Steven Belinsky

Summary

Affiliation: Lovelace Respiratory Research Institute
Country: USA

Publications

  1. ncbi request reprint Gene promoter methylation in plasma and sputum increases with lung cancer risk
    Steven A Belinsky
    Lovelace Respiratory Research Institute, Albuquerque, NM 87108, USA
    Clin Cancer Res 11:6505-11. 2005
  2. pmc Genome-wide unmasking of epigenetically silenced genes in lung adenocarcinoma from smokers and never smokers
    Mathewos Tessema
    Department of Lung Cancer, Lovelace Respiratory Research Institute, Albuquerque, NM 87108, USA, MDxHealth Inc, Irvine, CA 92618, USA, Department of Pathology, GROW School for Oncology and Developmental Biology, Maastricht University Medical Center, 6200 MD, Maastricht, The Netherlands and Department of Oncology, The Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins, Baltimore, MD 21287, USA
    Carcinogenesis 35:1248-57. 2014
  3. pmc Differential epigenetic regulation of TOX subfamily high mobility group box genes in lung and breast cancers
    Mathewos Tessema
    Lung Cancer Program, Lovelace Respiratory Research Institute, Albuquerque, New Mexico, United States of America
    PLoS ONE 7:e34850. 2012
  4. pmc Re-expression of CXCL14, a common target for epigenetic silencing in lung cancer, induces tumor necrosis
    M Tessema
    Lung Cancer Program, Lovelace Respiratory Research Institute, Albuquerque, NM, USA
    Oncogene 29:5159-70. 2010
  5. pmc SULF2 methylation is prognostic for lung cancer survival and increases sensitivity to topoisomerase-I inhibitors via induction of ISG15
    M Tessema
    Lung Cancer Program, Lovelace Respiratory Research Institute, Albuquerque, NM 87108, USA
    Oncogene 31:4107-16. 2012
  6. pmc Softwares and methods for estimating genetic ancestry in human populations
    Yushi Liu
    Lovelace Respiratory Research Institute, Albuquerque, NM 87108, USA
    Hum Genomics 7:1. 2013
  7. ncbi request reprint Role of the cytosine DNA-methyltransferase and p16INK4a genes in the development of mouse lung tumors
    S A Belinsky
    Lovelace Respiratory Research Institute, Albuquerque, New Mexico, USA
    Exp Lung Res 24:463-79. 1998
  8. ncbi request reprint Gene-promoter hypermethylation as a biomarker in lung cancer
    Steven A Belinsky
    Lung Cancer Program, Lovelace Respiratory Research Institute, Albuquerque, New Mexico 87108, USA
    Nat Rev Cancer 4:707-17. 2004
  9. ncbi request reprint Silencing of genes by promoter hypermethylation: key event in rodent and human lung cancer
    Steven A Belinsky
    Lung Cancer Program, Lovelace Respiratory Research Institute, 2425 Ridgecrest Drive SE, Albuquerque, NM 87108, USA
    Carcinogenesis 26:1481-7. 2005
  10. pmc Predicting gene promoter methylation in non-small-cell lung cancer by evaluating sputum and serum
    S A Belinsky
    Lung Cancer Program, Lovelace Respiratory Research Institute, 2425 Ridgecrest Dr SE, Albuquerque, NM 87108, USA
    Br J Cancer 96:1278-83. 2007

Collaborators

Detail Information

Publications55

  1. ncbi request reprint Gene promoter methylation in plasma and sputum increases with lung cancer risk
    Steven A Belinsky
    Lovelace Respiratory Research Institute, Albuquerque, NM 87108, USA
    Clin Cancer Res 11:6505-11. 2005
    ..The prevalence for methylation of seven and three genes was examined in DNA from sputum and plasma, respectively, from women at different risk for lung cancer...
  2. pmc Genome-wide unmasking of epigenetically silenced genes in lung adenocarcinoma from smokers and never smokers
    Mathewos Tessema
    Department of Lung Cancer, Lovelace Respiratory Research Institute, Albuquerque, NM 87108, USA, MDxHealth Inc, Irvine, CA 92618, USA, Department of Pathology, GROW School for Oncology and Developmental Biology, Maastricht University Medical Center, 6200 MD, Maastricht, The Netherlands and Department of Oncology, The Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins, Baltimore, MD 21287, USA
    Carcinogenesis 35:1248-57. 2014
    ..001). Collectively, this study has identified multiple, novel, epigenetically silenced genes in lung cancer and provides invaluable resources for the development of diagnostic and prognostic biomarkers...
