Although leptin and its receptor (ObR) have emerged as important cancer biomarkers, the role of the leptin system in brain tumor development remains unknown. We screened 87 human brain tumor biopsies using immunohistochemistry and detected leptin and ObR in 55.2% and 60.9% cases, respectively. In contrast, leptin and ObR were absent in 14 samples of normal brain tissue. The presence of leptin correlated with ObR with overall concordance 80.5%. The leptin/ObR system was highly expressed in glioblastomas and anaplastic astrocytomas, while lower expression of both markers was noted in low-grade astrocytomas and gangliogliomas. The association between leptin/ObR and the degree of tumor malignancy was highly significant (P 0.001). Using double immunofluorescence of glioblastoma tissues, we found co-expression of leptin with ObR and with the proliferation marker Ki-67 in 87% and 64% of cells, respectively. The leptin/ObR-positive tissues also expressed activated forms of STAT3 and Akt. In line with this finding, ObR-positive glioblastoma cells responded to leptin with cell growth and induction of the STAT3 and Akt pathways as well as inactivation of the cell cycle suppressor Rb. In summary, our data demonstrate that the leptin/ObR system is expressed in malignant brain tumors and might be involved in tumor progression.

Leptin and its receptor are overexpressed in brain tumors and correlate with the degree of malignancy / M., Riolfi; R., Ferla; L., Del Valle; S., Pina Oviedo; L., Scolaro; Micciolo, Rocco; M., Guidi; M., Terrasi; G. L., Cetto; E., Surmacz. - In: BRAIN PATHOLOGY. - ISSN 1015-6305. - STAMPA. - 20:2(2010), pp. 481-489. [10.1111/j.1750-3639.2009.00323.x]

Leptin and its receptor are overexpressed in brain tumors and correlate with the degree of malignancy

Micciolo, Rocco;
2010-01-01

Abstract

Although leptin and its receptor (ObR) have emerged as important cancer biomarkers, the role of the leptin system in brain tumor development remains unknown. We screened 87 human brain tumor biopsies using immunohistochemistry and detected leptin and ObR in 55.2% and 60.9% cases, respectively. In contrast, leptin and ObR were absent in 14 samples of normal brain tissue. The presence of leptin correlated with ObR with overall concordance 80.5%. The leptin/ObR system was highly expressed in glioblastomas and anaplastic astrocytomas, while lower expression of both markers was noted in low-grade astrocytomas and gangliogliomas. The association between leptin/ObR and the degree of tumor malignancy was highly significant (P 0.001). Using double immunofluorescence of glioblastoma tissues, we found co-expression of leptin with ObR and with the proliferation marker Ki-67 in 87% and 64% of cells, respectively. The leptin/ObR-positive tissues also expressed activated forms of STAT3 and Akt. In line with this finding, ObR-positive glioblastoma cells responded to leptin with cell growth and induction of the STAT3 and Akt pathways as well as inactivation of the cell cycle suppressor Rb. In summary, our data demonstrate that the leptin/ObR system is expressed in malignant brain tumors and might be involved in tumor progression.
2010
2
M., Riolfi; R., Ferla; L., Del Valle; S., Pina Oviedo; L., Scolaro; Micciolo, Rocco; M., Guidi; M., Terrasi; G. L., Cetto; E., Surmacz
Leptin and its receptor are overexpressed in brain tumors and correlate with the degree of malignancy / M., Riolfi; R., Ferla; L., Del Valle; S., Pina Oviedo; L., Scolaro; Micciolo, Rocco; M., Guidi; M., Terrasi; G. L., Cetto; E., Surmacz. - In: BRAIN PATHOLOGY. - ISSN 1015-6305. - STAMPA. - 20:2(2010), pp. 481-489. [10.1111/j.1750-3639.2009.00323.x]
File in questo prodotto:
File Dimensione Formato  
2010-Riolfi-BP.pdf

Solo gestori archivio

Tipologia: Post-print referato (Refereed author’s manuscript)
Licenza: Tutti i diritti riservati (All rights reserved)
Dimensione 891.46 kB
Formato Adobe PDF
891.46 kB Adobe PDF   Visualizza/Apri

I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione

Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11572/82704
Citazioni
  • ???jsp.display-item.citation.pmc??? ND
  • Scopus 58
  • ???jsp.display-item.citation.isi??? 51
social impact