Hong Wang

University of Texas MD Anderson Cancer Center, Houston, Texas, United States

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Publications (122)793.55 Total impact

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    ABSTRACT: Epithelial to mesenchymal transition (EMT) is a key process associated with tumor progression and metastasis. To define molecular features associated with EMT states, we undertook an integrative approach combining mRNA, microRNA, DNA methylation and proteomic profiles of 38 cell populations representative of the genomic heterogeneity in lung adenocarcinoma were integrated with functional profiles consisting of cell invasiveness, adhesion and motility. A subset of cell lines that were readily defined as epithelial or mesenchymal based on their morphology and E-cadherin and vimentin expression elicited distinctive molecular signatures. However, most cell populations displayed intermediate/hybrid states of EMT, with mixed epithelial and mesenchymal characteristics. A dominant proteomic feature of aggressive hybrid cell lines was upregulation of cytoskeletal and actin binding proteins, a signature shared with mesenchymal cell lines. Cytoskeletal reorganization preceded loss of E-cadherin in epithelial cells in which EMT was induced by TGFβ. A set of transcripts corresponding to the mesenchymal protein signature enriched in cytoskeletal proteins was found to be predictive of survival in independent datasets of lung adenocarcinomas. Our findings point to an association between cytoskeletal and actin-binding proteins, a mesenchymal or hybrid EMT phenotype and invasive properties of lung adenocarcinomas. Copyright © 2015, American Association for Cancer Research.
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    ABSTRACT: PNGase F-catalyzed glycosylation site 18O-labeling is a widely used method for glycoprotein quantitation owing to its efficiency and simplicity. However, PNGase F-catalyzed glycan 18O-labeling, which offers advantages for glycomics, has not been developed yet. In this study, PNGase F-mediated incorporation of 18O into Glycans during the N-glycans released from glycoproteins by PNGase F was finally realized, naming as PCGOL (PNGase F-catalyzed glycan 18O-labeling), which offers a potential strategy for relative glycan quantitation. This new method showed good linearity and high reproducibility within at least 2 orders of magnitude in dynamic range. Furthermore, PCGOL combined with our previously developed TOSIL method (Tandem 18O stable isotope labeling for N-glycoproteome quantitation) can be used for comprehensive N-glycosylation quantification, achieving simultaneous quantification of glycan, glycopeptide and glycoprotein in a single workflow, which was also used to analyze glycosylation changes in immunoglobulin G (IgG) associated with hepatocellular carcinoma in the present work.
    The Analyst 12/2014; 140(4). DOI:10.1039/C4AN02073A · 3.91 Impact Factor
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    ABSTRACT: Objective To evaluate whether uric acid (UA) predicts 4-yr incidence of metabolic syndrome (MetS) in non-diabetic participants of the Strong Heart Study (SHS) cohort. Design and Methods: In this population-based prospective study we analyzed 1499 American Indians (890 women), without diabetes or MetS, controlled during the 4th SHS exam and re-examined 4 years later during the 5th SHS exam. Participants were divided into sex-specific tertiles of UA and the first two tertiles (group N) were compared with the third tertile (group H). Results Body mass index (BMI =28.3±7 vs. 31.1±7 kg/m2), fat-free mass (FFM = 52.0±14 vs. 54.9±11 kg), waist-to-hip ratio, HOMA-IR (3.66 vs. 4.26), BP and indices of inflammation were significantly higher in group H than in group N (all p<0.001). Incident MetS at the time of the 5th exam was more frequent in group H than group N (35 vs. 28%, OR 1.44 (95% CI=1.10-1.91; p< 0.01). This association was still significant (OR= 1.13, p=0.04) independently of family relatedness, sex, history of hypertension, HOMA-IR, central adiposity and renal function, but disappeared when fat-free mass was included in the model. Conclusions In the SHS, UA levels are associated to parameters of insulin resistance and to indices of inflammation. UA levels, however, do not predict incident MetS independently of the initial obesity-related increased FFM.