  3. pmc Differential epigenetic regulation of TOX subfamily high mobility group box genes in lung and breast cancers
    Mathewos Tessema
    Lung Cancer Program, Lovelace Respiratory Research Institute, Albuquerque, New Mexico, United States of America
    PLoS ONE 7:e34850. 2012
    ....
  4. pmc Re-expression of CXCL14, a common target for epigenetic silencing in lung cancer, induces tumor necrosis
    M Tessema
    Lung Cancer Program, Lovelace Respiratory Research Institute, Albuquerque, NM, USA
    Oncogene 29:5159-70. 2010
    ..Together, these findings identify CXCL14 as an important tumor suppressor gene epigenetically silenced during lung carcinogenesis...
  5. pmc SULF2 methylation is prognostic for lung cancer survival and increases sensitivity to topoisomerase-I inhibitors via induction of ISG15
    M Tessema
    Lung Cancer Program, Lovelace Respiratory Research Institute, Albuquerque, NM 87108, USA
    Oncogene 31:4107-16. 2012
    ....
  6. pmc Softwares and methods for estimating genetic ancestry in human populations
    Yushi Liu
    Lovelace Respiratory Research Institute, Albuquerque, NM 87108, USA
    Hum Genomics 7:1. 2013
    ..In this review, we present an overview of genetic ancestry estimation in human disease studies, followed by a review of popular softwares and methods used for this estimation...
  7. ncbi request reprint Role of the cytosine DNA-methyltransferase and p16INK4a genes in the development of mouse lung tumors
    S A Belinsky
    Lovelace Respiratory Research Institute, Albuquerque, New Mexico, USA
    Exp Lung Res 24:463-79. 1998
    ..The inactivation of the p16 gene in murine cancers induced by NNK most likely arises as a late event via homozygous deletion...
  8. ncbi request reprint Gene-promoter hypermethylation as a biomarker in lung cancer
    Steven A Belinsky
    Lung Cancer Program, Lovelace Respiratory Research Institute, Albuquerque, New Mexico 87108, USA
    Nat Rev Cancer 4:707-17. 2004
    ..The detection of methylated genes in sputum could lead to the development of a screening test to non-invasively identify early cancer in high-risk people...
  9. ncbi request reprint Silencing of genes by promoter hypermethylation: key event in rodent and human lung cancer
    Steven A Belinsky
    Lung Cancer Program, Lovelace Respiratory Research Institute, 2425 Ridgecrest Drive SE, Albuquerque, NM 87108, USA
    Carcinogenesis 26:1481-7. 2005
    ....
  10. pmc Predicting gene promoter methylation in non-small-cell lung cancer by evaluating sputum and serum
    S A Belinsky
    Lung Cancer Program, Lovelace Respiratory Research Institute, 2425 Ridgecrest Dr SE, Albuquerque, NM 87108, USA
    Br J Cancer 96:1278-83. 2007
    ..These studies demonstrate that sputum can be used effectively as a surrogate for tumour tissue to predict the methylation status of advanced lung cancer where biopsy is not feasible...
  11. ncbi request reprint Plutonium targets the p16 gene for inactivation by promoter hypermethylation in human lung adenocarcinoma
    Steven A Belinsky
    Lovelace Respiratory Research Institute, Lung Cancer Program, 2425 Ridgecrest Drive SE, Albuquerque, NM 87108, USA
    Carcinogenesis 25:1063-7. 2004
    ..Here we demonstrate that exposure to plutonium may elevate the risk for adenocarcinoma through specifically targeting the p16 gene for inactivation by promoter methylation...
  12. ncbi request reprint Inhibition of DNA methylation and histone deacetylation prevents murine lung cancer
    Steven A Belinsky
    Lovelace Respiratory Research Institute, 2425 Ridgecrest Drive SE, Albuquerque, New Mexico 87108, USA
    Cancer Res 63:7089-93. 2003
    ..Thus, reduction in DNMT and histone deacetylase activities that likely block epigenetically mediated gene silencing might provide a novel clinical strategy to help prevent the leading cause of cancer death in the United States...
  13. ncbi request reprint Epigenetics is alive and growing
    Steven A Belinsky
    Lung Cancer Program, Lovelace Respiratory Research Institute, 2425 Ridgecrest Dr SE, Albuquerque, NM 87108, USA
    Trends Mol Med 8:53-4. 2002
    ..The conference 'Epigenetics of Cancer,' organized by the American Association for Cancer Research, was held 17-21 October 2001 in Palm Desert, CA...
