Overexpression of p16^〈INK4a〉 in Mastocytosis (Urticarial Pigmentosa)

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  • Tsujita Jun
    Department of Dermatology, Graduate School of Medical Sciences, Kyushu University
  • Doi Kazuko
    Department of Dermatology, Graduate School of Medical Sciences, Kyushu University
  • Nakahara Makiko
    Department of Dermatology, Graduate School of Medical Sciences, Kyushu University
  • Nakahara Takeshi
    Division of Skin Surface Sensing, Department of Dermatology, Graduate School of Medical Sciences, Kyushu University
  • Kaku Yumiko
    Department of Dermatology, Graduate School of Medical Sciences, Kyushu University
  • Nishio Kiichiro
    Department of Dermatology, Graduate School of Medical Sciences, Kyushu University
  • Kan Nagisa
    Department of Dermatology, Graduate School of Medical Sciences, Kyushu University
  • Sato Yuki
    Department of Dermatology, Graduate School of Medical Sciences Kyushu University
  • Nagata Shoko
    Department of Dermatology, Graduate School of Medical Sciences Kyushu University
  • Nakao. Asako
    Department of Dermatology, Graduate School of Medical Sciences, Kyushu University
  • Yoshida Maiko
    Department of Dermatology, Graduate School of Medical Sciences, Kyushu University
  • Uchi Hiroshi
    Department of Dermatology, Graduate School of Medical Sciences, Kyushu University
  • Furue Masutaka
    Department of Dermatology, Graduate School of Medical Sciences, Kyushu University | Division of Skin Surface Sensing, Department of Dermatology, Graduate School of Medical Sciences, Kyushu University | Research and Clinical Center for Yusho and Dioxin, Kyushu University Hospital

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Other Title
  • 肥満細胞症(色素性蕁麻疹)におけるp16^〈INK4a〉の高発現
  • Overexpression of p16INK4a in Mastocytosis (Urticarial Pigmentosa)

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Abstract

The expression of p16^〈INK4a〉 has been reported to induce cell-cycle arrest and cellular senescence. The p16^〈INK4a〉 expression has never been examined in human mast cells and mastocytosis. We immunohistologically examined the expression of p16^〈INK4a〉 and tryptase in 5 normal human skin and 4 mastocytosis. In normal mast cells, only 5.9 ± 3.4 (mean±standard deviation)％ of tryptase-positive mast cells coexpressed p16^〈INK4a〉. However, significantly higher percentage (86.0 ± 14.1％) of tryptase-positive tumor cells was immunoreactive to p16^〈INK4a〉 in all of 4 mastocytosis. The p16^〈INK4a〉 overexpression may induce the senescence of neoplastic mast cells to undergo spontaneous regression of mastocytosis.

Journal

  • 福岡醫學雜誌

    福岡醫學雜誌 107 (1), 12-17, 2016-01-25

    Fukuoka Medical Association

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