Maria Teresa Landi

Summary

Affiliation: National Institutes of Health
Country: USA

Publications

  1. ncbi request reprint DNA repair, dysplastic nevi, and sunlight sensitivity in the development of cutaneous malignant melanoma
    Maria Teresa Landi
    Genetic Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MD 20892 7236, USA
    J Natl Cancer Inst 94:94-101. 2002
  2. pmc Melanocortin-1 receptor, skin cancer and phenotypic characteristics (M-SKIP) project: study design and methods for pooling results of genetic epidemiological studies
    Sara Raimondi
    Division of Epidemiology and Biostatistics, European Institute of Oncology, Via Ramusio 1, Milan, 20141, Italy
    BMC Med Res Methodol 12:116. 2012
  3. pmc MicroRNA expression differentiates histology and predicts survival of lung cancer
    Maria Teresa Landi
    Genetic Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, Department of Health and Human Services, Bethesda, Maryland 20892 7236, USA
    Clin Cancer Res 16:430-41. 2010
  4. pmc A genome-wide association study of lung cancer identifies a region of chromosome 5p15 associated with risk for adenocarcinoma
    Maria Teresa Landi
    Division of Cancer Epidemiology, National Cancer Institute, National Institutes of Health, Department of Health and Human Services, Bethesda, MD 20892, USA
    Am J Hum Genet 85:679-91. 2009
  5. pmc Environment And Genetics in Lung cancer Etiology (EAGLE) study: an integrative population-based case-control study of lung cancer
    Maria Teresa Landi
    Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, Bethesda, MD, USA
    BMC Public Health 8:203. 2008
  6. ncbi request reprint MC1R germline variants confer risk for BRAF-mutant melanoma
    Maria Teresa Landi
    Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, Bethesda, MD 20892, USA
    Science 313:521-2. 2006
  7. ncbi request reprint MC1R, ASIP, and DNA repair in sporadic and familial melanoma in a Mediterranean population
    Maria Teresa Landi
    Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, DHHS, Bethesda, MD 20892 7236, USA
    J Natl Cancer Inst 97:998-1007. 2005
  8. ncbi request reprint CYP1A1 and CYP1B1 genotypes, haplotypes, and TCDD-induced gene expression in subjects from Seveso, Italy
    Maria Teresa Landi
    Genetic Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, 6120 Executive Blvd, EPS, Bethesda, MD 20892 7236, USA
    Toxicology 207:191-202. 2005
  9. ncbi request reprint TCDD-mediated alterations in the AhR-dependent pathway in Seveso, Italy, 20 years after the accident
    Maria Teresa Landi
    Genetic Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, Bethesda, MD 20892 7236, USA
    Carcinogenesis 24:673-80. 2003
  10. pmc Phase I metabolic genes and risk of lung cancer: multiple polymorphisms and mRNA expression
    Melissa Rotunno
    Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, United States of America
    PLoS ONE 4:e5652. 2009

Detail Information

Publications60

  1. ncbi request reprint DNA repair, dysplastic nevi, and sunlight sensitivity in the development of cutaneous malignant melanoma
    Maria Teresa Landi
    Genetic Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MD 20892 7236, USA
    J Natl Cancer Inst 94:94-101. 2002
    ..We designed this case-control study to determine whether DNA repair capacity (DRC) is associated with the risk of CMM and to identify risk factors that may interact biologically with DRC in the development of melanoma...
  2. pmc Melanocortin-1 receptor, skin cancer and phenotypic characteristics (M-SKIP) project: study design and methods for pooling results of genetic epidemiological studies
    Sara Raimondi
    Division of Epidemiology and Biostatistics, European Institute of Oncology, Via Ramusio 1, Milan, 20141, Italy
    BMC Med Res Methodol 12:116. 2012
    ..Pooled-analysis of epidemiological studies has many advantages over meta-analysis, and preliminary results may be obtained faster and with lower costs than with prospective consortia...
