER+ exists in about 90% in hereditary non-polyposis colorectal cancer and about 15-28% in sporadic cancers. The purpose of the study was to determine highly sensitive microsatellite markers which can be fast and efficient way of microsatellite screening for detection of HNPCC patients. Moreover, we have analysed the loss of heterozygosity of tumour suppressor genes which could have the diagnostic value in detection of HPNCC patients.

Indexed as

Genes, Tumor SuppressorMicrosatellite InstabilityAdaptor Proteins, Signal TransducingAdenocarcinomaAdenosine TriphosphatasesAdultCase-Control StudiesColorectal Neoplasms, Hereditary NonpolyposisDNA-Binding ProteinsDNA Repair EnzymesFemaleGenetic TestingHumansLoss of HeterozygosityMaleMiddle AgedAdaptor Proteins, Signal TransducingAdenosine TriphosphatasesDNA-Binding ProteinsDNA Repair EnzymesMismatch Repair Endonuclease PMS2MLH1 protein, humanMSH2 protein, humanMutL Protein Homolog 1MutL ProteinsMutS Homolog 2 ProteinNeoplasm ProteinsNuclear ProteinsNucleotidesPMS1 protein, humanPMS2 protein, human

Identifiers

PMID19284389

DOI10.17305/bjbms.2009.2850

PMCPMC5645541

OpenAlexW2441860493

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.