Paracrine Signaling Through MYCN Enhances Tumor-Vascular Interactions in Neuroblastoma-Reference-Cited by-同舟云学术

Paracrine Signaling Through MYCN Enhances Tumor-Vascular Interactions in Neuroblastoma

Published:2012-01-04 Issue:115 Volume:4 Page:
ISSN:1946-6234
Container-title:Science Translational Medicine
language:en
Short-container-title:Sci. Transl. Med.

Author:

Chanthery Yvan H.¹²³⁴,Gustafson W. Clay²³⁴⁵,Itsara Melissa²³⁴⁵,Persson Anders²³⁴⁵,Hackett Christopher S.¹²³⁴,Grimmer Matt²³⁴⁵,Charron Elise²³⁴⁵,Yakovenko Slava²³⁴⁵,Kim Grace⁶,Matthay Katherine K.²³⁵,Weiss William A.¹²³⁴⁵

Affiliation:

1. Biomedical Science Graduate Program, University of California, San Francisco, 1450 Third Street, MC0520, San Francisco, CA 94158–9001, USA.

2. Department of Neurology, University of California, San Francisco, San Francisco, CA 94158–9001, USA.

3. Department of Pediatrics, University of California, San Francisco, San Francisco, CA 94158–9001, USA.

4. Department of Neurological Surgery and Brain Tumor Research Center, University of California, San Francisco, San Francisco, CA 94158–9001, USA.

5. Helen Diller Family Comprehensive Cancer Center, University of California, San Francisco, San Francisco, CA 94158–9001, USA.

6. Department of Pathology, University of California, San Francisco, San Francisco, CA 94158–9001, USA.

Abstract

PI3K/mTOR inhibitors inhibit angiogenesis by blocking MYCN-dependent paracrine signaling between tumor and endothelial cells.

Publisher

American Association for the Advancement of Science (AAAS)

Subject

General Medicine

Reference36 articles.

1. Recent Advances in Neuroblastoma

2. Targeted expression of MYCN causes neuroblastoma in transgenic mice

3. Genome-wide array CGH analysis of murine neuroblastoma reveals distinct genomic aberrations which parallel those in human tumors.;Hackett C. S.;Cancer Res.,2003

4. Tumor angiogenesis correlates with metastatic disease, N-myc amplification, and poor outcome in human neuroblastoma.

5. c-Myc is essential for vasculogenesis and angiogenesis during development and tumor progression

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