  3. pmc MicroRNA expression differentiates histology and predicts survival of lung cancer
    Maria Teresa Landi
    Genetic Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, Department of Health and Human Services, Bethesda, Maryland 20892 7236, USA
    Clin Cancer Res 16:430-41. 2010
    ..The molecular drivers that determine histology in lung cancer are largely unknown. We investigated whether microRNA (miR) expression profiles can differentiate histologic subtypes and predict survival for non-small cell lung cancer...
  4. pmc A genome-wide association study of lung cancer identifies a region of chromosome 5p15 associated with risk for adenocarcinoma
    Maria Teresa Landi
    Division of Cancer Epidemiology, National Cancer Institute, National Institutes of Health, Department of Health and Human Services, Bethesda, MD 20892, USA
    Am J Hum Genet 85:679-91. 2009
    ..In conclusion, a lung cancer GWAS identified a distinct hereditary contribution to adenocarcinoma...
  5. pmc Environment And Genetics in Lung cancer Etiology (EAGLE) study: an integrative population-based case-control study of lung cancer
    Maria Teresa Landi
    Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, Bethesda, MD, USA
    BMC Public Health 8:203. 2008
    ..A new framework of research is needed to address the challenges offered by this complex disease...
  6. ncbi request reprint MC1R germline variants confer risk for BRAF-mutant melanoma
    Maria Teresa Landi
    Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, Bethesda, MD 20892, USA
    Science 313:521-2. 2006
    ..In this tumor subtype, the risk for melanoma associated with MC1R is due to an increase in risk of developing melanomas with BRAF mutations...
  7. ncbi request reprint MC1R, ASIP, and DNA repair in sporadic and familial melanoma in a Mediterranean population
    Maria Teresa Landi
    Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, DHHS, Bethesda, MD 20892 7236, USA
    J Natl Cancer Inst 97:998-1007. 2005
    ..We examined MC1R and ASIP genotypes in relation to phenotypic characteristics, sporadic and familial melanoma risk, and melanoma thickness as an indicator of disease progression in a Mediterranean population...
  8. ncbi request reprint CYP1A1 and CYP1B1 genotypes, haplotypes, and TCDD-induced gene expression in subjects from Seveso, Italy
    Maria Teresa Landi
    Genetic Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, 6120 Executive Blvd, EPS, Bethesda, MD 20892 7236, USA
    Toxicology 207:191-202. 2005
    ..Genetic variation in cytochrome P450 induction may identify subjects with variable responsiveness to TCDD and potentially increased risk of disease...
  9. ncbi request reprint TCDD-mediated alterations in the AhR-dependent pathway in Seveso, Italy, 20 years after the accident
    Maria Teresa Landi
    Genetic Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, Bethesda, MD 20892 7236, USA
    Carcinogenesis 24:673-80. 2003
    ....
  10. pmc Phase I metabolic genes and risk of lung cancer: multiple polymorphisms and mRNA expression
    Melissa Rotunno
    Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, United States of America
    PLoS ONE 4:e5652. 2009
    ..Our findings emphasize the necessity of post-GWAS fine mapping and SNP functional assessment to further elucidate cancer risk associations...
  11. pmc Alcohol consumption and lung cancer risk in the Environment and Genetics in Lung Cancer Etiology (EAGLE) study
    Vincenzo Bagnardi
    Genetic Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, 6120 Executive Blvd, EPS 7114, Bethesda, MD 20892 7236, USA
    Am J Epidemiol 171:36-44. 2010
    ..Although residual confounding by tobacco smoking cannot be ruled out, this finding may reflect interplay between alcohol and smoking, emphasizing the need for preventive measures...
  12. ncbi request reprint Aryl-hydrocarbon receptor-dependent pathway and toxic effects of TCDD in humans: a population-based study in Seveso, Italy
    Andrea Baccarelli
    Genetic Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, DHHS, Bethesda, MD 20892 7236, USA
    Toxicol Lett 149:287-93. 2004
    ..Markers within the AhR pathway were correlated with one another. Our findings suggest the presence of long-term effects in the subjects exposed to TCDD after the Seveso accident...
