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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 immunoh...istologically 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.
p16^〈INK4a〉は細胞増殖を停止させ細胞老化を誘導することが知られている．ヒト肥満細胞および肥満細胞症におけるp16^〈INK4a〉の発現はこれまで検討されていない．我々は，5例の健常皮膚および4 例の肥満細胞症のp16^〈INK4a〉，トリプターゼの発現を免疫組織学的に検討した．健常皮膚では，トリプターゼ陽性の肥満細胞のうち5.9 ± 3.4％のみがp16^〈INK4a〉を発現していた．一方，肥満細胞症におけるトリプターゼ陽性肥満細胞のp16^〈INK4a〉発現率は86.0 ± 14.1 ％にのぼり，健常肥満細胞にくらべ有意に高発現していた．肥満細胞症におけるp16^〈INK4a〉の高発現は，肥満細胞症を構成する腫瘍細胞の増殖を制御し，その自然消褪に関与しているかもしれない．show more
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