  14. ncbi request reprint Aberrant CpG island methylation of the p16(INK4a) and estrogen receptor genes in rat lung tumors induced by particulate carcinogens
    Steven A Belinsky
    Lovelace Respiratory Research Institute, Lung Cancer Program, 2425 Ridgecrest Drive SE, Albuquerque, NM 87108, USA
    Carcinogenesis 23:335-9. 2002
    ..Furthermore, the inactivation of the p16 gene by these carcinogenic exposures supports a possible role for oxidative stress and inflammation in the etiology of human lung cancer...
  15. ncbi request reprint Aberrant promoter methylation in bronchial epithelium and sputum from current and former smokers
    Steven A Belinsky
    Lung Cancer Program, Lovelace Respiratory Research Institute, 2425 Ridgecrest Drive SE, Albuquerque, New Mexico 87108, USA
    Cancer Res 62:2370-7. 2002
    ....
  16. pmc Combination therapy with vidaza and entinostat suppresses tumor growth and reprograms the epigenome in an orthotopic lung cancer model
    Steven A Belinsky
    Lung Cancer Program, Lovelace Respiratory Research Institute, Albuquerque, New Mexico 87108, USA
    Cancer Res 71:454-62. 2011
    ....
  17. ncbi request reprint Aberrant promoter hypermethylation of the death-associated protein kinase gene is early and frequent in murine lung tumors induced by cigarette smoke and tobacco carcinogens
    Leah C Pulling
    Lung Cancer Program, Lovelace Respiratory Research Institute, Albuquerque, New Mexico 87108, USA
    Cancer Res 64:3844-8. 2004
    ..This study is the first to use a murine model of cigarette smoke-induced lung cancer and demonstrate commonality for inactivation by promoter hypermethylation of a gene implicated in the development of this disease in humans...
  18. ncbi request reprint Gene promoter hypermethylation in mouse lung tumors
    Brian R Vuillemenot
    Lung Cancer Program, Lovelace Respiratory Research Institute, 2425 Ridgecrest Drive Southeast, Albuquerque, NM 87108, USA
    Mol Cancer Res 4:267-73. 2006
    ....
  19. doi request reprint Promoter methylation of genes in and around the candidate lung cancer susceptibility locus 6q23-25
    Mathewos Tessema
    Lung Cancer Program, Lovelace Respiratory Research Institute, Albuquerque, NM 87108, USA
    Cancer Res 68:1707-14. 2008
    ..Together, our results indicate that frequent inactivation of multiple candidate tumor suppressor genes within chromosome 6q likely contributes to development of sporadic lung cancer...
  20. ncbi request reprint Carcinogen exposure differentially modulates RAR-beta promoter hypermethylation, an early and frequent event in mouse lung carcinogenesis
    Brian R Vuillemenot
    Lung Cancer Program, Lovelace Respiratory Research Institute, 2425 Ridgecrest Drive SE, Albuquerque, NM 87108, USA
    Carcinogenesis 25:623-9. 2004
    ..These studies demonstrate that aberrant methylation of RAR-beta is an early and common alteration in murine lung tumors induced by several environmentally relevant exposures...
  21. pmc Wood smoke exposure and gene promoter methylation are associated with increased risk for COPD in smokers
    Akshay Sood
    University of New Mexico School of Medicine, Albuquerque, New Mexico, USA
    Am J Respir Crit Care Med 182:1098-104. 2010
    ..Wood smoke-associated chronic obstructive pulmonary disease (COPD) is common in women in developing countries but has not been adequately described in developed countries...
  22. ncbi request reprint Aberrant promoter methylation of the transcription factor genes PAX5 alpha and beta in human cancers
    William A Palmisano
    Lovelace Respiratory Research Institute, Lung Cancer Program, 2425 Ridgecrest Avenue S E, Albuquerque, New Mexico 87108, USA
    Cancer Res 63:4620-5. 2003
    ..Recent studies have demonstrated the importance of PAX5 gene alterations in human cancer. Our results are the first to identify aberrant promoter methylation as a common mechanism for dysregulation of these genes in solid tumors...
  23. ncbi request reprint Multiplicity of abnormal promoter methylation in lung adenocarcinomas from smokers and never smokers
    Kevin K Divine
    Lung Cancer Program, Lovelace Respiratory Research Institute, Albuquerque, NM 87108, USA
    Int J Cancer 114:400-5. 2005
    ..Adenocarcinomas may develop through 2 distinct processes: multiple gene inactivations through promoter hypermethylation and activation of the K-ras gene...
