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Germline PTPRD mutations in Ewing sarcoma: biologic and clinical implications.

Yunyun Jiang1, Filip Janku, Vivek Subbiah

  • 1Department of Investigational Cancer Therapeutics (Phase I Clinical Trials Program), The University of Texas MD Anderson Cancer Center, Houston, TX, USA.

Oncotarget
|June 27, 2013
PubMed
Summary

Germline mutations in the PTPRD gene were found in 37.5% of metastatic Ewing sarcoma patients. These mutations may impact STAT3 activation and suggest potential therapies targeting the insulin growth factor receptor (IGF-1R).

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Area of Science:

  • Oncology
  • Genetics
  • Molecular Biology

Background:

  • Ewing sarcoma is a cancer affecting young people.
  • High STAT3 signaling is implicated in Ewing sarcoma tumorigenesis.
  • Protein tyrosine phosphatase delta (PTPRD) normally suppresses STAT3 activation.

Purpose of the Study:

  • To investigate germline mutations in the PTPRD gene in Ewing sarcoma patients.
  • To explore the potential role of PTPRD germline mutations in Ewing sarcoma development.
  • To assess the therapeutic implications of PTPRD germline mutations.

Main Methods:

  • Genetic analysis of PTPRD in a cohort of Ewing sarcoma patients.
  • Functional assessment of identified PTPRD mutations.
  • Correlation of PTPRD mutation status with treatment response.

Main Results:

  • A novel germline mutation in PTPRD was identified in 37.5% of metastatic Ewing sarcoma patients.
  • One identified mutation (W775stop) is predicted to cause loss of PTPRD's STAT3 inhibitory function.
  • Two patients with PTPRD germline mutations responded durably to IGF-1R targeted therapy.

Conclusions:

  • Germline PTPRD mutations may contribute to Ewing sarcoma development.
  • PTPRD mutations could predict response to IGF-1R-targeted therapies in Ewing sarcoma.
  • Targeting IGF-1R may be a viable therapeutic strategy for Ewing sarcoma patients with PTPRD germline mutations.