Nathan A Ellis

Summary

Affiliation: Memorial Sloan-Kettering Cancer Center
Country: USA

Publications

  1. pmc No major association between TGFBR1*6A and prostate cancer
    Virginia Kaklamani
    Cancer Genetics Program, Division of Hematology Oncology, Department of Medicine, Robert H Lurie Comprehensive Cancer Center, Feinberg School of Medicine, Northwestern University, Chicago, Illinois, USA
    BMC Genet 5:28. 2004
  2. pmc The Ashkenazic Jewish Bloom syndrome mutation blmAsh is present in non-Jewish Americans of Spanish ancestry
    N A Ellis
    Department of Human Genetics, Memorial Sloan Kettering Cancer Center, 1275 York Avenue, USA
    Am J Hum Genet 63:1685-93. 1998
  3. pmc Transfection of BLM into cultured bloom syndrome cells reduces the sister-chromatid exchange rate toward normal
    N A Ellis
    Department of Human Genetics, Memorial Sloan Kettering Cancer Center, New York, NY, U S A
    Am J Hum Genet 65:1368-74. 1999
  4. ncbi request reprint Back mutation can produce phenotype reversion in Bloom syndrome somatic cells
    N A Ellis
    Department of Human Genetics, Memorial Sloan Kettering Cancer Center, New York, NY 10021, USA
    Hum Genet 108:167-73. 2001
  5. ncbi request reprint Value of immunohistochemical detection of DNA mismatch repair proteins in predicting germline mutation in hereditary colorectal neoplasms
    Jinru Shia
    Department of Pathology, Memorial Sloan Kettering, Cancer Center, New York, NY 10021, USA
    Am J Surg Pathol 29:96-104. 2005
  6. ncbi request reprint A636P testing in Ashkenazi Jews
    Jose G Guillem
    Department of Surgery, Memorial Sloan Kettering Cancer Center, New York, NY 10021, USA
    Fam Cancer 3:223-7. 2004
  7. pmc Single-amplicon MSH2 A636P mutation testing in Ashkenazi Jewish patients with colorectal cancer: role in presurgical management
    Jose G Guillem
    Department of Surgery, Memorial Sloan Kettering Cancer Center, New York, NY 10021, USA
    Ann Surg 245:560-5. 2007
  8. ncbi request reprint Localization of breast cancer susceptibility loci by genome-wide SNP linkage disequilibrium mapping
    Nathan A Ellis
    Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, NY 10021, USA
    Genet Epidemiol 30:48-61. 2006
  9. ncbi request reprint Localization of cancer susceptibility genes by genome-wide single-nucleotide polymorphism linkage-disequilibrium mapping
    Nandita Mitra
    Department of Epidemiology and Biostatistics, and Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, New York 10021, USA
    Cancer Res 64:8116-25. 2004
  10. ncbi request reprint Value of histopathology in predicting microsatellite instability in hereditary nonpolyposis colorectal cancer and sporadic colorectal cancer
    Jinru Shia
    Department of Pathology, Memorial Sloan Kettering Cancer Center, New York, NY 10002, USA
    Am J Surg Pathol 27:1407-17. 2003