  24. ncbi request reprint Promoter hypermethylation of the O6-methylguanine-DNA methyltransferase gene: more common in lung adenocarcinomas from never-smokers than smokers and associated with tumor progression
    Leah C Pulling
    Lung Cancer Program, Lovelace Respiratory Research Institute, Albuquerque, New Mexico 87108 L C P, K K D, D M K, S A B
    Cancer Res 63:4842-8. 2003
    ..This study also suggests that K-ras activation is independent of MGMT methylation...
  25. ncbi request reprint Life-span inhalation exposure to mainstream cigarette smoke induces lung cancer in B6C3F1 mice through genetic and epigenetic pathways
    Julie A Hutt
    Lovelace Respiratory Research Institute, Albuquerque, NM 87108, USA
    Carcinogenesis 26:1999-2009. 2005
    ..These results emphasize the importance of the activation of K-ras and silencing of DAP-kinase and RAR-beta in lung cancer development, and confirm the relevance of this mouse model for studying lung tumorigenesis...
  26. ncbi request reprint SPRR1B overexpression enhances entry of cells into the G0 phase of the cell cycle
    Yohannes Tesfaigzi
    Lovelace Respiratory Research Inst, 2425 Ridgecrest Dr, SE, Albuquerque, NM 87108, USA
    Am J Physiol Lung Cell Mol Physiol 285:L889-98. 2003
    ....
  27. pmc Dual promoter regulation of death-associated protein kinase gene leads to differentially silenced transcripts by methylation in cancer
    Leah C Pulling
    Lung Cancer Program, Lovelace Respiratory Research Institute, Albuquerque, NM 87108, USA
    Carcinogenesis 30:2023-30. 2009
    ..These studies show for the first time dual promoter regulation of DAPK, a tumor suppressor gene silenced in many cancers, and substantiate the importance of screening for silencing of both transcripts in tumors...
  28. doi request reprint Carcinogen-induced gene promoter hypermethylation is mediated by DNMT1 and causal for transformation of immortalized bronchial epithelial cells
    LEAH A DAMIANI
    Lung Cancer Program, Lovelace Respiratory Research Institute, Albuquerque, New Mexico 87108, USA
    Cancer Res 68:9005-14. 2008
    ..This finding supports the development of demethylation strategies for primary prevention of lung cancer in smokers...
  29. pmc Concomitant promoter methylation of multiple genes in lung adenocarcinomas from current, former and never smokers
    Mathewos Tessema
    Lung Cancer Program, Lovelace Respiratory Research Institute, 2425 Ridgecrest Drive Southeast, Albuquerque, NM 87108, USA
    Carcinogenesis 30:1132-8. 2009
    ..23). These results demonstrate a high degree of commonality for targeted silencing of genes between lung and other solid tumors and suggest that promoter hypermethylation in cancer is a highly co-ordinated event...
  30. pmc Genotypes in matrix metalloproteinase 9 are a risk factor for COPD
    Yohannes Tesfaigzi
    Lovelace Respiratory Research Institute, 2425 Ridgecrest Drive, SE, Albuquerque, NM 87108, USA
    Int J Chron Obstruct Pulmon Dis 1:267-78. 2006
    ..No association of this polymorphism was found with decline in pulmonary function. These studies show that variants of the MMP-9 gene are associated with COPD in this cohort of veterans...
  31. ncbi request reprint Nested multigene MSP/DHPLC method for analyzing promoter hypermethylation status in clinical samples
    Kevin K Divine
    Lovelace Respiratory Research Institute, Albuquerque, NM 87108 5127, USA
    Biotechniques 40:40, 42, 44 passim. 2006
  32. ncbi request reprint Promoter hypermethylation of multiple genes in sputum precedes lung cancer incidence in a high-risk cohort
    Steven A Belinsky
    Lung Cancer Program, Lovelace Respiratory Research Institute, Albuquerque, New Mexico 87108, USA
    Cancer Res 66:3338-44. 2006
    ....
  33. ncbi request reprint Chronic inhalation exposure to mainstream cigarette smoke increases lung and nasal tumor incidence in rats
    Joe L Mauderly
    Lovelace Respiratory Research Institute, Albuquerque, New Mexico 87108, USA
    Toxicol Sci 81:280-92. 2004
    ..3%, C = 0.4% for combined genders). These results demonstrate that chronic whole-body exposure of rats to cigarette smoke can induce lung cancer...
  34. pmc Multivitamins, folate, and green vegetables protect against gene promoter methylation in the aerodigestive tract of smokers
    Christine A Stidley
    Department of Internal Medicine, University of New Mexico, New Mexico, USA
    Cancer Res 70:568-74. 2010
    ..Novel interventions to prevent lung cancer should be developed based on the ability of diet and dietary supplements to affect reprogramming of the epigenome...
