E R Fearon

Summary

Affiliation: University of Michigan
Country: USA

Publications

  1. ncbi request reprint DCC: is there a connection between tumorigenesis and cell guidance molecules?
    E R Fearon
    Department of Internal Medicine, University of Michigan Medical School, Ann Arbor 48019 0638, USA
    Biochim Biophys Acta 1288:M17-23. 1996
  2. ncbi request reprint Human cancer syndromes: clues to the origin and nature of cancer
    E R Fearon
    Department of Internal Medicine, University of Michigan Medical Center, 4301 MSRB III, 1150 West Medical Center Drive, Ann Arbor, MI 48109 0638, USA
    Science 278:1043-50. 1997
  3. ncbi request reprint Characterization of human homologs of the Drosophila seven in absentia (sina) gene
    G Hu
    Department of Internal Medicine, University of Michigan Medical School, Ann Arbor 48109, USA
    Genomics 46:103-11. 1997
  4. ncbi request reprint Netrin-1: interaction with deleted in colorectal cancer (DCC) and alterations in brain tumors and neuroblastomas
    J A Meyerhardt
    Department of Internal Medicine, University of Michigan Medical Center, Ann Arbor 48109 0638, USA
    Cell Growth Differ 10:35-42. 1999
  5. pmc Siah-1 N-terminal RING domain is required for proteolysis function, and C-terminal sequences regulate oligomerization and binding to target proteins
    G Hu
    Division of Molecular Medicine and Genetics, Department of Internal Medicine, University of Michigan Medical Center, Ann Arbor, Michigan
    Mol Cell Biol 19:724-32. 1999
  6. pmc Neoplastic transformation of RK3E by mutant beta-catenin requires deregulation of Tcf/Lef transcription but not activation of c-myc expression
    F T Kolligs
    Division of Molecular Medicine and Genetics and the Cancer Center, Departments of Internal Medicine, University of Michigan School of Medicine, Ann Arbor, Michigan 48109, USA
    Mol Cell Biol 19:5696-706. 1999
  7. ncbi request reprint Beta- and gamma-catenin mutations, but not E-cadherin inactivation, underlie T-cell factor/lymphoid enhancer factor transcriptional deregulation in gastric and pancreatic cancer
    K Caca
    Department of Internal Medicine, The Cancer Center, University of Michigan Medical School, Ann Arbor 48109, USA
    Cell Growth Differ 10:369-76. 1999
  8. pmc Loss of CDX2 expression and microsatellite instability are prominent features of large cell minimally differentiated carcinomas of the colon
    T Hinoi
    Department of Internal Medicine, University of Michigan, Ann Arbor, Michigan 48109, USA
    Am J Pathol 159:2239-48. 2001
  9. pmc MSX2 is an oncogenic downstream target of activated WNT signaling in ovarian endometrioid adenocarcinoma
    Y Zhai
    Department of Pathology, The University of Michigan Medical School, Ann Arbor, MI, USA
    Oncogene 30:4152-62. 2011
  10. pmc Organ-specific molecular classification of primary lung, colon, and ovarian adenocarcinomas using gene expression profiles
    T J Giordano
    Department of Pathology, The University of Michigan, Ann Arbor, Michigan 48109 0054, USA
    Am J Pathol 159:1231-8. 2001

