Min Shen

National Institutes of Health, 베서스다, Maryland, United States

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Publications (77)394.45 Total impact

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    ABSTRACT: Formaldehyde has been proposed to be a human myeloid leukemogen. However, the mechanistic basis for this association is still debated. We aimed to evaluate whether circulating immune/inflammation markers were altered in workers occupationally exposed to formaldehyde. Using a multiplexed bead-based assay, we measured serum levels of 38 immune/inflammation markers in a cross-sectional study of 43 formaldehyde-exposed and 51 unexposed factory workers in Guangdong, China. Linear regression models adjusting for potential confounders were used to compare marker levels in exposed and unexposed workers. We found significantly lower circulating levels of two markers among exposed factory workers compared to unexposed controls that remained significant after adjusting for potential confounders and multiple comparisons using a false discovery rate (FDR) of 10%, including chemokine (C-X-C motif) ligand 11 (CXCL11; 36.2 pg/ml in exposed versus 48.4 pg/ml in controls, P=0.0008) and thymus and activation regulated chemokine (TARC; 52.7 pg/ml in exposed versus 75.0 pg/ml in controls, P=0.0028), suggesting immunosuppression among formaldehyde-exposed workers. Our findings are consistent with recently emerging understanding that immunosuppression might be associated with myeloid diseases. These findings, if replicated in a larger study, may provide insights into the mechanisms by which formaldehyde promotes leukemogenesis. Published by Oxford University Press 2015.
    Carcinogenesis 04/2015; DOI:10.1093/carcin/bgv055 · 5.27 Impact Factor
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    ABSTRACT: Exposure to benzene, a known leukemogen and probable lymphomagen, has been demonstrated to result in oxidative stress, which has previously been associated with altered telomere length (TL). TL specifically has been associated with several health outcomes in epidemiologic studies, including cancer risk, and has been demonstrated to be altered following exposure to a variety of chemical agents. To evaluate the association between benzene exposure and TL, we measured TL by monochrome multiplex quantitative PCR in 43 workers exposed to high levels of benzene and 43 age and sex-matched unexposed workers in Shanghai, China. Benzene exposure levels were monitored using organic vapor passive dosimetry badges before phlebotomy. The median benzene exposure level in exposed workers was 31 ppm. The mean TL in controls, workers exposed to levels of benzene below the median (≤31 ppm), and above the median (>31 ppm) was 1.26 ± 0.17, 1.25 ± 0.16, and 1.37 ± 0.23, respectively. Mean TL was significantly elevated in workers exposed to >31 ppm of benzene compared with controls (P = 0.03). Our findings provide evidence that high levels of occupational benzene exposure are associated with TL. Environ. Mol. Mutagen., 2014. Published [2014]. This article is a U.S. Government work and is in the public domain in the USA.
    Environmental and Molecular Mutagenesis 10/2014; 55(8). DOI:10.1002/em.21880 · 2.55 Impact Factor
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    ABSTRACT: Genome-wide association studies (GWAS) have mapped risk alleles for at least ten distinct cancers to a small region of 63,000 bp on chromosome 5p15.33. This region harbors the TERT and CLPTM1L genes; the former encodes the catalytic subunit of telomerase reverse transcriptase and the latter may play a role in apoptosis. To investigate further the genetic architecture of common susceptibility alleles in this region, we conducted an agnostic subset-based meta-analysis (ASSET) across six distinct cancers in 34,248 cases and 45,036 controls. Based on sequential conditional analysis, we identified as many as six independent risk loci marked by common single nucleotide polymorphisms (SNPs): five in the TERT gene (region 1: rs7726159, P=2.10x10-39; region 3: rs2853677, P=3.30x10-36 and PConditional=2.36x10-8; region 4: rs2736098, P=3.87x10-12 and PConditional=5.19x10-6, region 5: rs13172201, P=0.041 and PConditional=2.04x10-6; and region 6: rs10069690, P=7.49x10-15 and PConditional=5.35x10-7) and one in the neighboring CLPTM1L gene (region 2: rs451360; P=1.90x10-18 and PConditional=7.06x10-16). Between three and five cancers mapped to each independent locus with both risk-enhancing and protective effects. Allele specific effects on DNA methylation were seen for a subset of risk loci indicating that methylation and subsequent effects on gene expression may contribute to the biology of risk variants on 5p15.33. Our results provide strong support for extensive pleiotropy across this region of 5p15.33, to an extent not previously observed in other cancer susceptibility loci.