Collaborators

Detail Information

Publications30

  1. pmc No major association between TGFBR1*6A and prostate cancer
    Virginia Kaklamani
    Cancer Genetics Program, Division of Hematology Oncology, Department of Medicine, Robert H Lurie Comprehensive Cancer Center, Feinberg School of Medicine, Northwestern University, Chicago, Illinois, USA
    BMC Genet 5:28. 2004
    ..080) but the differences in TGFBR1*6A genotype distribution between cases and controls did not reach statistical significance (p = 0.67). Our data suggest that TGFBR1*6A does not contribute to the development of prostate cancer...
  2. pmc The Ashkenazic Jewish Bloom syndrome mutation blmAsh is present in non-Jewish Americans of Spanish ancestry
    N A Ellis
    Department of Human Genetics, Memorial Sloan Kettering Cancer Center, 1275 York Avenue, USA
    Am J Hum Genet 63:1685-93. 1998
    ..This striking observation underscores the complexity of Jewish history and demonstrates the importance of migration and genetic drift in the formation of human populations...
  3. pmc Transfection of BLM into cultured bloom syndrome cells reduces the sister-chromatid exchange rate toward normal
    N A Ellis
    Department of Human Genetics, Memorial Sloan Kettering Cancer Center, New York, NY, U S A
    Am J Hum Genet 65:1368-74. 1999
    ..These experiments prove that BLM cDNA encodes a functional protein capable of restoring to or toward normal the uniquely characteristic high-SCE phenotype of BS cells...
  4. ncbi request reprint Back mutation can produce phenotype reversion in Bloom syndrome somatic cells
    N A Ellis
    Department of Human Genetics, Memorial Sloan Kettering Cancer Center, New York, NY 10021, USA
    Hum Genet 108:167-73. 2001
    ....
  5. ncbi request reprint Value of immunohistochemical detection of DNA mismatch repair proteins in predicting germline mutation in hereditary colorectal neoplasms
    Jinru Shia
    Department of Pathology, Memorial Sloan Kettering, Cancer Center, New York, NY 10021, USA
    Am J Surg Pathol 29:96-104. 2005
    ....
  6. ncbi request reprint A636P testing in Ashkenazi Jews
    Jose G Guillem
    Department of Surgery, Memorial Sloan Kettering Cancer Center, New York, NY 10021, USA
    Fam Cancer 3:223-7. 2004
    ..In addition, we summarize our initial experience with a prospective A636P testing protocol aimed at Ashkenazi Jewish patients at high or intermediate risk for harboring the A636P mutation...
  7. pmc Single-amplicon MSH2 A636P mutation testing in Ashkenazi Jewish patients with colorectal cancer: role in presurgical management
    Jose G Guillem
    Department of Surgery, Memorial Sloan Kettering Cancer Center, New York, NY 10021, USA
    Ann Surg 245:560-5. 2007
    ..This study summarizes our initial experience with prospective, single-amplicon (mutation-specific) A636P testing in Ashkenazi Jewish patients at risk for Hereditary Nonpolyposis Colorectal Cancer (HNPCC)...
  8. ncbi request reprint Localization of breast cancer susceptibility loci by genome-wide SNP linkage disequilibrium mapping
    Nathan A Ellis
    Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, NY 10021, USA
    Genet Epidemiol 30:48-61. 2006
    ..While these results demonstrate the feasibility of genome-wide association strategies, further application of this approach will critically depend on optimizing the density and distribution of SNPs and the size and type of study design...
  9. ncbi request reprint Localization of cancer susceptibility genes by genome-wide single-nucleotide polymorphism linkage-disequilibrium mapping
    Nandita Mitra
    Department of Epidemiology and Biostatistics, and Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, New York 10021, USA
    Cancer Res 64:8116-25. 2004
    ..This work demonstrates the power of the LD mapping approach in an isolated population and its general applicability to the identification of novel cancer-causing genes...
  10. ncbi request reprint Value of histopathology in predicting microsatellite instability in hereditary nonpolyposis colorectal cancer and sporadic colorectal cancer
    Jinru Shia
    Department of Pathology, Memorial Sloan Kettering Cancer Center, New York, NY 10002, USA
    Am J Surg Pathol 27:1407-17. 2003
    ..Using a stepwise logistic regression model, a formula was generated that could be used to calculate the probability of a colorectal carcinoma being MSI-H based on morphologic features...
  11. ncbi request reprint Frequency of BRCA1 and BRCA2 mutations in unselected Ashkenazi Jewish patients with colorectal cancer
    Tomas Kirchhoff
    Clinical Genetics Service, Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, NY 10021, USA
    J Natl Cancer Inst 96:68-70. 2004
    ..22 to 1.14). We thus recommend that counseling for colorectal cancer screening and prevention in individuals with BRCA mutations be based on the personal and family history of colorectal cancer or associated syndromic malignancies...
  12. ncbi request reprint BRCA mutations and risk of prostate cancer in Ashkenazi Jews
    Tomas Kirchhoff
    Clinical Genetics Service, Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, New York 10021, USA
    Clin Cancer Res 10:2918-21. 2004
    ..Several series looking at the frequency of BRCA mutations in unselected patients with prostate cancer have not confirmed this finding. To clarify this issue, we conducted a large case-control study...
  13. ncbi request reprint MSH6 germline mutations are rare in colorectal cancer families
    Paolo Peterlongo
    Cell Biology Program, Sloan Kettering Institute, Memorial Sloan Kettering Cancer Center, New York, NY 10021, USA
    Int J Cancer 107:571-9. 2003
    ..Altogether, our results indicate that disease-causing germline mutations of MSH6 are rare in HNPCC and HNPCC-like families...
  14. pmc Analysis of genetic variation in Ashkenazi Jews by high density SNP genotyping
    Adam B Olshen
    Surgery, Memorial Sloan Kettering Cancer Center, New York, NY, USA
    BMC Genet 9:14. 2008
    ..435,632 SNPs overlapped and met annotation criteria in the two groups...