  13. pmc Nucleotide diversity and population differentiation of the melanocortin 1 receptor gene, MC1R
    Sharon A Savage
    Clinical Genetics Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Department of Health and Human Services, USA
    BMC Genet 9:31. 2008
    ..The melanocortin 1 receptor gene (MC1R) is responsible for normal pigment variation in humans and is highly polymorphic with numerous population-specific alleles. Some MC1R variants have been associated with skin cancer risk...
  14. pmc Chronic obstructive pulmonary disease and altered risk of lung cancer in a population-based case-control study
    Jill Koshiol
    Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Department of Health and Human Services, Bethesda, Maryland, United States of America
    PLoS ONE 4:e7380. 2009
    ..Chronic obstructive pulmonary disease (COPD) has been consistently associated with increased risk of lung cancer. However, previous studies have had limited ability to determine whether the association is due to smoking...
  15. pmc Family history of cancer and nonmalignant lung diseases as risk factors for lung cancer
    Ying Gao
    Division of Cancer Epidemiology and Genetics, Genetic Epidemiology Branch, National Cancer Institute, NIH, DHHS, Bethesda, MD 20892 7236, USA
    Int J Cancer 125:146-52. 2009
    ..23-1.80) and decreased (OR = 0.73, 95% CI = 0.61-0.87) lung cancer risk, respectively. FH of lung cancer and nonmalignant lung diseases affected lung cancer risk independently, and did not appear to be modified by FH of smoking...
  16. pmc On the interplay of telomeres, nevi and the risk of melanoma
    Clara Bodelon
    Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, Maryland, United States of America
    PLoS ONE 7:e52466. 2012
    ..Larger studies across different populations are necessary to clarify these associations...
  17. pmc Are women who smoke at higher risk for lung cancer than men who smoke?
    Sara De Matteis
    Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MD 20892, USA
    Am J Epidemiol 177:601-12. 2013
    ..g., tobacco type, inhalation depth, Fagerström-assessed nicotine dependence). These findings do not support a higher female susceptibility to tobacco-related lung cancer...
  18. pmc Influence of quercetin-rich food intake on microRNA expression in lung cancer tissues
    Tram K Lam
    Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, Bethesda, MD 20892, USA
    Cancer Epidemiol Biomarkers Prev 21:2176-84. 2012
    ..A quercetin-rich diet might modulate microRNA (miR) expression; however, this mechanism has not been fully examined...
  19. doi request reprint Genome-wide association analysis identifies new lung cancer susceptibility loci in never-smoking women in Asia
    Qing Lan
    Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MD, USA
    Nat Genet 44:1330-5. 2012
    ..3. We observed no evidence of association for lung cancer at 15q25 in never-smoking women in Asia, providing strong evidence that this locus is not associated with lung cancer independent of smoking...
  20. pmc A gene expression signature from peripheral whole blood for stage I lung adenocarcinoma
    Melissa Rotunno
    Division of Cancer Epidemiology and Genetics, NCI, NIH, Department of Health and Human Services, Bethesda, MD 20892, USA
    Cancer Prev Res (Phila) 4:1599-608. 2011
    ..81, 95% CI = 0.74-0.87). Our finding suggests the use of gene expression from PWB for the identification of early detection markers of lung cancer in the future...
  21. pmc A multi-stage genome-wide association study of bladder cancer identifies multiple susceptibility loci
    Nathaniel Rothman
    Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, Maryland, USA
    Nat Genet 42:978-84. 2010
    ..Our findings on common variants associated with bladder cancer risk should provide new insights into the mechanisms of carcinogenesis...
  22. pmc Genome-wide and candidate gene association study of cigarette smoking behaviors
    Neil Caporaso
    Division of Cancer Epidemiology and Genetics, NCI, Bethesda, Maryland, United States of America
    PLoS ONE 4:e4653. 2009
    ..4x10(-5)), our analysis provides independent replication of the association between the chr15q25.1 region and smoking intensity and data for multiple other loci associated with smoking behavior that merit further follow-up...
