A Proteogenomic Approach to Understanding MYC Function in Metastatic Medulloblastoma Tumors
Brain tumors are the leading cause of cancer-related deaths in children, and medulloblastoma is the most prevalent malignant childhood/pediatric brain tumor. Providing effective treatment for these cancers, with minimal damage to the still-developing brain, remains one of the greatest challenges fac...
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Format: | Article |
Language: | English |
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MDPI AG
2016-10-01
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Series: | International Journal of Molecular Sciences |
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Online Access: | http://www.mdpi.com/1422-0067/17/10/1744 |
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author | Jerome A. Staal Yanxin Pei Brian R. Rood |
author_facet | Jerome A. Staal Yanxin Pei Brian R. Rood |
author_sort | Jerome A. Staal |
collection | DOAJ |
description | Brain tumors are the leading cause of cancer-related deaths in children, and medulloblastoma is the most prevalent malignant childhood/pediatric brain tumor. Providing effective treatment for these cancers, with minimal damage to the still-developing brain, remains one of the greatest challenges faced by clinicians. Understanding the diverse events driving tumor formation, maintenance, progression, and recurrence is necessary for identifying novel targeted therapeutics and improving survival of patients with this disease. Genomic copy number alteration data, together with clinical studies, identifies c-MYC amplification as an important risk factor associated with the most aggressive forms of medulloblastoma with marked metastatic potential. Yet despite this, very little is known regarding the impact of such genomic abnormalities upon the functional biology of the tumor cell. We discuss here how recent advances in quantitative proteomic techniques are now providing new insights into the functional biology of these aggressive tumors, as illustrated by the use of proteomics to bridge the gap between the genotype and phenotype in the case of c-MYC-amplified/associated medulloblastoma. These integrated proteogenomic approaches now provide a new platform for understanding cancer biology by providing a functional context to frame genomic abnormalities. |
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id | doaj.art-3aa0e346b6164bb18cd9b3b2f07aa103 |
institution | Directory Open Access Journal |
issn | 1422-0067 |
language | English |
last_indexed | 2024-04-12T00:31:54Z |
publishDate | 2016-10-01 |
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series | International Journal of Molecular Sciences |
spelling | doaj.art-3aa0e346b6164bb18cd9b3b2f07aa1032022-12-22T03:55:18ZengMDPI AGInternational Journal of Molecular Sciences1422-00672016-10-011710174410.3390/ijms17101744ijms17101744A Proteogenomic Approach to Understanding MYC Function in Metastatic Medulloblastoma TumorsJerome A. Staal0Yanxin Pei1Brian R. Rood2Multiple Sclerosis Department, Florey Institute of Neuroscience and Mental Health, Melbourne, VIC 3052, AustraliaCenter for Cancer and Immunology Research, Children’s National Medical Center, Washington, DC 20010, USACenter for Cancer and Immunology Research, Children’s National Medical Center, Washington, DC 20010, USABrain tumors are the leading cause of cancer-related deaths in children, and medulloblastoma is the most prevalent malignant childhood/pediatric brain tumor. Providing effective treatment for these cancers, with minimal damage to the still-developing brain, remains one of the greatest challenges faced by clinicians. Understanding the diverse events driving tumor formation, maintenance, progression, and recurrence is necessary for identifying novel targeted therapeutics and improving survival of patients with this disease. Genomic copy number alteration data, together with clinical studies, identifies c-MYC amplification as an important risk factor associated with the most aggressive forms of medulloblastoma with marked metastatic potential. Yet despite this, very little is known regarding the impact of such genomic abnormalities upon the functional biology of the tumor cell. We discuss here how recent advances in quantitative proteomic techniques are now providing new insights into the functional biology of these aggressive tumors, as illustrated by the use of proteomics to bridge the gap between the genotype and phenotype in the case of c-MYC-amplified/associated medulloblastoma. These integrated proteogenomic approaches now provide a new platform for understanding cancer biology by providing a functional context to frame genomic abnormalities.http://www.mdpi.com/1422-0067/17/10/1744medulloblastomaMYCquantitative proteomics |
spellingShingle | Jerome A. Staal Yanxin Pei Brian R. Rood A Proteogenomic Approach to Understanding MYC Function in Metastatic Medulloblastoma Tumors International Journal of Molecular Sciences medulloblastoma MYC quantitative proteomics |
title | A Proteogenomic Approach to Understanding MYC Function in Metastatic Medulloblastoma Tumors |
title_full | A Proteogenomic Approach to Understanding MYC Function in Metastatic Medulloblastoma Tumors |
title_fullStr | A Proteogenomic Approach to Understanding MYC Function in Metastatic Medulloblastoma Tumors |
title_full_unstemmed | A Proteogenomic Approach to Understanding MYC Function in Metastatic Medulloblastoma Tumors |
title_short | A Proteogenomic Approach to Understanding MYC Function in Metastatic Medulloblastoma Tumors |
title_sort | proteogenomic approach to understanding myc function in metastatic medulloblastoma tumors |
topic | medulloblastoma MYC quantitative proteomics |
url | http://www.mdpi.com/1422-0067/17/10/1744 |
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