    Human Molecular Genetics 07/2014; DOI:10.1093/hmg/ddu363 · 6.68 Impact Factor
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    ABSTRACT: Lung cancer rates in Xuanwei are the highest in China. In-home use of smoky coal has been associated with lung cancer risk, and the association of smoking and lung cancer risk strengthened after stove improvement. Here, we explored the differential association of tobacco use and lung cancer risk by the intensity, duration, and type of coal used. We conducted a population-based case-control study of 260 male lung cancer cases and 260 age-matched male controls. Odds ratios (OR) and 95% confidence interval (CI) for tobacco use was calculated by conditional logistic regression. Use of smoky coal was significantly associated with an increased risk of lung cancer, and tobacco use was weakly and non-significantly associated with lung cancer risk. When the association was assessed by coal use, the cigarette-lung cancer risk association was null in hazardous coal users and elevated in less hazardous smoky coal users and non-smoky coal users. The risk of lung cancer per cigarette per day decreased as annual use of coal increased (>0-3tons: OR: 1.09; 95% CI: 1.03-1.17; >3tons: OR: 0.99; 95% CI: 0.95-1.03). Among more hazardous coal users, attenuation occured at even low levels of usage (>0-3tons: OR: 1.02; 95% CI: 0.91-1.14; >3tons: OR: 0.94; 95% CI: 0.97-1.03). We found evidence that smoky coal attenuated the tobacco and lung cancer risk association in males that lived in Xuanwei, particularly among users of hazardous coal where even low levels of smoky coal attenuated the association. Our results suggest that the adverse effects of tobacco may become more apparent as China's population continues to switch to cleaner fuels for the home, underscoring the urgent need for smoking cessation in China and elsewhere.
    Lung cancer (Amsterdam, Netherlands) 01/2014; 84(1). DOI:10.1016/j.lungcan.2014.01.004 · 3.74 Impact Factor
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    ABSTRACT: Objectives Lung cancer rates in Xuanwei are the highest in China. In-home use of smoky coal was associated with lung cancer risk, and the association of smoking and lung cancer risk strengthens after stove improvement. Here, we explored the differential association of tobacco use and lung cancer risk by the intensity, duration, and type of coal used. Materials and Methods We conducted a population-based case–control study of 260 male lung cancer cases and 260 age-matched male controls. Odds ratios (OR) and 95% confidence interval (CI) for tobacco use was calculated by conditional logistic regression. Results Use of smoky coal was significantly associated with an increased risk of lung cancer risk, and tobacco use was weakly and non-significantly associated with lung cancer risk. When the association was assessed by coal use, the cigarette-lung cancer risk association was null in hazardous coal users and elevated in less hazardous smoky coal users and non-smoky coal users. The risk of lung cancer per cigarette per day decreased as annual use of coal increased (>0-3 tons: OR: 1.09; 95% CI: 1.03-1.17; >3 tons: OR: 0.99; 95% CI: 0.95-1.03). Among more hazardous coal users, attenuation occurs at even low levels of usage (>0-3 tons: OR: 1.02; 95% CI: 0.91-1.14; >3 tons: OR: 0.94; 95% CI: 0.97-1.03). Conclusion Smoky coal attenuates the tobacco and lung cancer risk association in males that lived in Xuanwei, particularly among users of the hazardous coal where low levels of smoky coal attenuate the association. Our results suggest that the adverse effects of tobacco may become more apparent as China's population continues to switch to using cleaner fuels for the home, underscoring the urgent need for smoking cessation in China and elsewhere.
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    ABSTRACT: To evaluate the immunotoxicity of trichloroethylene (TCE), we conducted a cross-sectional molecular epidemiology study in China of workers exposed to TCE. We measured serum levels of IL-6, IL-10, and TNF-α, which play a critical role in regulating various components of the immune system, in 71 exposed workers and 78 unexposed control workers. Repeated personal exposure measurements were taken in workers before blood collection using 3 M organic vapor monitoring badges. Compared to unexposed workers, the serum concentration of IL-10 in workers exposed to TCE was decreased by 70% (P = 0.001) after adjusting for potential confounders. Further, the magnitude of decline in IL-10 was >60% and statistically significant in workers exposed to <12 ppm as well as in workers with exposures ≥ 12 ppm of TCE, compared to unexposed workers. No significant differences in levels of IL-6 or TNF-α were observed among workers exposed to TCE compared to unexposed controls. Given that IL-10 plays an important role in immunologic processes, including mediating the Th1/Th2 balance, our findings provide additional evidence that TCE is immunotoxic in humans. Environ. Mol. Mutagen., 2013. © 2013 Wiley Periodicals, Inc.