  23. pmc Dietary quercetin, quercetin-gene interaction, metabolic gene expression in lung tissue and lung cancer risk
    Tram Kim Lam
    Cancer Prevention Fellowship Program, Office of Preventive Oncology, National Cancer Institute, National Institutes of Health, Department of Health and Human Services, Bethesda, MD 20892, USA
    Carcinogenesis 31:634-42. 2010
    ..Our findings suggest an interplay between quercetin intake, tobacco smoking, and lung cancer risk. Further research on this relationship is warranted...
  24. ncbi request reprint High-risk melanoma susceptibility genes and pancreatic cancer, neural system tumors, and uveal melanoma across GenoMEL
    Alisa M Goldstein
    Genetic Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, DHHS, Bethesda, Maryland 20892 7236, USA
    Cancer Res 66:9818-28. 2006
    ..This GenoMEL study provides the most extensive characterization of mutations in high-risk melanoma susceptibility genes in families with three or more melanoma patients yet available...
  25. pmc Genetic variation in innate immunity and inflammation pathways associated with lung cancer risk
    Meredith S Shiels
    Infections and Immunoepidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, Maryland 20892, USA
    Cancer 118:5630-6. 2012
    ....
  26. pmc GSTM1 and GSTT1 copy numbers and mRNA expression in lung cancer
    Melissa Rotunno
    Division of Cancer Epidemiology and Genetics, Department of Health and Human Services, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892 7248, USA
    Mol Carcinog 51:E142-50. 2012
    ..A protective effect of the same mutations may be operative in never-smokers and women, possibly because of reduced activity of other genotoxic chemicals...
  27. pmc Inherited variation at chromosome 12p13.33, including RAD52, influences the risk of squamous cell lung carcinoma
    Jianxin Shi
    Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, Department of Health and Human Services, Bethesda, Maryland 20892, USA
    Cancer Discov 2:131-9. 2012
    ..33 (RAD52, rs6489769) and replicated the association in 3 independent studies totaling 3,359 squamous cell lung carcinoma cases and 9,100 controls (OR = 1.20, P(combined) = 2.3 × 10(-8))...
  28. pmc Mood disorders and risk of lung cancer in the EAGLE case-control study and in the U.S. Veterans Affairs inpatient cohort
    David E Capo-Ramos
    Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, United States of America
    PLoS ONE 7:e42945. 2012
    ..Mood disorders may affect lung cancer risk. We evaluated this hypothesis in two large studies...
  29. pmc Evaluation of normalization methods for two-channel microRNA microarrays
    Yingdong Zhao
    Division of Cancer Treatment and Diagnosis, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA
    J Transl Med 8:69. 2010
    ..Findings from previous studies have sometimes been inconclusive or contradictory. Further studies to determine optimal normalization methods for miR microarrays are needed...
  30. pmc Lower risk of lung cancer after multiple pneumonia diagnoses
    Jill Koshiol
    Division of Cancer Epidemiology and Genetics, National Cancer Institute, 6120 Executive Boulevard, MSC 7248, Bethesda, MD 20892 7248, USA
    Cancer Epidemiol Biomarkers Prev 19:716-21. 2010
    ..Although pneumonia has been suggested as a risk factor for lung cancer, previous studies have not evaluated the influence of number of pneumonia diagnoses in relation to lung cancer risk...
  31. pmc Common genetic polymorphisms modify the effect of smoking on absolute risk of bladder cancer
    Montserrat Garcia-Closas
    Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MD, USA
    Cancer Res 73:2211-20. 2013
    ..Our findings could have implications for targeted prevention strategies. However, other smoking-related diseases, as well as practical and ethical considerations, need to be considered before any recommendations could be made...
  32. pmc A flexible Bayesian model for studying gene-environment interaction
    Kai Yu
    Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, Maryland, USA
    PLoS Genet 8:e1002482. 2012
    ....
  33. ncbi request reprint Handling of dioxin measurement data in the presence of non-detectable values: overview of available methods and their application in the Seveso chloracne study
    Andrea Baccarelli
    Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, DHHS, 6120 Executive Boulevard, Bethesda, MD 20852, USA
    Chemosphere 60:898-906. 2005
    ..6% of plasma TCDD measurements were non-detects. We suggest that distribution-based multiple imputation be the preferred method to analyze environmental data when substantial proportions of observations are non-detects...