  35. pmc Rosiglitazone prevents the progression of preinvasive lung cancer in a murine model
    Christopher M Lyon
    Lung Cancer Program, Lovelace Respiratory Research Institute, Albuquerque, NM 87108, USA
    Carcinogenesis 30:2095-9. 2009
    ..These studies demonstrate for the first time that chronic in vivo administration of rosiglitazone, used in the management of diabetes mellitus, can significantly block the progression of premalignant lung cancer in the A/J mouse model...
  36. pmc Double-strand break damage and associated DNA repair genes predispose smokers to gene methylation
    Shuguang Leng
    Lung Cancer Program, Lovelace Respiratory Research Institute, Albuquerque, NM 87108, USA
    Cancer Res 68:3049-56. 2008
    ....
  37. ncbi request reprint A phase I study of 5-azacytidine and erlotinib in advanced solid tumor malignancies
    Julie Bauman
    Division of Hematology Oncology, University of New Mexico Cancer Center, Albuquerque, NM, USA
    Cancer Chemother Pharmacol 69:547-54. 2012
    ..Epigenetic therapy to reactivate tumor suppressor genes may enhance the anti-proliferative effect of erlotinib. This phase I study evaluated the combination of erlotinib and 5-azacytidine for safety and maximal tolerated dose (MTD)...
  38. ncbi request reprint Radiation-induced lung adenocarcinoma is associated with increased frequency of genes inactivated by promoter hypermethylation
    Christopher M Lyon
    Lovelace Respiratory Research Institute, Lung Cancer Program, Albuquerque, New Mexico 87108, USA
    Radiat Res 168:409-14. 2007
    ..Increased frequency for inactivation of genes by promoter hypermethylation and targeting of tumor suppressor genes such as GATA5 may be factors that contribute to the increased risk for lung cancer associated with radiation exposure...
  39. pmc Difference in airflow obstruction between Hispanic and non-Hispanic White female smokers
    Akshay Sood
    Lovelace Respiratory Research Institute, S E, Albuquerque, NM, USA
    COPD 5:274-81. 2008
    ..05 for all analyses). Hispanic female smokers in this New Mexico-based cohort had lower risk of airflow obstruction and better lung function than NHW female smokers. Further, smoking history did not completely explain these associations...
  40. ncbi request reprint Association between common genetic variation in Cockayne syndrome A and B genes and nucleotide excision repair capacity among smokers
    Shuguang Leng
    Lung Cancer Program, Lovelace Respiratory Research Institute, 2425 Ridgecrest Drive South East, Albuquerque, NM 87108, USA
    Cancer Epidemiol Biomarkers Prev 17:2062-9. 2008
    ..035). This study implicates transcription-coupled repair in protecting the cell from BPDE-induced DNA damage...
  41. pmc Haplotypes of DNMT1 and DNMT3B are associated with mutagen sensitivity induced by benzo[a]pyrene diol epoxide among smokers
    Shuguang Leng
    Lung Cancer Program, Lovelace Respiratory Research Institute, 2425 Ridgecrest Drive Southeast, Albuquerque, NM 87108, USA
    Carcinogenesis 29:1380-5. 2008
    ..004). The association between sequence variants of DNMT1 and 3B and mutagen sensitivity induced by BPDE supports the involvement of these DNMTs in protecting the cell from DNA damage...
  42. ncbi request reprint A critical role of luteolin-induced reactive oxygen species in blockage of tumor necrosis factor-activated nuclear factor-kappaB pathway and sensitization of apoptosis in lung cancer cells
    Wei Ju
    Molecular Biology and Lung Cancer Program, Lovelace Respiratory Research Institute, Albuquerque, NM 87108, USA
    Mol Pharmacol 71:1381-8. 2007
    ..Taken together, these results suggest that the accumulation of ROS induced by luteolin plays a pivotal role in suppression of NF-kappaB and potentiation of JNK to sensitize lung cancer cells to undergo TNF-induced apoptosis...
  43. pmc Acquired activation of the Akt/cyclooxygenase-2/Mcl-1 pathway renders lung cancer cells resistant to apoptosis
    Wenjie Chen
    Molecular Biology and Lung Cancer Program, Lovelace Respiratory Research Institute, 2425 Ridgecrest Dr, SE, Albuquerque, NM 87108, USA
    Mol Pharmacol 77:416-23. 2010
    ..Our results establish a novel pathway that consists of Akt, COX-2, and Mcl-1 for acquired apoptosis resistance, which could be a molecular target for circumventing acquired chemoresistance in lung cancer...