    Nutrition Metabolism and Cardiovascular Diseases 12/2014; DOI:10.1016/j.numecd.2014.06.002 · 3.88 Impact Factor
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    ABSTRACT: p53 is commonly mutated in lung adenocarcinoma. Mutant p53 loses wild-type function and some missense mutations further acquire oncogenic functions, while p53 wild-type may also induce pro-survival signaling. Therefore identification of signatures based on p53 mutational status has relevance to our understanding of p53 signaling pathways in cancer and identification of new therapeutic targets. To this end, we compared proteomic profiles of three cellular compartments (whole cell extract (WCE), cell surface, and media) from 28 human lung adenocarcinoma cell lines that differ based on p53 mutational status. In total, 11598 11569 and 9090 protein forms were identified in WCE, cell surface, and media, respectively. Bioinformatic analysis revealed that representative pathways associated with epithelial adhesion, immune and stromal cells, and mitochondrial function were highly significant in p53 missense mutations, p53 loss and wild-type p53 cell lines, respectively. Of note, mRNA levels of PGC1-α, a transcription co-activator that promotes mitochondrial oxidative phosphorylation and mitochondrial biogenesis, was substantially higher in p53 wild-type cell lines compared to either cell lines with p53 loss or with missense mutation. siRNA targeting PGC1-α inhibited cell proliferation in p53 wild-type cell lines, indicative of PGC1-α and its downstream molecules as potential therapeutic targets in p53 wild-type lung adenocarcinoma.This article is protected by copyright. All rights reserved
    Proteomics 12/2014; 14(23-24). DOI:10.1002/pmic.201400378 · 3.97 Impact Factor
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    ABSTRACT: Non-uniform distribution of drug-eluting stent struts may cause uneven drug deposition associated with an adverse neointimal response and clinical events. This study assesses circumferential stent strut distribution in bare-metal (BMS) and paclitaxel-eluting (Taxus) stents post implantation and at 9-month follow-up, as well as its impact on intimal hyperplasia (IH).
    The Journal of invasive cardiology 10/2014; 26(10):501-11. · 0.82 Impact Factor
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    ABSTRACT: Purpose: We evaluated the relationship between dietary fiber, fruit and vegetable intake, and the risk of kidney stone formation. Materials and Methods: Overall 83,922 postmenopausal women from the Women's Health Initiative observational study were included in the analysis and followed prospectively. Cox proportional hazards regression analyses were used to evaluate the associations between total dietary fiber, fruit and vegetable intake, and the risk of incident kidney stone formation, adjusting for nephrolithiasis risk factors (age, race/ethnicity, geographic region, diabetes mellitus, calcium supplementation, hormone therapy use, body mass index and calibrated caloric intake; and dietary water, sodium, animal protein and calcium intake). Women with a history of kidney stones (3,471) were analyzed separately. Results: Mean age of the women was 64 +/- 7 years, 85% were white and 2,937 (3.5%) experienced a kidney stone in a median followup of 8 years. In women with no history of kidney stones higher total dietary fiber (6% to 26% decreased risk, p < 0.001), greater fruit intake (12% to 25% decreased risk, p < 0.001) and greater vegetable intake (9% to 22% decreased risk, p = 0.002) were associated with a decreased risk of incident kidney stone formation in separate adjusted models. In women with a history of stones there were no significant protective effects of fiber, fruit or vegetable intake on the risk of kidney stone recurrence. Conclusions: Greater dietary intake of fiber, fruits and vegetables was associated with a reduced risk of incident kidney stones in postmenopausal women. The protective effects were independent of other known risk factors for kidney stones. In contrast, there was no reduction in risk in women with a history of stones.
    The Journal of Urology 05/2014; 192(6). DOI:10.1016/j.juro.2014.05.086 · 3.75 Impact Factor
  • Gastroenterology 05/2014; 146(5):S-816. DOI:10.1016/S0016-5085(14)62954-1 · 13.93 Impact Factor
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    ABSTRACT: Objectives. We determined all-cause, cardiovascular disease (CVD), and cancer mortality in western Alaska Native people and examined agreement between death certificate information and adjudicated cause of deaths. Methods. Data from 4 cohort studies were consolidated. Death certificates and medical records were reviewed and adjudicated according to standard criteria. We compared adjudicated CVD and cancer deaths with death certificates by calculating sensitivity, specificity, predictive values, and κ statistics. Results. Men (n = 2116) and women (n = 2453), aged 18 to 95 years, were followed an average of 6.7 years. The major cause of death in men was trauma (25%), followed by CVD (19%) and cancer (13%). The major cause of death in women was CVD (24%), followed by cancer (19%) and trauma (8%). Stroke rates in both genders were higher than those of US Whites. Only 56% of deaths classified as CVD by death certificate were classified as CVD by standard criteria; discordance was higher among men (55%) than women (32%; κs = 0.4 and 0.7). Conclusions. We found lower rates for coronary heart disease death but high rates of stroke mortality. Death certificates overestimated CVD mortality; concordance between the 2 methods is better for cancer mortality. The results point to the importance of cohort studies in this population in providing data to assist in health care planning. (Am J Public Health. Published online ahead of print April 22, 2014: e1-e7. doi:10.2105/AJPH.2013.301614).
