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1.
J Stroke Cerebrovasc Dis ; 28(3): 587-594, 2019 Mar.
Artículo en Inglés | MEDLINE | ID: mdl-30472175

RESUMEN

BACKGROUND: Many studies concentrated on the relationships between different types of family history and stroke, but they have not arrived at an unified conclusion. We conducted a comprehensive systematic review to further evaluate the associations. METHODS: Different databases were searched for related studies published from 1990 to August 2017. The relative risk was considered as the common measure of association across different studies. Heterogeneity of effects across studies was quantified by I2. RESULTS: Sixteen published studies (total participants: 655,552) were eligible in this study. The pooled multifactorial adjusted relative risk (RR) (95% confidence interval [CI]) was 1.40 (1.18, 1.67) for individuals with paternal history, 1.36 (1.20, 1.53) for those with maternal history, and 1.44 (1.17, 1.77) for those with sibling history. Based on cohort studies, the pooled adjusted RRs (95%CIs) for paternal, maternal, and sibling history were 1.33 (1.11-1.59), 1.28 (1.14-1.45), and 1.24 (1.01-1.51), respectively, all of which were smaller than those based on case-control and cross-sectional studies. In studies with large sample size, the respective adjusted RR (95%CI) of stroke for paternal, maternal, and sibling history was 1.30 (1.09, 1.56), 1.30 (1.18, 1.44), and 1.26 (1.02, 1.56), which was lower than that in studies with small sample size. CONCLUSIONS: Each type of family history of stroke was associated with an increased stroke risk. We could not find significant differences among stroke risks relating to different types of family history of stroke. Thus, paternal, maternal, and sibling history require our equal attention in the stroke prevention and control work.


Asunto(s)
Núcleo Familiar , Accidente Cerebrovascular/genética , Factores de Edad , Padre , Femenino , Predisposición Genética a la Enfermedad , Herencia , Humanos , Masculino , Madres , Linaje , Fenotipo , Medición de Riesgo , Factores de Riesgo , Factores Sexuales , Hermanos , Accidente Cerebrovascular/diagnóstico , Accidente Cerebrovascular/epidemiología , Accidente Cerebrovascular/prevención & control
2.
Pathol Res Pract ; 236: 153988, 2022 Aug.
Artículo en Inglés | MEDLINE | ID: mdl-35759938

RESUMEN

BACKGROUND: Systematic research on the associations between vital single nucleotide polymorphisms (SNPs) in MALAT1 and cancer risk was still lacking. Thus, we performed this study. MATERIALS AND METHODS: The literature searches were until April 1, 2022. The pooled association-analysis results were assessed by odds ratios (ORs) and the corresponding 95% confidence intervals (CIs) in three genetic models. In addition, we explored the potential functions of MALAT1 and its vital SNPs based on several public websites. RESULTS: Eighteen articles about four SNPs (rs619586, rs664589, rs1194338, and rs3200401) involving 11,843 cancer cases and 14,682 controls were collected. Rs619586, rs664589, and rs1194338 were associated with cancer risk (all P-value < 0.05). Each SNP of the three was significantly related to the risk of colorectal cancer (CRC), and rs619586 correlated with hepatocellular carcinoma (HCC) risk (all P-value < 0.05). The three SNPs might affect the transcription factor, promoter, or enhancer functions. MALAT1 expressed significantly higher in CRC and HCC than in normal tissues. The respective area under the receiver operating characteristic curve of MALAT1 for CRC and HCC patients was 0.783 and 0.864. Moreover, survival analysis indicated that MALAT1 might be a potential prognostic marker of CRC and HCC (all relevant P-value < 0.05). CONCLUSIONS: The functional SNPs in MALAT1 correlated with cancer risk. MALAT1 and its vital functional SNPs might be potential biomarkers for predicting the risk and prognosis of two types of cancer, especially CRC. Further investigations are needed to confirm our present findings.


Asunto(s)
Carcinoma Hepatocelular , Neoplasias Hepáticas , ARN Largo no Codificante/genética , Carcinoma Hepatocelular/genética , Predisposición Genética a la Enfermedad , Humanos , Neoplasias Hepáticas/genética , Polimorfismo de Nucleótido Simple/genética
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