  44. pmc Mining the epigenome for methylated genes in lung cancer
    Mathewos Tessema
    Lovelace Respiratory Research Institute, 2425 Ridgecrest Dr SE, Albuquerque, NM 87108, USA
    Proc Am Thorac Soc 5:806-10. 2008
    ....
  45. pmc Akt-mediated eminent expression of c-FLIP and Mcl-1 confers acquired resistance to TRAIL-induced cytotoxicity to lung cancer cells
    Xia Wang
    Molecular Biology and Lung Cancer Program, Lovelace Respiratory Research Institute, 2425 Ridgecrest Drive Southeast, Albuquerque, NM 87108, USA
    Mol Cancer Ther 7:1156-63. 2008
    ..Taken together, these results identify c-FLIP(L) and Mcl-1(L) as the major determinants of acquired TRAIL resistance and could be molecular targets for improving the therapeutic value of TRAIL against lung cancer...
  46. ncbi request reprint 17-allylamino-17-demethoxygeldanamycin synergistically potentiates tumor necrosis factor-induced lung cancer cell death by blocking the nuclear factor-kappaB pathway
    Xia Wang
    Molecular Biology and Lung Cancer Program, Lovelace Respiratory Research Institute, 2425 Ridgecrest Drive SE, Albuquerque, NM 87108, USA
    Cancer Res 66:1089-95. 2006
    ....
  47. ncbi request reprint Glutathione S-transferase P1 and NADPH quinone oxidoreductase polymorphisms are associated with aberrant promoter methylation of P16(INK4a) and O(6)-methylguanine-DNA methyltransferase in sputum
    Frank D Gilliland
    Keck School of Medicine, Department of Preventive Medicine and Norris Comprehensive Cancer Center, University of Southern California, Los Angeles, CA 90089 9021, USA
    Cancer Res 62:2248-52. 2002
    ....
  48. ncbi request reprint Hypermethylation of ASC/TMS1 is a sputum marker for late-stage lung cancer
    Emi Ota Machida
    The Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins, Baltimore, Maryland 21231, USA
    Cancer Res 66:6210-8. 2006
    ..Thus, hypermethylation of ASC/TMS1 is a marker for late-stage lung cancer and, in sputum, could predict prognosis in patients resected for early-stage disease...
  49. ncbi request reprint Tobacco carcinogen-induced cellular transformation increases activation of the phosphatidylinositol 3'-kinase/Akt pathway in vitro and in vivo
    Kip A West
    Cancer Therapeutics Branch, Cell and Cancer Biology Branch, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, Maryland, USA
    Cancer Res 64:446-51. 2004
    ....
  50. ncbi request reprint Hypermethylation of a small CpGuanine-rich region correlates with loss of activator protein-2alpha expression during progression of breast cancer
    Donna B Douglas
    The Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins, Baltimore, MD 21231, USA
    Cancer Res 64:1611-20. 2004
    ....
  51. ncbi request reprint Towards Clinical Application of Methylated DNA Sequences as Cancer Biomarkers: A Joint NCI's EDRN and NIST Workshop on Standards, Methods, Assays, Reagents and Tools
    Jacob Kagan
    Cancer Biomarkers Research Group, Division of Cancer Prevention, National Cancer Institute, NIH, Bethesda, Maryland, USA
    Cancer Res 67:4545-9. 2007
    ....
  52. doi request reprint DNA methylation markers and early recurrence in stage I lung cancer
    Malcolm V Brock
    Johns Hopkins Hospital, Baltimore, USA
    N Engl J Med 358:1118-28. 2008
    ..Despite optimal and early surgical treatment of non-small-cell lung cancer (NSCLC), many patients die of recurrent NSCLC. We investigated the association between gene methylation and recurrence of the tumor...
  53. doi request reprint Silencing of DUOX NADPH oxidases by promoter hypermethylation in lung cancer
    Sylvia Luxen
    Department of Immunology, The Scripps Research Institute, La Jolla, California 92037, USA
    Cancer Res 68:1037-45. 2008
    ..Our results suggest that an area on chromosome 15 that includes DUOX1, DUOX2, and their maturation factors is a frequent target for epigenetic silencing in lung cancer...
  54. pmc A SNP in a let-7 microRNA complementary site in the KRAS 3' untranslated region increases non-small cell lung cancer risk
    Lena J Chin
    Department of Molecular, Yale University, New Haven, Connecticut 06520, USA
    Cancer Res 68:8535-40. 2008
    ..The LCS6 variant allele in a KRAS miRANA complementary site is significantly associated with increased risk for NSCLC among moderate smokers and represents a new paradigm for let-7 miRNAs in lung cancer susceptibility...