    American Journal of Public Health 04/2014; 104(7). DOI:10.2105/AJPH.2013.301614 · 4.23 Impact Factor
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    ABSTRACT: AST-120 (spherical carbon adsorbent) was previously reported to be effective for perianal fistula healing in Japanese patients with mild-to-moderate Crohn's disease. To evaluate the efficacy and safety of AST-120 in a Western population, a phase 3, multicenter, randomized, double-blind, placebo-controlled, study (FHAST-1) was conducted in adult patients with at least 1 draining perianal fistula and a Crohn's disease activity index <400. Patients received either AST-120 or matching placebo at a dose of 2 g 3 times daily for 8 weeks. The primary endpoint was the proportion of patients with treatment success, defined as a 50% reduction in the number of draining fistulae, at both weeks 4 and 8. A multivariate model was generated to assess covariates for treatment success among baseline variables. Two hundred forty-nine patients were randomized (AST-120; n = 122; placebo, n = 127). The proportions of patients achieving the primary endpoint were no different between treatment groups (13.9% versus 16.5%, P = 0.6). No differences in fistula response were noted at week 4 (23.0% versus 25.2%, P = 0.77) or week 8 (27.0 versus 34.6%, P = 0.22). Serum C-reactive protein concentrations >0.6 mg/dL and Crohn's disease activity index scores >151 at baseline were associated with a reduced likelihood of treatment success (odds ratio, 0.40; confidence interval, 0.19-0.87; P = 0.02; and odds ratio, 0.45; confidence interval, 0.21-0.97; P = 0.04, respectively). In this largest placebo-controlled trial to date to evaluate the impact of a therapeutic agent on perianal fistulae in Crohn's disease, the efficacy of AST-120 could not be confirmed. An inverse relationship was observed between both inflammatory and clinical disease activity and fistula response.
    Inflammatory Bowel Diseases 04/2014; DOI:10.1097/MIB.0000000000000031 · 5.48 Impact Factor
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    ABSTRACT: Background: The sex-determining region Y-box 17 (SOX17) is a member of the high mobility group (HMG) transcription factor family, which plays critical roles in the regulation of development and stem/precursor cell function. Recent evidence demonstrated that SOX17 acts as a tumor-suppressor gene, at least partly though repression of Wnt pathway activity. Methods: Here we report that SOX17 methylation was detected in THP-1 and SKM-1 cell lines and SOX17 mRNA levels was up-regulated by 5-aza-dC. To clarify the role of SOX17 in MDS, methylation-specific PCR (MSP) was employed to examine the methylation status of SOX17 in 164 adult de novo MDS patients and 6 normal samples. Results: We found that SOX17 methylation was presented in 58.5% (n = 96) of these patients and none of the normal samples. Methylation was correlated significantly with World Health Organization (WHO) subtypes and international prognostic scoring system (IPSS) risk group. Patients with advanced stages of WHO subtypes (69.6% vs. 44.4%, p = 0.001) and higher risk IPSS subgroups (69.8% vs. 48.8%, p = 0.010) exhibited a significantly higher frequency of SOX17 methylation. Though multivariate analysis indicated that SOX17 methylation status was not the independent factor that impacted overall survival (OS) (HR = 0.097), there were significant differences in marrow blast levels and the IPSS risk subgroups between patients with and without SOX17 methylation. Conclusions: These findings suggest that the hypermethylation of SOX17 promoter may be one of the early events in the development of MDS and predicts poor prognosis.
    Clinical laboratory 01/2014; 60(9):1465-74. DOI:10.7754/Clin.Lab.2013.130414 · 1.08 Impact Factor
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    ABSTRACT: Lectin array is becoming important in profiling targeted glycan/glycoprotein, but weak interaction between lectin and glycan causes low sensitivity of the approach. This study aims to develop a bead-based lectin array for improving the sensitivity of glycosylation profiling. Lectins are chemically coupled to fluorescent dye coated microbeads, and glycan-lectin recognition is carried out three-dimensionally. The performance of this platform was evaluated, and the limit of detection of lectin Ricinus communis agglutinin 120 (RCA120) was 50 pg/mL (1 pM) of asialofetuin, providing the bead-based lectin microarray with the highest sensitivity among the reported lectin microarrays. Furthermore, multiplexed assay was performed, which allowed the simultaneous detection of multiple carbohydrate epitopes in a single reaction vessel. The glycosylation patterns of hepatocellular carcinoma associated immunoglobulin G were analyzed, and increased (α-1, 6) core fucosylation and (α-2, 6) sialylation patterns were observed, which may provide significant clinical evidence for disease diagnosis. This article is protected by copyright. All rights reserved.