    Environmental and Molecular Mutagenesis 07/2013; DOI:10.1002/em.21789 · 2.55 Impact Factor
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    ABSTRACT: BACKGROUND: Formaldehyde is used in many occupational settings, most notably in manufacturing, health care, and embalming. Formaldehyde has been classified as a human carcinogen, but its mechanism of action remains uncertain. METHODS: We carried out a cross-sectional study of 43 formaldehyde-exposed workers and 51 unexposed age and sex-matched controls in Guangdong, China to study formaldehyde's early biologic effects. To follow up our previous report that the total lymphocyte count was decreased in formaldehyde-exposed workers compared with controls, we evaluated each major lymphocyte subset (i.e., CD4(+) T cells, CD8(+) T cells, natural killer [NK] cells, and B cells) and T cell lymphocyte subset (CD4(+) naïve and memory T cells, CD8(+) naïve and memory T cells, and regulatory T cells). Linear regression of each subset was used to test for differences between exposed workers and controls, adjusting for potential confounders. RESULTS: Total NK cell and T cell counts were about 24% (P = 0.037) and 16% (P = 0.0042) lower, respectively, among exposed workers. Among certain T cell subsets, decreased counts among exposed workers were observed for CD8(+) T cells (P = 0.026), CD8(+) effector memory T cells (P = 0.018), and regulatory T cells (CD4(+) FoxP3(+) : P = 0.04; CD25(+) FoxP3(+) : P = 0.008). CONCLUSIONS: Formaldehyde-exposed workers experienced decreased counts of NK cells, regulatory T cells, and CD8(+) effector memory T cells; however, due to the small sample size; these findings need to be confirmed in larger studies. Am. J. Ind. Med. © 2012 Wiley Periodicals, Inc.
    American Journal of Industrial Medicine 02/2013; 56(2). DOI:10.1002/ajim.22088 · 1.59 Impact Factor
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    ABSTRACT: Epidemiological studies suggest that trichloroethylene (TCE) exposure may be associated with renal cancer. The biological mechanisms involved are not exactly known although nephrotoxicity is believed to play a role. Studies on TCE nephrotoxicity among humans, however, have been largely inconsistent. We studied kidney toxicity in Chinese factory workers exposed to TCE using novel sensitive nephrotoxicity markers. Eighty healthy workers exposed to TCE and 45 comparable unexposed controls were included in the present analyses. Personal TCE exposure measurements were taken over a 2-week period before urine collection. Ninety-six percent of workers were exposed to TCE below the current US Occupational Safety and Health Administration permissible exposure limit (100 ppm 8h TWA), with a mean (SD) of 22.2 (35.9) ppm. Kidney injury molecule-1 (KIM-1) and Pi-glutathione S transferase (GST) alpha were elevated among the exposed subjects as compared with the unexposed controls with a strong exposure-response association between individual estimates of TCE exposure and KIM-1 (P < 0.0001). This is the first report to use a set of sensitive nephrotoxicity markers to study the possible effects of TCE on the kidneys. The findings suggest that at relatively low occupational exposure levels a toxic effect on the kidneys can be observed. This finding supports the biological plausibility of linking TCE exposure and renal cancer.
    Carcinogenesis 06/2012; 33(8):1538-41. DOI:10.1093/carcin/bgs191 · 5.27 Impact Factor
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    ABSTRACT: Benzene exposure causes acute myeloid leukemia and hematotoxicity, shown as suppression of mature blood and myeloid progenitor cell numbers. As the leukemia-related aneuploidies monosomy 7 and trisomy 8 previously had been detected in the mature peripheral blood cells of exposed workers, we hypothesized that benzene could cause leukemia through the induction of these aneuploidies in hematopoietic stem and progenitor cells. We measured loss and gain of chromosomes 7 and 8 by fluorescence in situ hybridization in interphase colony-forming unit-granulocyte-macrophage (CFU-GM) cells cultured from otherwise healthy benzene-exposed (n=28) and unexposed (n=14) workers. CFU-GM monosomy 7 and 8 levels (but not trisomy) were significantly increased in subjects exposed to benzene overall, compared with levels in the control subjects (P=0.0055 and P=0.0034, respectively). Levels of monosomy 7 and 8 were significantly increased in subjects exposed to <10 p.p.m. (20%, P=0.0419 and 28%, P=0.0056, respectively) and 10 p.p.m. (48%, P=0.0045 and 32%, 0.0354) benzene, compared with controls, and significant exposure-response trends were detected (P(trend)=0.0033 and 0.0057). These data show that monosomies 7 and 8 are produced in a dose-dependent manner in the blood progenitor cells of workers exposed to benzene, and may be mechanistically relevant biomarkers of early effect for benzene and other leukemogens.Leukemia advance online publication, 22 June 2012; doi:10.1038/leu.2012.143.