  55. ncbi request reprint Transcriptional regulation of basal cyclooxygenase-2 expression in murine lung tumor-derived cell lines by CCAAT/enhancer-binding protein and activating transcription factor/cAMP response element-binding protein
    Sarah A Wardlaw
    Department of Thoracic Head and Neck Medical Oncology, The University of Texas M D Anderson Cancer Center, Houston, Texas 77030, USA
    Mol Pharmacol 62:326-33. 2002
    ....

Research Grants38

  1. Biomarkers to Assess Selenium Chemoprevention for NSCLC
    Steven Belinsky; Fiscal Year: 2006
    ..Our findings could identify molecular markers to monitor the efficacy of selenium supplementation in future prevention trials in cancer-free subjects with a history of smoking. ..
  2. TUMOR SUPPRESSOR GENE METHYLATION IN LUNG ADENOCARCINOMA
    Steven Belinsky; Fiscal Year: 2006
    ..Transient transfection of minimized promoters into cell lines with an endogenously active or silenced gene will be used to elucidate the sequence of changes involved in repression of promoter activity. REVISED: July 7, 2005 ..
  3. Biomarkers to Assess Selenium Chemoprevention for NSCLC
    Steven Belinsky; Fiscal Year: 2007
    ..Our findings could identify molecular markers to monitor the [efficacy of selenium supplementation in future prevention trials in cancer-free subiects with a history of smoking. ..
  4. TUMOR SUPPRESSOR GENE METHYLATION IN LUNG ADENOCARCINOMA
    Steven Belinsky; Fiscal Year: 2007
    ..Transient transfection of minimized promoters into cell lines with an endogenously active or silenced gene will be used to elucidate the sequence of changes involved in repression of promoter activity. REVISED: July 7, 2005 ..
  5. Biomarkers to Assess Selenium Chemoprevention for NSCLC
    Steven Belinsky; Fiscal Year: 2006
    ..Our findings could identify molecular markers to monitor the efficacy of selenium supplementation in future prevention trials in cancer-free subjects with a history of smoking. ..
  6. Factors for Epigenetic Silencing of Lung Cancer Genes
    Steven Belinsky; Fiscal Year: 2007
    ..Finally we will describe the gene-specific promoter hypermethylation patterns at study entry and at 18-month follow-up. ..
  7. TUMOR SUPPRESSOR GENE METHYLATION IN LUNG ADENOCARCINOMA
    Steven Belinsky; Fiscal Year: 2009
    ..Transient transfection of minimized promoters into cell lines with an endogenously active or silenced gene will be used to elucidate the sequence of changes involved in repression of promoter activity. REVISED: July 7, 2005 ..
  8. Biomarkers to Assess Selenium Chemoprevention for NSCLC
    Steven Belinsky; Fiscal Year: 2009
    ..Studies will also assess whether these same biomarkers can predict cancer recurrence. Finally, a cocktail of agents with minimal side effects is being evaluated that could ultimately be used in the prevention of lung cancer in humans. ..
  9. Genetic and Epigenetic Biomarkers for SCC of the Lung
    Steven Belinsky; Fiscal Year: 2009
    ..Ultimately approaches could be developed that modify the activity of the affected genes to prevent or treat lung cancer. ..
  10. Biomarkers to Assess Selenium Chemoprevention for NSCLC
    Steven A Belinsky; Fiscal Year: 2010
    ..Studies will also assess whether these same biomarkers can predict cancer recurrence. Finally, a cocktail of agents with minimal side effects is being evaluated that could ultimately be used in the prevention of lung cancer in humans. ..
  11. TUMOR SUPPRESSOR GENE METHYLATION IN LUNG ADENOCARCINOMA
    Steven A Belinsky; Fiscal Year: 2010
    ..Transient transfection of minimized promoters into cell lines with an endogenously active or silenced gene will be used to elucidate the sequence of changes involved in repression of promoter activity. REVISED: July 7, 2005 ..
  12. Biomarkers to Assess Selenium Chemoprevention for NSCLC
    Steven Belinsky; Fiscal Year: 2009
    ....
  13. Genetic and Epigenetic Biomarkers for SCC of the Lung
    Steven A Belinsky; Fiscal Year: 2010
    ..Ultimately approaches could be developed that modify the activity of the affected genes to prevent or treat lung cancer. ..
