Premium
Expression of leucocyte adhesion molecules on 66 clinical neuroblastoma specimens
Author(s) -
Favrot Marie C.,
Combaret Valérie,
Goillot Evelyne,
Tabone Eric,
Bouffet Eric,
Dolbeau Dominique,
Bouvier Rolande,
Coze Carole,
Michon Jean,
Philip Thierry
Publication year - 1991
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/ijc.2910480405
Subject(s) - ganglioneuroblastoma , ganglioneuroma , neuroblastoma , neuroblast , pathology , biology , cancer research , medicine , cell culture , microbiology and biotechnology , genetics , neurogenesis
Abstract LFA‐3, ICAM‐1, HLA.ABC and HLA.DR expression was analyzed on 66 neuroblastoma specimens. HLA.ABC was expressed on 26 specimens, HLA.DR on 2, LFA‐3 on 20 and ICAM‐1 on 10. HLA.ABC and LFA‐3 were positive on ganglioneuroblastoma or ganglioneuroma, but they were negative on neuroblastoma, independently of the clinical staging; HLA.ABC and LFA‐3 were induced in vivo by chemotherapy in parallel with tumoral cell differentiation, in both the primary and the metastases. The expression of ICAM‐1 was restricted to 5 of the 10 low‐grade stage‐1 or stage‐2 specimens, 1 stage‐3 specimen, and the primary tumors of 2 patients with stage‐4 disease, analyzed hence at diagnosis and after chemotherapy (4 specimens); metastatic cells obtained in 1 of these patients were negative. HLA.ABC and LFA‐3 expressed on both myc N‐negative and ‐positive specimens, whereas ICAM‐1 was restricted to MYCN‐negative specimens. LFA‐3 diffusely stained partially differentiated neuroblasts, Schwann cells and ganglion cells. The expression of HLA.ABC on differentiated neuroblasts varied from one sample to another and within the same tumor; Schwann cells were strongly positive, but ganglion cells were negative. In positive samples, ICAM‐1 was expressed on differentiated neuroblasts and Schwann cells, but negative on ganglion cells; however, most of the differentiated tumors were ICAM‐1‐negative, suggesting ICAM‐1 induction by unknown local signal. The 4 markers were negative on undifferentiated neuroblasts. The distribution of these 4 markers on clinical specimens was in agreement with their reactivity on fetal tissues, as well as with results obtained on neuroblastoma cell lines before and after in vitro treatment with IFN‐γ.