    Leukemia: official journal of the Leukemia Society of America, Leukemia Research Fund, U.K 05/2012; DOI:10.1038/leu.2012.143 · 9.38 Impact Factor
  • Cancer Research 07/2011; 71(8 Supplement):1876-1876. DOI:10.1158/1538-7445.AM2011-1876 · 9.28 Impact Factor
  • Cancer Research 07/2011; 71(8 Supplement):4645-4645. DOI:10.1158/1538-7445.AM2011-4645 · 9.28 Impact Factor
  • Cancer Research 07/2011; 71(8 Supplement):4646-4646. DOI:10.1158/1538-7445.AM2011-4646 · 9.28 Impact Factor
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    ABSTRACT: Immune deficiency is one of the best characterized and strongest known risk factors for non-Hodgkin lymphoma (NHL). We studied the association between single nucleotide polymorphisms (SNPs) in integrin genes that are important components in human innate immunity and the risk of NHL in a population-based case-control study of women in Connecticut, USA. A total of 373 tag SNPs in 33 gene regions were included in the analysis of 448 cases and 525 controls. The ADAM19 rs11466782 SNP was associated with an increased risk of lymphoma (OR, 1.73; 95% CI, 1.28-2.35; Padditive=0.0004), and the ICAM3 rs2304240 (OR, 0.67; 95% CI, 0.52-0.86; Padditive=0.002) and the PTGDR rs708486 SNPs (OR, 0.75; 95% CI, 0.63-0.90; Padditive=0.002) were associated with reduced risk of lymphoma. Two gene regions (ADAM19 (P=0.009) and ICAM3 (P=0.009)) displayed global associations with lymphoma risk at the P<0.01 level. While our results suggest that genetic polymorphisms in integrin genes may play a role in the genesis of lymphoma in women, they should be viewed as exploratory until they are replicated in additional populations.
    Leukemia research 07/2011; 35(7):968-70. DOI:10.1016/j.leukres.2010.12.012 · 2.69 Impact Factor
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    ABSTRACT: Telomeres play a key role in the maintenance of chromosome integrity and stability, and telomere shortening is involved in initiation and progression of malignancies. A series of epidemiological studies have examined the association between shortened telomeres and risk of cancers, but the findings remain conflicting. A dataset composed of 11,255 cases and 13,101 controls from 21 publications was included in a meta-analysis to evaluate the association between overall cancer risk or cancer-specific risk and the relative telomere length. Heterogeneity among studies and their publication bias were further assessed by the χ(2)-based Q statistic test and Egger's test, respectively. The results showed that shorter telomeres were significantly associated with cancer risk (OR = 1.35, 95% CI = 1.14-1.60), compared with longer telomeres. In the stratified analysis by tumor type, the association remained significant in subgroups of bladder cancer (OR = 1.84, 95% CI = 1.38-2.44), lung cancer (OR = 2.39, 95% CI = 1.18-4.88), smoking-related cancers (OR = 2.25, 95% CI = 1.83-2.78), cancers in the digestive system (OR = 1.69, 95% CI = 1.53-1.87) and the urogenital system (OR = 1.73, 95% CI = 1.12-2.67). Furthermore, the results also indicated that the association between the relative telomere length and overall cancer risk was statistically significant in studies of Caucasian subjects, Asian subjects, retrospective designs, hospital-based controls and smaller sample sizes. Funnel plot and Egger's test suggested that there was no publication bias in the current meta-analysis (P = 0.532). The results of this meta-analysis suggest that the presence of shortened telomeres may be a marker for susceptibility to human cancer, but single larger, well-design prospective studies are warranted to confirm these findings.
