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Isolation, Enrichment, and Maintenance of Medulloblastoma Stem Cells
06:32

Isolation, Enrichment, and Maintenance of Medulloblastoma Stem Cells

Published on: September 1, 2010

Differential expression of somatostatin receptors, P44/42 MAPK, and mTOR activation in medulloblastomas and primitive

Mahlon D Johnson1, Mary J O'Connell, Howard Silberstein

  • 1*Department of Pathology, Division of Neuropathology Departments of †Pediatric Neurosurgery ‡Pediatric Oncology, University of Rochester School of Medicine and Dentistry, Rochester, NY.

Applied Immunohistochemistry & Molecular Morphology : AIMM
|March 5, 2013
PubMed

Insights

Somatostatin receptors (SSR) show promise for treating medulloblastomas and primitive neuroectodermal tumors (PNETs). Targeting SSRs and mTOR pathways may enhance chemotherapy effectiveness, particularly in PNETs.

Area of Science:

  • Neuro-oncology
  • Molecular biology
  • Pharmacology

Background:

  • Somatostatin receptors (SSR) are identified on medulloblastomas and PNETs.
  • SSR activation inhibits tumor growth via MEK/MAPK and PI3K/Akt/mTOR pathways.
  • SSR-inhibited pathways in these tumors require characterization for combined chemotherapy strategies.

Purpose of the Study:

  • To evaluate SSR1 and SSR2 expression in medulloblastomas and PNETs.
  • To correlate SSR expression with the activation status of MEK/MAPK and PI3K/Akt/mTOR signaling pathways.
  • To explore potential combined chemotherapy targets.

Main Methods:

  • Immunohistochemistry was used to assess SSR1, SSR2, p44/42 MAPK, phosphorylated p44/42 MAPK, and phosphorylated mTOR expression.
  • 22 medulloblastomas and 9 PNETs were analyzed.
  • Expression levels and coexpression patterns were correlated.

Main Results:

  • SSR1 was detected in 50% of medulloblastomas and 78% of PNETs; SSR2 in 18% of medulloblastomas and 33% of PNETs.
  • Activated p44/42 MAPK was found in 82% of medulloblastomas and 62.5% of PNETs.
  • Activated mTOR was present in 18% of medulloblastomas and 88% of PNETs, with SSR1 coexpression in 75% of PNETs.

Conclusions:

  • SSR1 is frequently expressed in medulloblastomas and PNETs.
  • Combined targeting of SSR agonists and mTOR inhibitors may be a promising therapeutic strategy for PNETs.
  • Immunohistochemical detection of mTOR activation can guide clinical trial development and treatment decisions for PNETs.

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