Occurrence of a glioblastoma-associated Tenascin-C isoform in cerebral cavernomas and neighboring vessels

Giuseppe L. Viale, Patrizia Castellani, Alessandra Dorcaratto, Antonio Pau, Elke Sehrbundt, Annalisa Siri, Attila Birò, Luciano Zardi, Maciej S. Lesniak, Daniele Rigamonti, Joseph M. Piepmeier

Research output: Contribution to journalArticle

7 Citations (Scopus)

Abstract

OBJECTIVE: Regrowth of cerebral cavernomas after apparently complete excision, de novo occurrence, and evidence of proliferation-related patterns raise the question as to their intrinsic growth potential. A particular isoform (Type III repeat c) of the glycoprotein tenascin-C (TN-C), typically associated with the vessels of anaplastic gliomas, is regarded as a marker of vascular proliferation in lesions growing within brain tissue. This study sought to ascertain whether this isoform is expressed in cerebral cavernomas to gain further insight into the growth potential of these lesions. METHODS: Sixteen cerebral cavernomas and three fragments of normal brain underwent immunohistochemical examinations via two antibody fragments obtained by phage display technology. Previous characterization demonstrated that the fragment TN-12 recognizes the epidermal growth factor-like repeat, common to all TN-C isoforms. On the contrary, the fragment TN-11 was found to be highly specific for the Type III repeat c isoform. RESULTS: Accumulation of total TN-C was found in the vascular walls and in the interspaces between the blood cavities of all examined cavernomas. When the antibody fragment TN-11 was used, staining of the subendothelial layers occurred in both the bulk of the cavernomas and vessels of the white matter surrounding the lesions, but staining was absent in the control specimens. CONCLUSION: The distribution of the Type III repeat c isoform of TN-C, a putative marker of vascular proliferation, within cerebral cavernomas is consistent with the hypothesis of a growth potential of cerebral cavernomas. Enlargement of these lesions might involve recruitment of neighboring vasculature, which is possibly dependent on environmental conditions.

Original languageEnglish
Pages (from-to)838-842
Number of pages5
JournalNeurosurgery
Volume50
Issue number4
DOIs
Publication statusPublished - Apr 1 2002

Fingerprint

Tenascin
Glioblastoma
Protein Isoforms
Blood Vessels
Immunoglobulin Fragments
Growth
Staining and Labeling
Brain
Epidermal Growth Factor
Glioma
Bacteriophages
Technology

Keywords

  • Angiogenesis
  • Cavernomas
  • Cavernous angiomas
  • Tenascin-C

ASJC Scopus subject areas

  • Clinical Neurology
  • Surgery

Cite this

Occurrence of a glioblastoma-associated Tenascin-C isoform in cerebral cavernomas and neighboring vessels. / Viale, Giuseppe L.; Castellani, Patrizia; Dorcaratto, Alessandra; Pau, Antonio; Sehrbundt, Elke; Siri, Annalisa; Birò, Attila; Zardi, Luciano; Lesniak, Maciej S.; Rigamonti, Daniele; Piepmeier, Joseph M.

In: Neurosurgery, Vol. 50, No. 4, 01.04.2002, p. 838-842.

Research output: Contribution to journalArticle

Viale, GL, Castellani, P, Dorcaratto, A, Pau, A, Sehrbundt, E, Siri, A, Birò, A, Zardi, L, Lesniak, MS, Rigamonti, D & Piepmeier, JM 2002, 'Occurrence of a glioblastoma-associated Tenascin-C isoform in cerebral cavernomas and neighboring vessels', Neurosurgery, vol. 50, no. 4, pp. 838-842. https://doi.org/10.1097/00006123-200204000-00028
Viale, Giuseppe L. ; Castellani, Patrizia ; Dorcaratto, Alessandra ; Pau, Antonio ; Sehrbundt, Elke ; Siri, Annalisa ; Birò, Attila ; Zardi, Luciano ; Lesniak, Maciej S. ; Rigamonti, Daniele ; Piepmeier, Joseph M. / Occurrence of a glioblastoma-associated Tenascin-C isoform in cerebral cavernomas and neighboring vessels. In: Neurosurgery. 2002 ; Vol. 50, No. 4. pp. 838-842.
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AU - Viale, Giuseppe L.

AU - Castellani, Patrizia

AU - Dorcaratto, Alessandra

AU - Pau, Antonio

AU - Sehrbundt, Elke

AU - Siri, Annalisa

AU - Birò, Attila

AU - Zardi, Luciano

AU - Lesniak, Maciej S.

AU - Rigamonti, Daniele

AU - Piepmeier, Joseph M.

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N2 - OBJECTIVE: Regrowth of cerebral cavernomas after apparently complete excision, de novo occurrence, and evidence of proliferation-related patterns raise the question as to their intrinsic growth potential. A particular isoform (Type III repeat c) of the glycoprotein tenascin-C (TN-C), typically associated with the vessels of anaplastic gliomas, is regarded as a marker of vascular proliferation in lesions growing within brain tissue. This study sought to ascertain whether this isoform is expressed in cerebral cavernomas to gain further insight into the growth potential of these lesions. METHODS: Sixteen cerebral cavernomas and three fragments of normal brain underwent immunohistochemical examinations via two antibody fragments obtained by phage display technology. Previous characterization demonstrated that the fragment TN-12 recognizes the epidermal growth factor-like repeat, common to all TN-C isoforms. On the contrary, the fragment TN-11 was found to be highly specific for the Type III repeat c isoform. RESULTS: Accumulation of total TN-C was found in the vascular walls and in the interspaces between the blood cavities of all examined cavernomas. When the antibody fragment TN-11 was used, staining of the subendothelial layers occurred in both the bulk of the cavernomas and vessels of the white matter surrounding the lesions, but staining was absent in the control specimens. CONCLUSION: The distribution of the Type III repeat c isoform of TN-C, a putative marker of vascular proliferation, within cerebral cavernomas is consistent with the hypothesis of a growth potential of cerebral cavernomas. Enlargement of these lesions might involve recruitment of neighboring vasculature, which is possibly dependent on environmental conditions.

AB - OBJECTIVE: Regrowth of cerebral cavernomas after apparently complete excision, de novo occurrence, and evidence of proliferation-related patterns raise the question as to their intrinsic growth potential. A particular isoform (Type III repeat c) of the glycoprotein tenascin-C (TN-C), typically associated with the vessels of anaplastic gliomas, is regarded as a marker of vascular proliferation in lesions growing within brain tissue. This study sought to ascertain whether this isoform is expressed in cerebral cavernomas to gain further insight into the growth potential of these lesions. METHODS: Sixteen cerebral cavernomas and three fragments of normal brain underwent immunohistochemical examinations via two antibody fragments obtained by phage display technology. Previous characterization demonstrated that the fragment TN-12 recognizes the epidermal growth factor-like repeat, common to all TN-C isoforms. On the contrary, the fragment TN-11 was found to be highly specific for the Type III repeat c isoform. RESULTS: Accumulation of total TN-C was found in the vascular walls and in the interspaces between the blood cavities of all examined cavernomas. When the antibody fragment TN-11 was used, staining of the subendothelial layers occurred in both the bulk of the cavernomas and vessels of the white matter surrounding the lesions, but staining was absent in the control specimens. CONCLUSION: The distribution of the Type III repeat c isoform of TN-C, a putative marker of vascular proliferation, within cerebral cavernomas is consistent with the hypothesis of a growth potential of cerebral cavernomas. Enlargement of these lesions might involve recruitment of neighboring vasculature, which is possibly dependent on environmental conditions.

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