    PLoS ONE 06/2011; 6(6):e20466. DOI:10.1371/journal.pone.0020466 · 3.53 Impact Factor
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    ABSTRACT: Benzene, a recognized hematotoxicant and carcinogen, can damage the human immune system. We studied the association between single nucleotide polymorphisms (SNPs) in genes involved in innate immunity and benzene hematotoxicity in a cross-sectional study of workers exposed to benzene (250 workers and 140 controls). A total of 1,236 tag SNPs in 149 gene regions of six pathways were included in the analysis. Six gene regions were significant for their association with white blood cell (WBC) counts (MBP, VCAM1, ALOX5, MPO, RAC2, and CRP) based on gene-region (P<0.05) and SNP analyses (FDR<0.05). VCAM1 rs3176867, ALOX5 rs7099684, and MPO rs2071409 were the three most significant SNPs. They showed similar effects on WBC subtypes, especially granulocytes, lymphocytes, and monocytes. A 3-SNP block in ALOXE3 (rs7215658, rs9892383, and rs3027208) showed a global association (omnibus P = 0.0008) with WBCs even though the three SNPs were not significant individually. Our study suggests that polymorphisms in innate immunity genes may play a role in benzene-induced hematotoxicity; however, independent replication is necessary.
    Experimental and Molecular Medicine 05/2011; 43(6):374-8. DOI:10.3858/emm.2011.43.6.041 · 2.46 Impact Factor
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    ABSTRACT: Telomere length plays an important role in chromosomal stability and tumorigenesis, and its measurement in peripheral white blood cell DNA may be a predictor of the development of lung cancer. Using a new method - monochrome multiplex quantitative PCR - which reduces measurement variability, we compared telomere length relative to standard DNA in white blood cell DNA in 229 incident male lung cancer cases and 229 matched controls within the prospective Alpha-Tocopherol, Beta-Carotene Cancer Prevention (ATBC) Study of male smokers. Median (10th, 90th percentile) telomere length was 1.13 (0.86, 1.45) in cases and 1.08 (0.85, 1.38) in controls (P=0.038). Telomere length was inversely associated with pack-years of smoking (Spearman's correlation r=-0.16, P=0.02) among controls. Compared to subjects with shorter telomere length (≤median), subjects with greater telomere length (>median) had a 1.6-fold (95% CI, 1.06-2.36) increased risk of lung cancer. There was a significant linear relationship between quartiles of telomere length and risk of lung cancer (odds ratios (95% confidence intervals) by quartile: 1.00, 0.98 (0.55-1.73), 1.62 (0.95-2.77), and 1.50 (0.84-2.68); P(trend)=0.05). In addition, subgroup analysis showed that greater telomere length was associated with an increased risk of lung cancer among longer-term smokers (>38 years) (OR, 1.90; 95% CI, 1.00-3.59) but not among shorter-term smokers (≤38 years) (OR, 1.08; 95% CI, 0.56-2.11) (P(interaction)=0.01). Our results suggest that greater telomere length may be associated with higher risk of lung cancer among male smokers.
    Lung cancer (Amsterdam, Netherlands) 04/2011; 73(2):133-7. DOI:10.1016/j.lungcan.2010.11.009 · 3.74 Impact Factor
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    ABSTRACT: Evidence suggests that de novo, therapy-related and benzene-induced acute myeloid leukemias (AML) occur via similar cytogenetic and genetic pathways, several of which involve aneuploidy, the loss or gain of chromosomes. Aneuploidy of specific chromosomes has been detected in benzene-related leukemia patients as well as in healthy benzene-exposed workers, suggesting that aneuploidy precedes and may be a potential mechanism underlying benzene-induced leukemia. Here, we analyzed the peripheral blood lymphocytes of 47 exposed workers and 27 unexposed controls using a novel OctoChrome fluorescence in situ hybridization (FISH) technique that simultaneously detects aneuploidy in all 24 chromosomes. Through this chromosome-wide aneuploidy study (CWAS) approach, we found heterogeneity in the monosomy and trisomy rates of the 22 autosomes when plotted against continuous benzene exposure. In addition, statistically significant, chromosome-specific increases in the rates of monosomy [5, 6, 7, 10, 16 and 19] and trisomy [5, 6, 7, 8, 10, 14, 16, 21 and 22] were found to be dose dependently associated with benzene exposure. Furthermore, significantly higher rates of monosomy and trisomy were observed in a priori defined 'susceptible' chromosome sets compared with all other chromosomes. Together, these findings confirm that benzene exposure is associated with specific chromosomal aneuploidies in hematopoietic cells, which suggests that such aneuploidies may play roles in benzene-induced leukemogenesis.