Collaborators

Detail Information

Publications16

  1. ncbi request reprint DCC: is there a connection between tumorigenesis and cell guidance molecules?
    E R Fearon
    Department of Internal Medicine, University of Michigan Medical School, Ann Arbor 48019 0638, USA
    Biochim Biophys Acta 1288:M17-23. 1996
    ..Though many additional studies are needed to characterize DCC function more definitively, it seems reasonable to predict that such studies are likely to provide new insights into growth control pathways in normal and cancer tissues...
  2. ncbi request reprint Human cancer syndromes: clues to the origin and nature of cancer
    E R Fearon
    Department of Internal Medicine, University of Michigan Medical Center, 4301 MSRB III, 1150 West Medical Center Drive, Ann Arbor, MI 48109 0638, USA
    Science 278:1043-50. 1997
    ..Further investigation of inherited mutations that affect susceptibility to cancer will aid efforts to effectively prevent, detect, and treat the disease...
  3. ncbi request reprint Characterization of human homologs of the Drosophila seven in absentia (sina) gene
    G Hu
    Department of Internal Medicine, University of Michigan Medical School, Ann Arbor 48109, USA
    Genomics 46:103-11. 1997
    ..Furthermore, given the role of sina in Drosophila photoreceptor development, SIAH2 is a candidate for the Usher syndrome type 3 gene at chromosome 3q21-q25...
  4. ncbi request reprint Netrin-1: interaction with deleted in colorectal cancer (DCC) and alterations in brain tumors and neuroblastomas
    J A Meyerhardt
    Department of Internal Medicine, University of Michigan Medical Center, Ann Arbor 48109 0638, USA
    Cell Growth Differ 10:35-42. 1999
    ..Furthermore, the binding of netrin-1 to DCC appears to depend on the presence of a coreceptor or accessory proteins...
  5. pmc Siah-1 N-terminal RING domain is required for proteolysis function, and C-terminal sequences regulate oligomerization and binding to target proteins
    G Hu
    Division of Molecular Medicine and Genetics, Department of Internal Medicine, University of Michigan Medical Center, Ann Arbor, Michigan
    Mol Cell Biol 19:724-32. 1999
    ..The data indicate that the Siah-1 N-terminal RING domain is required for its proteolysis function, while the C-terminal sequences regulate oligomerization and binding to target proteins, such as DCC...
  6. pmc Neoplastic transformation of RK3E by mutant beta-catenin requires deregulation of Tcf/Lef transcription but not activation of c-myc expression
    F T Kolligs
    Division of Molecular Medicine and Genetics and the Cancer Center, Departments of Internal Medicine, University of Michigan School of Medicine, Ann Arbor, Michigan 48109, USA
    Mol Cell Biol 19:5696-706. 1999
    ..Our findings underscore the role of beta-cat mutations and Tcf/Lef activation in cancer and illustrate a useful system for defining critical factors in beta-cat transformation...
  7. ncbi request reprint Beta- and gamma-catenin mutations, but not E-cadherin inactivation, underlie T-cell factor/lymphoid enhancer factor transcriptional deregulation in gastric and pancreatic cancer
    K Caca
    Department of Internal Medicine, The Cancer Center, University of Michigan Medical School, Ann Arbor 48109, USA
    Cell Growth Differ 10:369-76. 1999
    ..Furthermore, these data imply that the consequences of APC and beta-cat mutations are distinct from the effects of E-cad inactivation...
  8. pmc Loss of CDX2 expression and microsatellite instability are prominent features of large cell minimally differentiated carcinomas of the colon
    T Hinoi
    Department of Internal Medicine, University of Michigan, Ann Arbor, Michigan 48109, USA
    Am J Pathol 159:2239-48. 2001
    ..CDX2 alterations and DNA mismatch repair defects have particularly prominent roles in the development of LCMDCs...
  9. pmc MSX2 is an oncogenic downstream target of activated WNT signaling in ovarian endometrioid adenocarcinoma
    Y Zhai
    Department of Pathology, The University of Michigan Medical School, Ann Arbor, MI, USA
    Oncogene 30:4152-62. 2011
    ..Our findings indicate MSX2 is a direct downstream transcriptional target of β-catenin/TCF and has a key contributing role in the cancer phenotype of OEAs carrying WNT/β-catenin pathway defects...
  10. pmc Organ-specific molecular classification of primary lung, colon, and ovarian adenocarcinomas using gene expression profiles
    T J Giordano
    Department of Pathology, The University of Michigan, Ann Arbor, Michigan 48109 0054, USA
    Am J Pathol 159:1231-8. 2001
    ....
  11. pmc The transcription factor snail represses Crumbs3 expression and disrupts apico-basal polarity complexes
    E L Whiteman
    Department of Internal Medicine, University of Michigan, Ann Arbor, MI 48109, USA
    Oncogene 27:3875-9. 2008
    ..Our findings provide new insights into the links between the transcriptional repression function of Snail and its role in antagonizing key apico-basal polarity factors during EMT...
  12. ncbi request reprint Cancer genetics: tumor suppressor meets oncogene
    E R Fearon
    Division of Molecular Medicine and Genetics, Department of Internal Medicine, Human Genetics, University of Michigan Cancer Center, Ann Arbor, 48109 0638 USA
    Curr Biol 9:R62-5. 1999
    ..A recent study has revealed that alterations in the APC signaling pathway can result in the transcriptional activation of the c-MYC gene...
  13. ncbi request reprint Identification and characterization of neogenin, a DCC-related gene
    J A Meyerhardt
    Department of Internal Medicine, University of Michigan Medical Center, Ann Arbor, USA
    Oncogene 14:1129-36. 1997
    ..However, the chromosomal location and ubiquitous expression of NGN in various human tumors suggest it is infrequently altered in cancer...
  14. ncbi request reprint Extinction of E-cadherin expression in breast cancer via a dominant repression pathway acting on proximal promoter elements
    K M Hajra
    Program in Cellular and Molecular Biology, University of Michigan Medical School, Ann Arbor, Michigan, MI 48109 USA
    Oncogene 18:7274-9. 1999
    ..Our findings suggest loss of E-cadherin expression in some breast cancers may be due to dominant repression of the trans-acting pathways that regulate E-cadherin transcription...
  15. pmc Mammalian homologs of seven in absentia regulate DCC via the ubiquitin-proteasome pathway
    G Hu
    Division of Molecular Medicine and Genetics, University of Michigan Medical Center, Ann Arbor, Michigan 48109 0638 USA
    Genes Dev 11:2701-14. 1997
    ..Taken together, the data imply that the Sina/Siah proteins regulate DCC and perhaps other proteins via the ubiquitin-proteasome pathway...
  16. ncbi request reprint Diverse mechanisms of beta-catenin deregulation in ovarian endometrioid adenocarcinomas
    R Wu
    Department of Pathology, The University of Michigan Medical School, 1150 West Medical Center Drive, Ann Arbor, MI 48109, USA
    Cancer Res 61:8247-55. 2001
    ..e., OEAs. Although mutations in the CTNNB1 gene are the most common mechanism of beta-catenin deregulation in OEAs, beta-catenin deregulation may also result from mutations in the APC, AXIN1, and AXIN2 genes...