  34. pmc Genome-wide association studies of pigmentation and skin cancer: a review and meta-analysis
    Meg R Gerstenblith
    Genetic Epidemiology Branch Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Department of Health and Human Services, Bethesda, MD, USA
    Pigment Cell Melanoma Res 23:587-606. 2010
    ..As with any GWAS, the identified loci may not include the causal variants and may need confirmation by direct genome sequencing...
  35. pmc Genetic variant in TP63 on locus 3q28 is associated with risk of lung adenocarcinoma among never-smoking females in Asia
    H Dean Hosgood
    Division of Cancer Epidemiology and Genetics, National Cancer Institute, 6120 Executive Blvd, EPS 8118, MCS 7240, Bethesda, MD 20892 7240, USA
    Hum Genet 131:1197-203. 2012
    ..037; allelic risk = 0.82, 95% CI = 0.67-0.99). Our findings provide strong evidence that genetic variation in TP63 is associated with the risk of lung adenocarcinoma among Asian females in the absence of tobacco smoking...
  36. pmc Large-scale pathway-based analysis of bladder cancer genome-wide association data from five studies of European background
    Idan Menashe
    Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, Maryland, United States of America
    PLoS ONE 7:e29396. 2012
    ..Identification of the aromatic amine metabolism pathway provides support for the ability of this approach to identify pathways with established relevance to bladder carcinogenesis...
  37. ncbi request reprint Instrumental measurements of skin color and skin ultraviolet light sensitivity and risk of cutaneous malignant melanoma: a case-control study in an Italian population
    Alina V Brenner
    Radiation Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MD 20892 7362, USA
    Am J Epidemiol 156:353-62. 2002
    ..Epidemiologic studies of CMM may benefit from the inclusion of colorimetric and MED measurements along with traditional risk factors to obtain more accurate, quantitative, and objective information...
  38. pmc Intakes of red meat, processed meat, and meat mutagens increase lung cancer risk
    Tram Kim Lam
    Cancer Prevention Fellowship Program, Office of Preventive Oncology, National Cancer Institute, NIH, Department of Health and Human Services, corrected Bethesda, Maryland 20892 7236, USA
    Cancer Res 69:932-9. 2009
    ..In summary, red meat, processed meat, and meat mutagens were independently associated with increased risk of lung cancer...
  39. pmc Immunologic effects of dioxin: new results from Seveso and comparison with other studies
    Andrea Baccarelli
    Genetic Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, Maryland 20892, USA
    Environ Health Perspect 110:1169-73. 2002
    ..The possible long-term immunologic effects of TCDD exhibited by the participants of the present study, coupled with the increased incidence of lymphatic tumors in the area of the accident, warrant further investigation...
  40. pmc Gene expression signature of cigarette smoking and its role in lung adenocarcinoma development and survival
    Maria Teresa Landi
    Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health NIH, Department of Health and Human Services DHHS, Bethesda, Maryland, USA
    PLoS ONE 3:e1651. 2008
    ..Tobacco smoking is responsible for over 90% of lung cancer cases, and yet the precise molecular alterations induced by smoking in lung that develop into cancer and impact survival have remained obscure...
  41. pmc A genome-wide association study of bladder cancer identifies a new susceptibility locus within SLC14A1, a urea transporter gene on chromosome 18q12.3
    Montserrat Garcia-Closas
    Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MD, USA
    Hum Mol Genet 20:4282-9. 2011
    ..Our findings suggest that genetic variation in SLC14A1 could provide new etiological insights into bladder carcinogenesis...
  42. pmc Assessment of human papillomavirus in lung tumor tissue
    Jill Koshiol
    Infections and Immunoepidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MD 20892 7248, USA
    J Natl Cancer Inst 103:501-7. 2011
    ..Lung cancer kills more than 1 million people worldwide each year. Whereas several human papillomavirus (HPV)-associated cancers have been identified, the role of HPV in lung carcinogenesis remains controversial...