    Proteomics 01/2014; 14(1). DOI:10.1002/pmic.201200544 · 3.97 Impact Factor
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    ABSTRACT: To study the complex cellular interactions involved in wound healing, it is essential to have an animal model that adequately mimics the human wound microenvironment. Currently available murine models are limited because wound contraction introduces bias into wound surface area measurements. The purpose of this study was to demonstrate utility of a human-mouse xenograft model for studying human wound healing. Normal human skin was harvested from elective abdominoplasty surgery, xenografted onto athymic nude (nu/nu) mice, and allowed to engraft for 3 months. The graft was then wounded using a 2-mm punch biopsy. Wounds were harvested on sequential days to allow tissue-based markers of wound healing to be followed sequentially. On the day of wound harvest, mice were injected with XenoLight RediJect cyclooxygenase-2 (COX-2) probe and imaged according to package instructions. Immunohistochemistry confirms that this human-mouse xenograft model is effective for studying human wound healing in vivo. Additionally, in vivo fluorescent imaging for inducible COX-2 demonstrated upregulation from baseline to day 4 (P = 0·03) with return to baseline levels by day 10, paralleling the reepithelialisation of the wound. This human-mouse xenograft model, combined with in vivo fluorescent imaging provides a useful mechanism for studying molecular pathways of human wound healing.
    International Wound Journal 12/2013; DOI:10.1111/iwj.12205 · 2.02 Impact Factor
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    ABSTRACT: Obesity is a strong risk factor for nephrolithiasis, but the role of physical activity and caloric intake remains poorly understood. We evaluated this relationship in 84,225 women with no history of stones as part of the Women's Health Initiative Observational Study, a longitudinal, prospective cohort of postmenopausal women enrolled from 1993 to 1998 with 8 years' median follow-up. The independent association of physical activity (metabolic equivalents [METs]/wk), calibrated dietary energy intake, and body mass index (BMI) with incident kidney stone development was evaluated after adjustment for nephrolithiasis risk factors. Activity intensity was evaluated in stratified analyses. Compared with the risk in inactive women, the risk of incident stones decreased by 16% in women with the lowest physical activity level (adjusted hazard ratio [aHR], 0.84; 95% confidence interval [95% CI], 0.74 to 0.97). As activity increased, the risk of incident stones continued to decline until plateauing at a decrease of approximately 31% for activity levels ≥10 METs/wk (aHR, 0.69; 95% CI, 0.60 to 0.79). Intensity of activity was not associated with stone formation. As dietary energy intake increased, the risk of incident stones increased by up to 42% (aHR, 1.42; 95% CI, 1.02 to 1.98). However, intake <1800 kcal/d did not protect against stone formation. Higher BMI category was associated with increased risk of incident stones. In summary, physical activity may reduce the risk of incident kidney stones in postmenopausal women independent of caloric intake and BMI, primarily because of the amount of activity rather than exercise intensity. Higher caloric intake further increases the risk of incident stones.
    Journal of the American Society of Nephrology 12/2013; 25(2). DOI:10.1681/ASN.2013050548 · 9.47 Impact Factor
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    ABSTRACT: No plasma biomarkers are associated with the response of acute graft-versus-host disease (GVHD) to therapy after allogeneic hematopoietic stem-cell transplantation. We compared 12 biomarkers in plasma obtained a median of 16 days after therapy initiation from 10 patients with a complete response by day 28 after therapy initiation and in plasma obtained from 10 patients with progressive GVHD during therapy. The lead biomarker, suppression of tumorigenicity 2 (ST2), was measured at the beginning of treatment for GVHD in plasma from 381 patients and during the first month after transplantation in three independent sets totaling 673 patients to determine the association of this biomarker with treatment-resistant GVHD and 6-month mortality after treatment or transplantation. Of the 12 markers, ST2 had the most significant association with resistance to GVHD therapy and subsequent death without relapse. As compared with patients with low ST2 values at therapy initiation, patients with high ST2 values were 2.3 times as likely to have treatment-resistant GVHD (95% confidence interval [CI], 1.5 to 3.6) and 3.7 times as likely to die within 6 months after therapy (95% CI, 2.3 to 5.9). Patients with low ST2 values had lower mortality without relapse than patients with high ST2 values, regardless of the GVHD grade (11% vs. 31% among patients with grade I or II GVHD and 14% vs. 67% among patients with grade III or IV GVHD, P<0.001 for both comparisons). Plasma ST2 values at day 14 after transplantation were associated with 6-month mortality without relapse, regardless of the intensity of the conditioning regimen. ST2 levels measured at the initiation of therapy for GVHD and during the first month after transplantation improved risk stratification for treatment-resistant GVHD and death without relapse after transplantation. (Funded by the National Institutes of Health.)
