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  • CANCER  (2)
  • DISSEMINATED TUMOR-CELLS  (2)
  • 1
    Keywords: CANCER ; LUNG ; LUNG-CANCER ; DISEASE ; EPIDEMIOLOGY ; RISK ; GENE ; GENES ; GENETIC POLYMORPHISMS ; ASSOCIATION ; polymorphism ; HEALTH ; smoking ; SQUAMOUS-CELL CARCINOMA ; case-control studies ; lung neoplasms ; glutathione-S-transferase ; case-control study ; WORLDWIDE ; review ; METAANALYSIS ; GENOTYPE ; CHINESE POPULATION ; PUBLICATION BIAS ; DNA ADDUCT LEVELS ; NULL-GENOTYPE ; Asian continental ancestry group ; glutathione S-transferase pi ; GSTP1 ; HONG-KONG ; P1 POLYMORPHISMS ; PI-GENE
    Abstract: Lung cancer is the most common cancer worldwide. Polymorphisms in genes associated with carcinogen metabolism may modulate risk of disease. Glutathione S-transferase pi (GSTP1) detoxifies polycyclic aromatic hydrocarbons found in cigarette smoke and is the most highly expressed glutathione S-transferase in lung tissue. A polymorphism in the GSTP1 gene, an A-to-G transition in exon 5 (Ile105Val, 313A -〉 313G), results in lower activity among individuals who carry the valine allele. The authors present a meta- and a pooled analysis of case-control studies that examined the association between this polymorphism in GSTP1 and lung cancer risk (27 studies, 8,322 cases and 8,844 controls and 15 studies, 4,282 cases and 5,032 controls, respectively). Overall, the meta-analysis found no significant association between lung cancer risk and the GSTP1 exon 5 polymorphism. In the pooled analysis, there was an overall association (odds ratio = 1.11, 95% confidence interval: 1.03, 1.21) between lung cancer and carriage of the GSTP1 Val/Val or Ile/Val genotype compared with those carrying the Ile/Ile genotype. Increased risk varied by histologic type in Asians. There appears to be evidence for interaction between amount of smoking, the GSTP1 exon 5 polymorphism, and risk of lung cancer in whites
    Type of Publication: Journal article published
    PubMed ID: 19240225
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  • 2
    Keywords: CANCER ; CELLS ; EXPRESSION ; tumor ; carcinoma ; GENE ; GENE-EXPRESSION ; COMPLEXES ; BREAST-CANCER ; COMPARATIVE GENOMIC HYBRIDIZATION ; gene expression ; MUTATION ; METASTASIS ; SIGNALING PATHWAYS ; SOLID TUMORS ; PRIMARY TUMORS ; SUBTYPES ; GENETIC ALTERATIONS ; LYMPH-NODE METASTASES
    Abstract: Introduction: With the improvement of therapeutic options for the treatment of breast cancer, the development of brain metastases has become a major limitation to life expectancy in many patients. Therefore, our aim was to identify molecular markers associated with the development of brain metastases in breast cancer. Methods: Patterns of chromosomal aberrations in primary breast tumors and brain metastases were compared with array-comparative genetic hybridization (CGH). The most significant region was further characterized in more detail by microsatellite and gene-expression analysis, and finally, the possible target gene was screened for mutations. Results: The array CGH results showed that brain metastases, in general, display similar chromosomal aberrations as do primary tumors, but with a notably higher frequency. Statistically significant differences were found at nine different chromosomal loci, with a gain and amplification of EGFR (7p11.2) and a loss of 10q22.3-qter being among the most significant aberrations in brain metastases (P 〈 0.01; false discovery rate (fdr) 〈 0.04). Allelic imbalance (AI) patterns at 10q were further verified in 77 unmatched primary tumors and 21 brain metastases. AI at PTEN loci was found significantly more often in brain metastases (52%) and primary tumors with a brain relapse (59%) compared with primary tumors from patients without relapse (18%; P = 0.003) or relapse other than brain tumors (12%; P = 0.006). Loss of PTEN was especially frequent in HER2-negative brain metastases (64%). Furthermore, PTEN mRNA expression was significantly downregulated in brain metastases compared with primary tumors, and PTEN mutations were frequently found in brain metastases. Conclusions: These results demonstrate that brain metastases often show very complex genomic-aberration patterns, suggesting a potential role of PTEN and EGFR in brain metastasis formation
    Type of Publication: Journal article published
    PubMed ID: 22429330