  43. ncbi request reprint Association of MC1R variants and risk of melanoma in melanoma-prone families with CDKN2A mutations
    Alisa M Goldstein
    Genetic Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MD 20892 7236, USA
    Cancer Epidemiol Biomarkers Prev 14:2208-12. 2005
    ..Additional studies are needed to confirm these findings and to explore the mechanisms that may contribute to this relationship...
  44. ncbi request reprint [Risk factors of malignant skin melanoma in Italian population: review of results of a case-control study]
    Andrea Baccarelli
    Genetic Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute NIH 6120 Executive Blvd, EPS 7110, Bethesda, MD 20892 7236, USA
    Epidemiol Prev 26:293-9. 2002
    ..7; 95% CI: 2.4-18.6) than those lacking dysplastic nevi and with high DRC. These results may help identify high-risk subjects in the Mediterranean populations who would the benefit from preventive measures...
  45. pmc Association of genetic variants in CDK6 and XRCC1 with the risk of dysplastic nevi in melanoma-prone families
    Xueying Liang
    1 Division of Cancer Epidemiology and Genetics, NCI NIH, Bethesda, Maryland, USA 2 Office of In Vitro Diagnostics and Radiological Health, CDRH FDA, Silver Spring, Maryland, USA
    J Invest Dermatol 134:481-7. 2014
    ..0001). Our findings suggest that some genetic variants may contribute to DN risk independently of their association with CMM in melanoma-prone families. ..
  46. doi request reprint Genome-wide association study identifies two susceptibility loci for osteosarcoma
    Sharon A Savage
    Division of Cancer Epidemiology and Genetics, National Cancer Institute, US National Institutes of Health, Bethesda, MD, USA
    Nat Genet 45:799-803. 2013
    ..2 (rs7591996 and rs10208273; P = 1.0 × 10⁻⁸ and 2.9 × 10⁻⁷, respectively). These two loci warrant further exploration to uncover the biological mechanisms underlying susceptibility to osteosarcoma...
  47. pmc Impact of occupational carcinogens on lung cancer risk in a general population
    Sara De Matteis
    Unit of Epidemiology, Department of Preventive Medicine, Fondazione IRCCS Ca Granda Ospedale Maggiore Policlinico and EPOCA Research Centre, Department of Occupational and Environmental Health, Universita degli Studi di Milano, Milan, Italy
    Int J Epidemiol 41:711-21. 2012
    ..Most of the previous studies were in highly exposed industrial cohorts. Our aim was to quantify lung cancer burden attributable to occupational carcinogens in a general population...
  48. ncbi request reprint Comprehensive evaluation of allele frequency differences of MC1R variants across populations
    Meg R Gerstenblith
    Genetic Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Department of Health and Human Services, Bethesda, Maryland 20892 7236, USA
    Hum Mutat 28:495-505. 2007
    ....
  49. pmc Strengths and limitations of laboratory procedures for microRNA detection
    Jill Koshiol
    Infections and Immunepidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, 6120 Executive Boulevard, Room 7070, Rockville, MD 20852 7248, USA
    Cancer Epidemiol Biomarkers Prev 19:907-11. 2010
    ..MicroRNAs (miR) are endogenous, noncoding RNAs involved in many cellular processes and have been associated with the development and progression of cancer. There are many different ways to evaluate miRs...
  50. ncbi request reprint Mutations in the tyrosine kinase domain of the epidermal growth factor receptor in non-small cell lung cancer
    Sei Hoon Yang
    Laboratory of Population Genetics, Center for Cancer Research, National Cancer Institute NIH, 41 Library Drive, Bethesda, MD 20892, USA
    Clin Cancer Res 11:2106-10. 2005
    ..Screening subjects with EGFR mutations may identify patients whose tumors could respond to targeted therapy using tyrosine kinase inhibitors...