  14. Gene Methylation and Therapeutic Response in Lung Cancer
    Steven Belinsky; Fiscal Year: 2005
    ..The validation of these genes as biomarkers of lung cancer risk and their detection in sputum and/or serum could ultimately support chemoprevention trials for preventing lung cancer. ..
  15. TUMOR SUPPRESSOR GENE METHYLATION IN LUNG ADENOCARCINOMA
    Steven Belinsky; Fiscal Year: 1999
    ..time key methylation changes during adenocarcinoma, and provide an animal model in which to test intervention and prevention therapies directed against these genetic changes. ..
  16. MARKERS FOR LUNG CARCINOGENESIS IN BRONCHIAL EPITHELIUM
    Steven Belinsky; Fiscal Year: 1999
    ..f., simply markers of exposure) and help identify genetic alterations that are candidate markers of respiratory carcinogenesis. ..
  17. TUMOR SUPPRESSOR GENE METHYLATION IN LUNG ADENOCARCINOMA
    Steven Belinsky; Fiscal Year: 2000
    ..time key methylation changes during adenocarcinoma, and provide an animal model in which to test intervention and prevention therapies directed against these genetic changes. ..
  18. MARKERS FOR LUNG CARCINOGENESIS IN BRONCHIAL EPITHELIUM
    Steven Belinsky; Fiscal Year: 2000
    ..f., simply markers of exposure) and help identify genetic alterations that are candidate markers of respiratory carcinogenesis. ..
  19. TUMOR SUPPRESSOR GENE METHYLATION IN LUNG ADENOCARCINOMA
    Steven Belinsky; Fiscal Year: 2001
    ..time key methylation changes during adenocarcinoma, and provide an animal model in which to test intervention and prevention therapies directed against these genetic changes. ..
  20. MARKERS FOR LUNG CARCINOGENESIS IN BRONCHIAL EPITHELIUM
    Steven Belinsky; Fiscal Year: 2001
    ..f., simply markers of exposure) and help identify genetic alterations that are candidate markers of respiratory carcinogenesis. ..
  21. Gene Methylation and Therapeutic Response in Lung Cancer
    Steven Belinsky; Fiscal Year: 2001
    ..The validation of these genes as biomarkers of lung cancer risk and their detection in sputum and/or serum could ultimately support chemoprevention trials for preventing lung cancer. ..
  22. TUMOR SUPPRESSOR GENE METHYLATION IN LUNG ADENOCARCINOMA
    Steven Belinsky; Fiscal Year: 2002
    ..time key methylation changes during adenocarcinoma, and provide an animal model in which to test intervention and prevention therapies directed against these genetic changes. ..
  23. Gene Methylation and Therapeutic Response in Lung Cancer
    Steven Belinsky; Fiscal Year: 2002
    ..The validation of these genes as biomarkers of lung cancer risk and their detection in sputum and/or serum could ultimately support chemoprevention trials for preventing lung cancer. ..
  24. Biomarkers to Assess Selenium Chemoprevention for NSCLC
    Steven Belinsky; Fiscal Year: 2003
    ..Our findings could identify molecular markers to monitor the efficacy of selenium supplementation in future prevention trials in cancer-free subjects with a history of smoking. ..
  25. Gene Methylation and Therapeutic Response in Lung Cancer
    Steven Belinsky; Fiscal Year: 2003
    ..The validation of these genes as biomarkers of lung cancer risk and their detection in sputum and/or serum could ultimately support chemoprevention trials for preventing lung cancer. ..
  26. Biomarkers to Assess Selenium Chemoprevention for NSCLC
    Steven Belinsky; Fiscal Year: 2004
    ..Finally, aim 3 will determine the potency of selenium alone and in concert with HDAC inhibitors to prevent lung cancer development and to impede the progression of field cancerization in a murine lung tumor model. ..
  27. Factors for Epigenetic Silencing of Lung Cancer Genes
    Steven Belinsky; Fiscal Year: 2004
    ..Finally we will describe the gene-specific promoter hypermethylation patterns at study entry and at 18-month follow-up. ..
  28. Gene Methylation and Therapeutic Response in Lung Cancer
    Steven Belinsky; Fiscal Year: 2004
    ..The validation of these genes as biomarkers of lung cancer risk and their detection in sputum and/or serum could ultimately support chemoprevention trials for preventing lung cancer. ..
  29. Factors for Epigenetic Silencing of Lung Cancer Genes
    Steven A Belinsky; Fiscal Year: 2010
    ..S. PUBLIC HEALTH RELEVANCE: Studies in this application could lead to the development of a comprehensive model using clinical risk factors, genetic variation, and gene methylation in sputum for early lung cancer detection. ..