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Aberrant Localization of the Neuronal Class III β-Tubulin in Astrocytomas
Journal article   Peer reviewed

Aberrant Localization of the Neuronal Class III β-Tubulin in Astrocytomas

Christos D. Katsetos, Luis Del Valle, Jennian F. Geddes, Martha Assimakopoulou, Agustin Legido, James C. Boyd, Brian Balin, Nehal A. Parikh, Theodoros Maraziotis, Jean-Pierre de Chadarevian, …
Archives of pathology & laboratory medicine (1976), v 125(5), pp 613-624
01 May 2001
DOI: https://doi.org/10.5858/2001-125-0613-ALOTNC
PMID: 11300931
Featured in Collection :   UN Sustainable Development Goals @ Drexel

Abstract

Abstract Background.—The class III β-tubulin isotype (βIII) is widely regarded as a neuronal marker in development and neoplasia. In previous work, we have shown that the expression of βIII in neuronal/neuroblastic tumors is differentiation dependent. In contrast, the aberrant localization of this isotype in certain nonneuronal neoplasms, such as epithelial neuroendocrine lung tumors, is associated with anaplastic potential. Objective.—To test the generality of this observation, we investigated the immunoreactivity profile of βIII in astrocytomas. Design.—Sixty archival, surgically excised astrocytomas (8 pilocytic astrocytomas, WHO grade 1; 18 diffuse fibrillary astrocytomas, WHO grade 2; 4 anaplastic astrocytomas, WHO grade 3; and 30 glioblastomas, WHO grade 4), were studied by immunohistochemistry using anti-βIII monoclonal (TuJ1) and polyclonal antibodies. A monoclonal antibody to Ki-67 nuclear antigen (NC-MM1) was used as a marker for cell proliferation. Antibodies to glial fibrillary acidic protein (GFAP) and BM89 synaptic vesicle antigen/synaptophysin were used as glial and neuronal markers, respectively. Results.—The βIII immunoreactivity was significantly greater in high-grade astrocytomas (anaplastic astrocytomas and glioblastomas; median labeling index [MLI], 35%; interquartile range [IQR], 20%–47%) as compared with diffuse fibrillary astrocytomas (MLI, 4%; IQR, 0.2%–21%) (P < .0001) and was rarely detectable in pilocytic astrocytomas (MLI, 0%; IQR, 0%–0.5%) (P < .0001 vs high-grade astrocytomas; P < .01 vs diffuse fibrillary astrocytomas). A highly significant, grade-dependent relationship was observed between βIII and Ki-67 labeling and malignancy, but this association was stronger for Ki-67 than for βIII (βIII, P < .006; Ki-67, P < .0001). There was co-localization of βIII and GFAP in neoplastic astrocytes, but no BM89 synaptic vesicle antigen/synaptophysin staining was detected. Conclusions.—In the context of astrocytic gliomas, βIII immunoreactivity is associated with an ascending gradient of malignancy and thus may be a useful ancillary diagnostic marker. However, the significance of βIII-positive phenotypes in diffuse fibrillary astrocytomas with respect to prognostic and predictive value requires further evaluation. Under certain neoplastic conditions, βIII expression is not neuron specific, calling for a cautious interpretation of βIII-positive phenotypes in brain tumors.

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Domestic collaboration
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Web of Science research areas
Medical Laboratory Technology
Medicine, Research & Experimental
Pathology
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