  15. ncbi request reprint The utility of immunohistochemical detection of DNA mismatch repair gene proteins
    Jinru Shia
    Department of Pathology, Memorial Sloan Kettering Cancer Center, 1275 York Avenue, NY 10021, New York, USA
    Virchows Arch 445:431-41. 2004
    ....
  16. ncbi request reprint Increased frequency of disease-causing MYH mutations in colon cancer families
    Paolo Peterlongo
    Cell Biology Program, Memorial Sloan Kettering Cancer Center New York, NY, USA
    Carcinogenesis 27:2243-9. 2006
    ..These data further support a model in which low-penetrance alleles are enriched in MMR gene mutation-negative CRC families...
  17. ncbi request reprint Syndrome-causing mutations of the BLM gene in persons in the Bloom's Syndrome Registry
    James German
    Weill Medical College of Cornell University, New York, New York, USA
    Hum Mutat 28:743-53. 2007
    ..The presence of widespread founder mutations in persons with BS points to population genetic processes that repeatedly and pervasively generate mutations that recur in unrelated persons...
  18. ncbi request reprint Intra-nuclear trafficking of the BLM helicase to DNA damage-induced foci is regulated by SUMO modification
    Sonia Eladad
    Laboratory of Cancer Suspectibility, Department of Medicine, Cell Biology Program, Memorial Sloan Kettering Cancer Center, New York, NY 10021, USA
    Hum Mol Genet 14:1351-65. 2005
    ..These results constitute evidence that BLM is a DNA damage sensor that signals the formation of DDI, and they establish SUMO modification as a negative regulator of BLM's signaling function...
  19. ncbi request reprint A636P is associated with early-onset colon cancer in Ashkenazi Jews
    Jose G Guillem
    Department of Surgery, Memorial Sloan Kettering Cancer Center, New York, NY 10021, USA
    J Am Coll Surg 196:222-5. 2003
    ..This study seeks to characterize the proportion of individuals of Ashkenazi heritage with very early-onset colon cancer (diagnosed at age 40 or younger) that could be attributed to MSH2*1906C>G...
  20. pmc Genome-wide association study provides evidence for a breast cancer risk locus at 6q22.33
    Bert Gold
    Laboratory of Genomic Diversity, Human Genetics Section, National Cancer Institute Frederick, Frederick, MD 21702, USA
    Proc Natl Acad Sci U S A 105:4340-5. 2008
    ..Candidate genes in the 6q22.33 region include ECHDC1, which encodes a protein involved in mitochondrial fatty acid oxidation, and also RNF146, which encodes a ubiquitin protein ligase, both known pathways in breast cancer pathogenesis...
  21. pmc The BRCA1 Ashkenazi founder mutations occur on common haplotypes and are not highly correlated with anonymous single nucleotide polymorphisms likely to be used in genome-wide case-control association studies
    Lutecia H Mateus Pereira
    Laboratory of Population Genetics, National Cancer Institute, Bethesda, MD 20892, USA
    BMC Genet 8:68. 2007
    ..We evaluated LD using pairwise and haplotype-based methods, and assessed correlation of SNPs with the founder mutations using Pearson's correlation coefficient...
  22. ncbi request reprint Germline mutations of AXIN2 are not associated with nonsyndromic colorectal cancer
    Paolo Peterlongo
    Hum Mutat 25:498-500. 2005
  23. ncbi request reprint Analysis of mismatch repair defects in the familial occurrence of lymphoma and colorectal cancer
    J Teruya-Feldstein
    Department of Pathology, Memorial Sloan Kettering Cancer Center, Memorial Hospital, New York, NY 10021, USA
    Leuk Lymphoma 43:1619-26. 2002
    ....
  24. ncbi request reprint BLM heterozygosity and the risk of colorectal cancer
    Stephen B Gruber
    Departments of Internal Medicine and Epidemiology, University of Michigan, Ann Arbor, MI 48109, USA
    Science 297:2013. 2002
  25. ncbi request reprint SUMO: the glue that binds
    Michael J Matunis
    Department of Biochemistry and Molecular Biology, Johns Hopkins University, Bloomberg School of Public Health, Baltimore, Maryland 21205, USA
    Dev Cell 11:596-7. 2006
    ....
  26. ncbi request reprint Risk-reducing salpingo-oophorectomy in women with a BRCA1 or BRCA2 mutation
    Noah D Kauff
    Clinical Genetics Service, Memorial Sloan Kettering Cancer Center, New York 10021, USA
    N Engl J Med 346:1609-15. 2002
    ..We prospectively compared the effect of risk-reducing salpingo-oophorectomy with that of surveillance for ovarian cancer on the incidence of subsequent breast cancer and BRCA-related gynecologic cancers in women with BRCA mutations...
  27. ncbi request reprint The broken genome: genetic and pharmacologic approaches to breaking DNA
    Leslie L Woo
    Department of Biochemistry and Molecular Biology, University of Chicago, Chicago, IL 60637, USA
    Ann Med 39:208-18. 2007
    ..This review discusses the roles of RecQ helicases in genomic stability, the interplay between RecQ helicases and topoisomerase 3s, and current and future prospects for targeting these interactions to develop novel anticancer therapies...
  28. ncbi request reprint Colorectal cancer risk in individuals with biallelic or monoallelic mutations of MYH
    Paolo Peterlongo
    Int J Cancer 114:505-7. 2005
  29. pmc BLM helicase-dependent transport of p53 to sites of stalled DNA replication forks modulates homologous recombination
    Sagar Sengupta
    Laboratory of Human Carcinogenesis, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA
    EMBO J 22:1210-22. 2003
    ..These results indicate that p53 and BLM functionally interact during resolution of stalled DNA replication forks and provide insight into the mechanism of genomic fidelity maintenance by these nuclear proteins...
  30. pmc MDM2 SNP309 and TP53 Arg72Pro interact to alter therapy-related acute myeloid leukemia susceptibility
    Nathan A Ellis
    Department of Medicine, University of Chicago Cancer Research Center, University of Chicago, IL 60637, USA
    Blood 112:741-9. 2008
    ..These data indicate that the MDM2 and TP53 variants interact to modulate responses to genotoxic therapy and are determinants of risk for t-AML...