  51. doi request reprint Characterizing the genetic basis of methylome diversity in histologically normal human lung tissue
    Jianxin Shi
    Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, DHHS, Bethesda, Maryland 20892, USA
    Nat Commun 5:3365. 2014
    ..Thus, inherited genetic variation may affect lung carcinogenesis by regulating the human methylome. ..
  52. pmc Detectable clonal mosaicism and its relationship to aging and cancer
    Kevin B Jacobs
    Division of Cancer Epidemiology and Genetics, National Cancer Institute NCI, Rockville, Maryland, USA
    Nat Genet 44:651-8. 2012
    ..4; P = 3.8 × 10(-11)). These findings underscore the time-dependent nature of somatic events in the etiology of cancer and potentially other late-onset diseases...
  53. pmc Features associated with germline CDKN2A mutations: a GenoMEL study of melanoma-prone families from three continents
    Alisa M Goldstein
    Genetic Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, DHHS, Bethesda, Maryland 20892 7236, USA
    J Med Genet 44:99-106. 2007
    ....
  54. ncbi request reprint Genetic variation and willingness to participate in epidemiologic research: data from three studies
    Parveen Bhatti
    Radiation Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, Department of Health and Human Services, 6120 Executive Boulevard, EPS 7091, MSC 7238, Bethesda, MD 20892 7238, USA
    Cancer Epidemiol Biomarkers Prev 14:2449-53. 2005
    ..To the extent possible, investigators should evaluate their own genetic data for bias in response categories...
  55. pmc A comparison of CDKN2A mutation detection within the Melanoma Genetics Consortium (GenoMEL)
    Mark Harland
    Division of Epidemiology and Biostatistics, Leeds Institute of Molecular Medicine, Cancer Research UK Cancer Centre at Leeds, St James s University Hospital, Leeds, UK
    Eur J Cancer 44:1269-74. 2008
    ..The relatively low rate of CDKN2A mutation detection is not due to failure to detect mutations and implies the existence of other high penetrance melanoma susceptibility genes...
  56. pmc Neonatal thyroid function in Seveso 25 years after maternal exposure to dioxin
    Andrea Baccarelli
    Department of Environmental Health, Harvard School of Public Health, Boston, Massachusetts, United States of America
    PLoS Med 5:e161. 2008
    ....
  57. ncbi request reprint Correspondence re: K. Toide et al., Aryl hydrocarbon hydroxylase represents CYP1B1, and not CYP1A1, in human freshly isolated white cells: trimodal distribution of Japanese population according to induction of CYP1B1 mRNA by environmental dioxins. 12: 219
    Maria Teresa Landi
    Cancer Epidemiol Biomarkers Prev 12:1116-7; author reply 1118. 2003
  58. ncbi request reprint Microarray analysis of gene expression in peripheral blood mononuclear cells from dioxin-exposed human subjects
    Cliona M McHale
    School of Public Health, University of California, Berkeley, CA 94720 7360, USA
    Toxicology 229:101-13. 2007
    ..Further examination of the role of these genes in dioxin induced-toxicity is warranted...
  59. ncbi request reprint t(14;18) translocations in lymphocytes of healthy dioxin-exposed individuals from Seveso, Italy
    Andrea Baccarelli
    EPOCA Research Center for Occupational, Clinical and Environmental Epidemiology, Department of Occupational and Environmental Health, University of Milan, IRCCS Ospedale Maggiore Policlinico Mangiagalli e Regina Elena, Milan, Italy
    Carcinogenesis 27:2001-7. 2006
    ..Whether this change in t(14;18) frequency is an indicator of elevated lymphoma risk remains speculative and needs further investigation for its potential impact on public health...
  60. ncbi request reprint Identification of 14-3-3 theta as an antigen that induces a humoral response in lung cancer
    Sandra R Pereira-Faca
    Fred Hutchinson Cancer Research Center, Seattle, Washington 98109, USA
    Cancer Res 67:12000-6. 2007
    ..5 proteins previously identified as associated with autoantibodies in lung cancer, gave a sensitivity of 55% at 95% specificity (area under the curve, 0.838) in discriminating lung cancer at the preclinical stage from matched controls...