Evidence map›Paper›PMID 23645041›Full record

ArticleMolecular biology reports2013

Influence of survivin (BIRC5) and caspase-9 (CASP9) functional polymorphisms in renal cell carcinoma development: a study in a southern European population.

Inês Marques, Ana L Teixeira, Marta Ferreira, Joana Assis, Francisco Lobo, Joaquina Maurício, Rui Medeiros

Abstract readComparative Study
PubMed Publisher
In one paragraph

Article in Molecular biology reports, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 4 pooled it
1.2field-weighted citation impact, top 21% 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

12 citing papers in PubMed, 4 syntheses or guidelines pooled it, 23 citations in OpenAlex.

  1. Pooled it
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  4. Survivin rs9904341 (G>C) polymorphism contributes to cancer risk: an updated meta-analysis of 26 studies.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014
    Pooled it
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  12. Correlation between survivin genetic polymorphisms and lung cancer susceptibility.International journal of clinical and experimental pathology · 2015
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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.

Inês MarquesGrupo de Oncologia Molecular-CI, Edifício Laboratórios, Instituto Português de Oncologia do Porto Francisco Gentil, EPE, 4º piso, Rua Dr. António Bernardino de Almeida, 4200-072, Porto, Portugal.
Ana L Teixeira
Marta Ferreira
Joana Assis
Francisco Lobo
Joaquina Maurício
Rui Medeiros
Instituto Português de Oncologia Francisco Gentil · PTIPO Porto · PTUniversidade do Porto · PT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Renal cell carcinoma (RCC) is the most common cancer of the adult kidney and its incidence and mortality has increase in the last 20 years. The disruption of cellular death is one the mechanism involved in cancer development. This process is precise regulated by apoptotic and anti-apoptotic molecules. Survivin (BIRC5) is a member of the inhibitor of apoptosis protein family and has the ability to inhibit the activation of the pro-apoptotic caspase-9 (CASP9). Thus BIRC5 and CASP9 functional polymorphisms might modulate the apoptosis and consequently RCC development. Our purpose was to investigate the potential role of BIRC5-31G/C and CASP9+83C/T functional polymorphisms in the risk for the development of RCC and metastatic disease. We studied the BIRC5-31G/C and CASP9+83C/T functional polymorphisms by PCR-RFLP and allelic discrimination using the 7300 real-time polymerase chain reaction system, respectively, in 178 RCC patients and in 305 healthy individuals. Regarding the BIRC5-31G/C polymorphism, there is a trend to an overrepresentation of CC genotype in RCC group compared with normal controls (aOR, 1.94; P=0.053). We observed, after gender stratification and age-adjustment, that BIRC5-31CC and CASP9+83CT/TT genotypes were associated with an increased risk for RCC development in the female group of our southern European study population (aOR=3.85; P=0.019; aOR=2.98; P=0.028; respectively). Concerning the waiting time for onset of metastatic disease, we observed that BIRC5-31CC homozygous developed metastasis 8 years earlier than the G carriers using a Cox proportional hazard model with gender as covariate (HR=4.9, P=0.038, P bootstrap=0.009). The Cox regression proportional hazard model was validated using bootstrap statistic with 1,000 samples of the same number of patients as the original dataset. Our results suggest that individual differences influence the susceptibility to RCC and tumor behavior. This genetic profile may help to define higher risk groups that would benefit from individualized chemoprevention strategies and therapies.

Indexed as

AgedApoptosisCarcinoma, Renal CellCaspase 9FemaleGenetic Predisposition to DiseaseGenotypeHumansInhibitor of Apoptosis ProteinsMaleMiddle AgedNeoplasm MetastasisOdds RatioPolymorphism, Restriction Fragment LengthPolymorphism, Single NucleotidePortugalBIRC5 protein, humanCASP9 protein, humanCaspase 9Inhibitor of Apoptosis ProteinsSurvivin

Identifiers

PMID23645041
OpenAlexW2466146321

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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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.