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  • 3
    Keywords: CELL LUNG-CANCER ; GENE ; PROTEINS ; BREAST-CANCER ; METASTASIS ; DISSEMINATED TUMOR-CELLS ; IMBALANCES ; METHYLATION ; TUMORIGENESIS ; CHROMOSOME 4Q
    Abstract: For better lung cancer diagnosis and therapy, early detection markers of tumor dissemination are urgently needed, as most lung cancers do not show symptoms until extensive metastasis formation has already taken place. Our previous studies showed that in non-small cell lung cancer (NSCLC) early tumor dissemination is associated with a loss of chromosome 4q12-q32 and the presence of disseminated tumor cells (DTC) in the bone marrow. In order to identify the potential target gene in this region, a screen for methylation-dependent expression was performed. Lung cancer cell lines showing a loss of 4q as well as a normal bronchial epithelial cell line as control were treated with 5-aza-2'-deoxycytidine (5-aza-CdR) followed by expression profiling. Seven genes within the 4q target region, which have been associated with a positive DTC status before were found to be regulated by hypermethylation. QRT-PCR in an independent sample set identified HERC5 as a potential target gene. Quantitative methylation analysis of these lung tissue samples revealed that HERC5 promoter hypermethylation was significantly associated with positive DTC status (p=0.020) and occurrence of brain metastases (p=0.015). In addition, hypermethylation of the HERC5 promoter in NSCLC was identified as a predictor for poor survival for Stage I adenocarcinoma patients (p=0.022) and also for poor overall survival in metastatic lung cancer patients (p=0.028). In conclusion, HERC5 may function as a prognostic marker and is associated with tumor dissemination in lung cancer. What's new? In order to improve the diagnosis and therapy of lung cancer, early biomarkers of tumor dissemination are urgently needed. In this study, the authors found that the HERC5 gene on chromosome 4 may be involved in regulating the spread of non-small cell lung cancer (NSCLC) tumors. In cases where the promoter region of HERC5 was hypermethylated, the number of disseminated tumor cells (DTC) and metastases increased, and survival decreased. HERC5 may thus be a new metastasis-suppressor gene, and its methylation and expression status may provide prognostic biomarkers for NSCLC.
    Type of Publication: Journal article published
    PubMed ID: 25353388
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  • 4
    Keywords: EXPRESSION ; GENE ; PROTEIN ; DIFFERENTIATION ; METASTASIS ; DISSEMINATED TUMOR-CELLS ; micrometastasis ; MAMMARY-GLAND ; SELF-RENEWAL ; CTBP
    Abstract: Regulatory pathways that drive early hematogenous dissemination of tumor cells are insufficiently defined. Here, we used the presence of disseminated tumor cells (DTC) in the bone marrow to define patients with early disseminated breast cancer and identified low retinoic acid-induced 2 (RAI2) expression to be significantly associated with DTC status. Low RAI2 expression was also shown to be an independent poor prognostic factor in 10 different cancer datasets. Depletion of RAI2 protein in luminal breast cancer cell lines resulted in dedifferentiation marked by downregulation of ERalpha, FOXA1, and GATA3, together with increased invasiveness and activation of AKT signaling. Functional analysis of the previously uncharacterized RAI2 protein revealed molecular interaction with CtBP transcriptional regulators and an overlapping function in controlling the expression of a number of key target genes involved in breast cancer. These results suggest that RAI2 is a new metastasis-associated protein that sustains differentiation of luminal breast epithelial cells. SIGNIFICANCE: We identified downregulation of RAI2 as a novel metastasis-associated genetic alteration especially associated with early occurring bone metastasis in ERalpha-positive breast tumors. We specified the role of the RAI2 protein to function as a transcriptional regulator that controls the expression of several key regulators of breast epithelial integrity and cancer. Cancer Discov; 5(5); 506-19. (c)2015 AACR. See related commentary by Esposito and Kang, p. 466 This article is highlighted in the In This Issue feature, p. 453.
    Type of Publication: Journal article published
    PubMed ID: 25716347
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