    Carcinogenesis 03/2011; 32(4):605-12. DOI:10.1093/carcin/bgq286 · 5.27 Impact Factor
  • Cancer Research 01/2011; 70(8 Supplement):2994-2994. DOI:10.1158/1538-7445.AM10-2994 · 9.28 Impact Factor
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    ABSTRACT: Trichloroethylene (TCE) is a volatile chlorinated organic compound that is commonly used as a solvent for lipophilic compounds. Although recognized as an animal carcinogen, TCE's carcinogenic potential in humans is still uncertain. We have carried out a cross-sectional study of 80 workers exposed to TCE and 96 unexposed controls matched on age and sex in Guangdong, China to study TCE's early biologic effects. We previously reported that the total lymphocyte count and each of the major lymphocyte subsets (i.e., CD4(+) T cells, CD8(+) T cells, natural killer cells, and B cells) were decreased in TCE-exposed workers compared to controls, suggesting a selective effect on lymphoid progenitors, and/or lymphocyte survival. To explore which T lymphocyte subsets are affected in the same study population, we investigated the effect of TCE exposure on the numbers of CD4(+) naïve and memory T cells, CD8(+) naïve and memory T cells, and regulatory T cells by FACS analysis. Linear regression of each subset was used to test for differences between exposed workers and controls adjusting for potential confounders. We observed that CD4(+) and CD8(+) naïve T cell counts were about 8% (p = 0.056) and 17% (p = 0.0002) lower, respectively, among exposed workers. CD4(+) effector memory T cell counts were decreased by about 20% among TCE-exposed workers compared to controls (p = 0.001). The selective targeting of TCE on CD8(+) naive and possibly CD4(+) naive T cells, and CD4(+) effector memory T cells, provide further insights into the immunosuppression-related response of human immune cells upon TCE exposure.
    Frontiers in Oncology 01/2011; 1:53. DOI:10.3389/fonc.2011.00053
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    ABSTRACT: The genetic basis of chronic lymphocytic leukemia (CLL) has not been fully elucidated to date. Although it is the most common haematological malignancy in Caucasians, it is uncommon among Asians. A recent genome-wide scan of CLL in Caucasians, which was carried out in the UK, identified six variants showing strong association. We attempted to replicate these findings in 71 patients with CLL and 1273 controls in Hong Kong Chinese. Three of the six variants were significantly associated with CLL. The rs872071 variant (Odds Ratio (95% Confidence Interval) = 1.78 (1.25-2.53), P = 0.0013) in the IRF4 gene region showed the strongest association, similar to that reported in the UK study. Polymorphisms in SP140 and ACOXL were also associated with risk of CLL. Further, the mean allele frequencies of the six variants were moderately (59%) to extremely (0.5%) lower in the Chinese population compared with Caucasians. These results suggest that variants in three loci may contribute to risk of CLL among Chinese.
    European Journal Of Haematology 12/2010; 85(6):492-5. DOI:10.1111/j.1600-0609.2010.01518.x · 2.41 Impact Factor

Publication Stats

2k Citations
394.45 Total Impact Points

Institutions

  • 2008–2015
    • National Institutes of Health
      • • Division of Cancer Epidemiology and Genetics
      • • Branch of Occupational and Environmental Epidemiology
      베서스다, Maryland, United States
  • 2014
    • Interfaith Medical Center
      Brooklyn, New York, United States
  • 2005–2014
    • National Cancer Institute (USA)
      • • Division of Cancer Epidemiology and Genetics
      • • Occupational and Environmental Epidemiology
      Maryland, United States
  • 2012
    • Universiteit Utrecht
      • Institute for Risk Assessment Sciences (IRAS)
      Utrecht, Provincie Utrecht, Netherlands
  • 2006–2011
    • University of California, Berkeley
      • • Department of Environmental Health Sciences
      • • School of Public Health
      Berkeley, MO, United States
    • Finnish Cancer Registry, Helsinki
      Helsinki, Uusimaa, Finland
    • Yale University
      • Department of Molecular, Cellular and Developmental Biology
      New Haven, Connecticut, United States
  • 2005–2011
    • NCI-Frederick
      Maryland, United States
  • 2004–2009
    • Northern Inyo Hospital
      BIH, California, United States
  • 2007
    • University of North Carolina at Chapel Hill
      • Department of Environmental Sciences and Engineering
      Chapel Hill, NC, United States