    New England Journal of Medicine 08/2013; 369(6):529-39. DOI:10.1056/NEJMoa1213299 · 54.42 Impact Factor
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    ABSTRACT: PURPOSE: Proteomics technologies are well suited for harnessing the immune response to tumor antigens for diagnostic applications as in the case of breast cancer. We previously reported a substantial impact of hormone therapy (HT) on the proteome. Here we investigated the effect of HT on the immune response toward breast tumor antigens. EXPERIMENTAL DESIGN: Plasmas collected 0-10 months prior to diagnosis of ER+ breast cancer from 190 post-menopausal women and 190 controls that participated in the Women's Health Initiative (WHI) Observational Study were analyzed for the effect of HT on IgG reactivity against arrayed proteins from MCF-7 or SKBR3 breast cancer cell line lysates following extensive fractionation. RESULTS: HT user cases exhibited significantly reduced autoantibody reactivity against arrayed proteins compared to cases who were not current users. An associated reduced level of IL-6 and other immune-related cytokines was observed among HT users relative to non-users. CONCLUSION AND CLINICAL RELEVANCE: Our findings suggest occurrence of a global altered immune response to breast cancer derived proteins associated with HT. Thus a full understanding of factors that modulate the immune response is necessary to translate autoantibody panels into clinical applications.
    PROTEOMICS - CLINICAL APPLICATIONS 06/2013; 7(5-6). DOI:10.1002/prca.201200058 · 2.68 Impact Factor
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    Journal of Clinical Hypertension 04/2013; 15(4):299. DOI:10.1111/jch.12064 · 2.96 Impact Factor
  • The Journal of Urology 04/2013; 189(4):e28. DOI:10.1016/j.juro.2013.02.1445 · 3.75 Impact Factor
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    ABSTRACT: Linking an ester group to the imidazolium ring has been demonstrated to improve solar cell performance in terms of short-circuit photocurrent (Jsc), open-circuit photovoltage (Voc) and fill factor (FF) in particular, when the imidazolium iodide mixed with iodine and LiI is used as solid state electrolyte of dye-sensitized solar cells. Herein, the effect of ester group on solar cell performance has been investigated by means of intensity modulated photocurrent/photovoltage and electrochemical impedance spectroscopy. From the alkyl- to ester-functionalized imidazolium iodide, the increase in Jsc is attributed to the increased charge collection efficiency due to the enhanced conductivity, the increase in Voc is caused by the upward shift of conduction band edge of TiO2, which compensates for the voltage loss arising from the higher charge recombination rate, and the remarkable increase in FF is attributed to the decreased series resistance along with the increased Voc and decreased diode quality factor.
    ACS Applied Materials & Interfaces 03/2013; 5(8). DOI:10.1021/am4002293 · 5.90 Impact Factor
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    ABSTRACT: OBJECTIVES: This study sought to investigate into the biologically plausible interaction between the common haptoglobin (Hp) polymorphism rs#72294371 and glycosylated hemoglobin (HbA(1c)) on risk of coronary heart disease (CHD). BACKGROUND: Studies of the association between the Hp polymorphism and CHD report inconsistent results. Individuals with the Hp2-2 genotype produce Hp proteins with an impaired ability to prevent oxidative injury caused by elevated HbA(1c). METHODS: HbA(1c) concentration and Hp genotype were determined for 407 CHD cases matched 1:1 to controls (from the NHS [Nurses' Health Study]) and in a replication cohort of 2,070 individuals who served as the nontreatment group in the ICARE (Israel Cardiovascular Events Reduction With Vitamin E) study, with 29 CHD events during follow-up. Multivariate models were adjusted for lifestyle and CHD risk factors as appropriate. A pooled analysis was conducted of NHS, ICARE, and the 1 previously published analysis (a cardiovascular disease case-control sample from the Strong Heart Study). RESULTS: In the NHS, Hp2-2 genotype (39% frequency) was strongly related to CHD risk only among individuals with elevated HbA(1c) (≥6.5%), an association that was similar in the ICARE trial and the Strong Heart Study. In a pooled analysis, participants with both the Hp2-2 genotype and elevated HbA(1c) had a relative risk of 7.90 (95% confidence interval: 4.43 to 14.10) for CHD compared with participants with both an Hp1 allele and HbA(1c) <6.5% (p for interaction = 0.004), whereas the Hp2-2 genotype with HbA(1c) <6.5% was not associated with risk (relative risk: 1.34 [95% confidence interval: 0.73 to 2.46]). CONCLUSIONS: Hp genotype was a significant predictor of CHD among individuals with elevated HbA(1c).
