Cancer · 1998
Expression of the neural cell adhesion molecule in astrocytic tumors: an inverse correlation with malignancy.
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Sasaki H, Yoshida K, Ikeda E, Asou H, Inaba M, Otani M, Kawase T
Аннотация
BACKGROUND: Cell adhesion molecules are among the key factors in the development of the malignant potential of brain tumors. The aim of this study was to investigate the expression of the neural cell adhesion molecule (NCAM) in human astrocytic tumors and assess any relationship between NCAM expression and the degree of malignancy.
METHODS: The expression of NCAM was examined in 52 astrocytic tumors by Western blot analysis. From them the authors selected 23 adult supratentorial ordinary astrocytic tumors and performed quantitative Western blot analysis for each isoform (NCAM 172-180, NCAM 145, NCAM 125-130) to investigate any correlation between the expression of each NCAM isoform and the histologic and biologic malignancy (histology, proliferating cell indices [PCIs] determined by MIB-1 immunohistochemistry, and manifestation on magnetic resonance images [MRIs]). Immunohistochemistry with antihuman NCAM monoclonal antibody was also performed on the tumors from which cryostat sections were available.
RESULTS: Most of the astrocytomas and anaplastic astrocytomas revealed 3 bands at 180, 145, and 125-130kD, whereas in glioblastomas the bands tended to diminish. The expression of each NCAM isoform in astrocytic tumors decreased in proportion to the progression of the histologic malignancy, and the results were also corroborated by immunohistochemical evaluation. An inverse correlation was also observed between the amount of NCAM expression and MIB-1 PCIs. NCAM expression was hardly detectable in those tumors with highly invasive manifestation on MRIs.
CONCLUSIONS: To the authors' knowledge, this study provides the first direct evidence that NCAM is down-regulated in the development of the malignancy of astrocytic tumors; and it is suggested that reduced NCAM expression might be involved in the development of biologic malignancy.
METHODS: The expression of NCAM was examined in 52 astrocytic tumors by Western blot analysis. From them the authors selected 23 adult supratentorial ordinary astrocytic tumors and performed quantitative Western blot analysis for each isoform (NCAM 172-180, NCAM 145, NCAM 125-130) to investigate any correlation between the expression of each NCAM isoform and the histologic and biologic malignancy (histology, proliferating cell indices [PCIs] determined by MIB-1 immunohistochemistry, and manifestation on magnetic resonance images [MRIs]). Immunohistochemistry with antihuman NCAM monoclonal antibody was also performed on the tumors from which cryostat sections were available.
RESULTS: Most of the astrocytomas and anaplastic astrocytomas revealed 3 bands at 180, 145, and 125-130kD, whereas in glioblastomas the bands tended to diminish. The expression of each NCAM isoform in astrocytic tumors decreased in proportion to the progression of the histologic malignancy, and the results were also corroborated by immunohistochemical evaluation. An inverse correlation was also observed between the amount of NCAM expression and MIB-1 PCIs. NCAM expression was hardly detectable in those tumors with highly invasive manifestation on MRIs.
CONCLUSIONS: To the authors' knowledge, this study provides the first direct evidence that NCAM is down-regulated in the development of the malignancy of astrocytic tumors; and it is suggested that reduced NCAM expression might be involved in the development of biologic malignancy.