       Document 0093
 DOCN  M9640093
 TI    Malignant hemangioendothelioma.
 DT    9604
 AU    Ihda H; Tokura Y; Fushimi M; Yokote R; Hashizume H; Shirahama S;
       Iwatsuki K; Murakami K; Takigawa M; Department of Dermatology, Hamamatsu
       University School of; Medicine, Japan.
 SO    Int J Dermatol. 1995 Nov;34(11):811-6. Unique Identifier : AIDSLINE
       MED/96128708
 AB    BACKGROUND. The administration of interleukin-2 (IL-2) has recently been
       reported to be favorable for treating malignant hemangioendothelioma
       (MHE). METHODS. Two patients with MHE responded well to intralesional
       injections of recombinant IL-2 (rIL-2) without major side effects. The
       purpose of this study was to characterize cells infiltrating the
       regressing tumor following rIL-2 treatment. Immunohistochemical studies
       were performed on biopsy specimens taken from rIL-2-injected lesional
       skin. RESULTS. It was shown that CD8+ lymphocytes and CD56+ natural
       killer (NK) cells infiltrated at the rIL-2-injection sites, suggesting
       that these cells contributed to the tumor regression. In addition, MHE
       cells bore intercellular adhesion molecule-1 (ICAM-1) whose expression
       was augmented by rIL-2 injections. CONCLUSIONS. These findings
       suggested, that rIL-2 not only induces lymphokine-activated killer (LAK)
       cells and NK cells, but also facilitates these cytotoxic cells to adhere
       to MHE cells by enhancing ICAM-1 expression of tumor cells.
 DE    Aged  Case Report  CD8-Positive T-Lymphocytes/PATHOLOGY  Female
       *Hemangiosarcoma/IMMUNOLOGY/PATHOLOGY/THERAPY  Human
       Immunohistochemistry  Intercellular Adhesion Molecule-1/ANALYSIS
       Interleukin-2/THERAPEUTIC USE  Killer Cells,
       Natural/IMMUNOLOGY/PATHOLOGY  Male  Middle Age  Recombinant Proteins
       *Skin Neoplasms/IMMUNOLOGY/PATHOLOGY/THERAPY  JOURNAL ARTICLE

       SOURCE: National Library of Medicine.  NOTICE: This material may be
       protected by Copyright Law (Title 17, U.S.Code).