    Journal of the American College of Cardiology 01/2013; 61(7). DOI:10.1016/j.jacc.2012.09.063 · 15.34 Impact Factor
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    ABSTRACT: Activation of the Wnt signaling pathway has been implicated in the pathogenesis of many tumors as well as in leukemia. However, its role in myelodysplastic syndrome (MDS) is unknown. In this study, we employed methylation-specific PCR to examine the methylation status of six Wnt antagonist genes in 144 MDS patients and in the MDS cell line SKM-1. We also used real-time PCR to examine the expression of Wnt antagonist genes and Wnt pathway genes in the SKM-1 cell line after treatment with 5-aza-2'-deoxycytidine. We found that methylation of the gene promoters of each of the six genes were observed in MDS patients at the following methylation frequencies: 41 % for sFRP1, 89.6 % for sFRP2, 43.1 % for sFRP4, 50.7 % for sFRP5, 44.4 % for DKK-1, and 69.4 % for DKK-3. In the SKM-1 cell line, the gene promoters sFRP1, sFRP2, sFRP5, DKK-1, and DKK-3 were methylated, while sFRP4 was not methylated. Treatment of the SKM-1 cell line with 5-aza-2'-deoxycytidine induced re-expression of methylated Wnt antagonists and inactivation of the Wnt pathway. Survival analysis showed that methylation status of sFRP1, sFRP4, and sFRP5 was associated with worse survival in MDS and sFRP5 methylation also predicted a high risk of leukemia evolution (P = 0.018). Our results indicate that epigenetic regulation of the Wnt pathway in MDS cell line, and the methylation status of Wnt antagonists predicts prognoses of MDS patients.
    Annals of Hematology 10/2012; 92(2). DOI:10.1007/s00277-012-1595-y · 2.40 Impact Factor

Publication Stats

4k Citations
793.55 Total Impact Points

Institutions

  • 2014–2015
    • University of Texas MD Anderson Cancer Center
      • Department of Clinical Cancer Prevention
      Houston, Texas, United States
  • 2012–2014
    • Soochow University (PRC)
      Wu-hsien, Jiangsu Sheng, China
  • 2009–2014
    • Fudan University
      • Department of Chemistry
      Shanghai, Shanghai Shi, China
    • MedStar Health Research Institute
      هایتسویل، مریلند, Maryland, United States
    • Columbia University
      • Division of Cardiology
      New York, New York, United States
  • 2008–2014
    • Georgetown University
      Washington, Washington, D.C., United States
    • Beth Israel Deaconess Medical Center
      • Department of Medicine
      Boston, Massachusetts, United States
  • 2013
    • University of California, San Francisco
      San Francisco, California, United States
  • 2006–2013
    • Fred Hutchinson Cancer Research Center
      • • Division of Public Health Sciences
      • • Molecular Diagnostics Program
      Seattle, Washington, United States
  • 2008–2012
    • Boston Scientific
      Boston, Massachusetts, United States
  • 2011
    • Cleveland Clinic
      • Department of Internal Medicine
      Cleveland, Ohio, United States
  • 2010
    • Vanderbilt University
      • Department of Radiation Oncology
      Nashville, Michigan, United States
  • 2001–2008
    • University of Michigan
      • Division of Pediatric Genetics
      Ann Arbor, Michigan, United States
  • 2003–2005
    • Concordia University–Ann Arbor
      Ann Arbor, Michigan, United States
  • 2004
    • Harvard University
      • Department of Molecular and Cell Biology
      Cambridge, Massachusetts, United States