Pubmed-entry ::= {
  pmid 22431917,
  medent {
    em std {
      year 2012,
      month 3,
      day 20
    },
    cit {
      title {
        name "Merlin/NF2 regulates angiogenesis in schwannomas through a
 Rac1/semaphorin 3F-dependent mechanism."
      },
      authors {
        names ml {
          "Wong HK",
          "Shimizu A",
          "Kirkpatrick ND",
          "Garkavtsev I",
          "Chan AW",
          "di Tomaso E",
          "Klagsbrun M",
          "Jain RK"
        },
        affil str "The Steele Lab of Tumor Biology, Department of Radiation
 Oncology, Massachusetts General Hospital and Harvard Medical School, Boston,
 MA, USA; Center for Neurologic Diseases, Brigham and Women's Hospital and
 Harvard Medical School, Harvard Institutes of Medicine, Boston, MA 02115, USA."
      },
      from journal {
        title {
          iso-jta "Neoplasia",
          ml-jta "Neoplasia",
          issn "1476-5586",
          name "Neoplasia (New York, N.Y.)"
        },
        imp {
          date std {
            year 2012,
            month 2
          },
          volume "14",
          issue "2",
          pages "84-94",
          language "eng",
          pubstatus ppublish,
          history {
            {
              pubstatus received,
              date std {
                year 2011,
                month 11,
                day 16
              }
            },
            {
              pubstatus revised,
              date std {
                year 2012,
                month 2,
                day 3
              }
            },
            {
              pubstatus accepted,
              date std {
                year 2012,
                month 2,
                day 3
              }
            },
            {
              pubstatus other,
              date std {
                year 2012,
                month 3,
                day 21,
                hour 6,
                minute 0
              }
            },
            {
              pubstatus pubmed,
              date std {
                year 2012,
                month 3,
                day 21,
                hour 6,
                minute 0
              }
            },
            {
              pubstatus medline,
              date std {
                year 2012,
                month 4,
                day 20,
                hour 6,
                minute 0
              }
            }
          }
        }
      },
      ids {
        pubmed 22431917,
        other {
          db "pmc",
          tag str "PMC3306254"
        }
      }
    },
    abstract "Neurofibromatosis type 2 (NF2) is an autosomal-dominant multiple
 neoplasia syndrome that results from mutations in the NF2 tumor suppressor
 gene. Patients with NF2 develop hallmark schwannomas that require surgery or
 radiation, both of which have significant adverse effects. Recent studies
 have indicated that the tumor microenvironment-in particular, tumor blood
 vessels-of schwannomas may be an important therapeutic target. Furthermore,
 although much has been done to understand how merlin, the NF2 gene product,
 functions as a tumor suppressor gene in schwannoma cells, the functional role
 of merlin in the tumor microenvironment and the mechanism(s) by which merlin
 regulates angiogenesis to support schwannoma growth is largely unexplored.
 Here we report that the expression of semaphorin 3F (SEMA3F) was specifically
 downregulated in schwannoma cells lacking merlin/NF2. When we reintroduced
 SEMA3F in schwannoma cells, we observed normalized tumor blood vessels,
 reduced tumor burden, and extended survival in nude mice bearing
 merlin-deficient brain tumors. Next, using chemical inhibitors and gene
 knockdown with RNA interference, we found that merlin regulated expression of
 SEMA3F through Rho GTPase family member Rac1. This study shows that, in
 addition to the tumor-suppressing activity of merlin, it also functions to
 maintain physiological angiogenesis in the nervous system by regulating
 antiangiogenic factors such as SEMA3F. Restoring the relative balance of
 proangiogenic and antiangiogenic factors, such as increases in SEMA3F, in
 schwannoma microenvironment may represent a novel strategy to alleviate the
 clinical symptoms of NF2-related schwannomas.",
    mesh {
      {
        term "Animals"
      },
      {
        term "Blood Vessels",
        qual {
          {
            subh "metabolism"
          }
        }
      },
      {
        term "Brain Neoplasms",
        qual {
          {
            mp TRUE,
            subh "blood supply"
          },
          {
            subh "metabolism"
          },
          {
            subh "pathology"
          }
        }
      },
      {
        term "Cell Line, Tumor"
      },
      {
        term "Down-Regulation"
      },
      {
        term "Gene Expression Profiling"
      },
      {
        term "Gene Expression Regulation, Neoplastic"
      },
      {
        term "Human Umbilical Vein Endothelial Cells"
      },
      {
        term "Humans"
      },
      {
        term "Kaplan-Meier Estimate"
      },
      {
        term "Membrane Proteins",
        qual {
          {
            subh "genetics"
          },
          {
            mp TRUE,
            subh "metabolism"
          }
        }
      },
      {
        term "Mice"
      },
      {
        term "Mice, Nude"
      },
      {
        term "Neoplasm Transplantation"
      },
      {
        mp TRUE,
        term "Neovascularization, Pathologic"
      },
      {
        term "Nerve Tissue Proteins",
        qual {
          {
            subh "genetics"
          },
          {
            mp TRUE,
            subh "metabolism"
          }
        }
      },
      {
        term "Neurilemmoma",
        qual {
          {
            mp TRUE,
            subh "blood supply"
          },
          {
            subh "metabolism"
          },
          {
            subh "pathology"
          }
        }
      },
      {
        term "Neurofibromatosis 2",
        qual {
          {
            subh "metabolism"
          },
          {
            subh "pathology"
          }
        }
      },
      {
        term "Neurofibromin 2",
        qual {
          {
            subh "genetics"
          },
          {
            mp TRUE,
            subh "metabolism"
          }
        }
      },
      {
        term "Permeability"
      },
      {
        term "Signal Transduction"
      },
      {
        term "Thrombospondins",
        qual {
          {
            subh "genetics"
          },
          {
            subh "metabolism"
          }
        }
      },
      {
        term "rac1 GTP-Binding Protein",
        qual {
          {
            mp TRUE,
            subh "metabolism"
          }
        }
      }
    },
    substance {
      {
        type nameonly,
        name "Membrane Proteins"
      },
      {
        type nameonly,
        name "Nerve Tissue Proteins"
      },
      {
        type nameonly,
        name "Neurofibromin 2"
      },
      {
        type nameonly,
        name "RAC1 protein, human"
      },
      {
        type nameonly,
        name "SEMA3F protein, human"
      },
      {
        type nameonly,
        name "Thrombospondins"
      },
      {
        type nameonly,
        name "thrombospondin 2"
      },
      {
        type ec,
        cit "3.6.5.2",
        name "rac1 GTP-Binding Protein"
      }
    },
    idnum {
      "CA37392/CA/NCI NIH HHS",
      "CA45548/CA/NCI NIH HHS",
      "P01-CA80124/CA/NCI NIH HHS"
    },
    pmid 22431917,
    pub-type {
      "Journal Article",
      "Research Support, N.I.H., Extramural",
      "Research Support, Non-U.S. Gov't"
    },
    status medline
  }
}

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