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TRKA gene induction by ATRA in neuroblastoma

Research Project

Project/Area Number 09670850
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field Pediatrics
Research InstitutionOsaka Medical College

Principal Investigator

MIYAKE Munenori  Faculty of Medicine, Osaka Medical College, Research Associate, 医学部, 助手 (10268203)

Co-Investigator(Kenkyū-buntansha) MURATA Takuji  Faculty of Medicine, Osaka Medical College, Research Associate, 医学部, 助手 (30288708)
ASHIDA Akira  Faculty of Medicine, Osaka Medical College, Research Associate, 医学部, 助手 (80278514)
TAMAI Hiroshi  Faculty of Medicine, Osaka Medical College, Professor, 医学部, 教授 (30179874)
Project Period (FY) 1997 – 1999
Project Status Completed (Fiscal Year 1999)
Budget Amount *help
¥3,700,000 (Direct Cost: ¥3,700,000)
Fiscal Year 1999: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1998: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1997: ¥2,700,000 (Direct Cost: ¥2,700,000)
KeywordsNeuroblastoma / TRKA gene / All-trans retinoic acid / Nerve Growth Factor / 神経芽細胞種 / All-trans Retinoic acid / 神経芽腫 / all-trans retinoic acid / trkA / nerve growth factor / neuroblastoma / All-trans Retinoic oacid
Research Abstract

We have adapted the fluorescence-based detection system of the ABI automated DNA sequencer for the precise sizing and quantitation of PCR products. This system will be used to provide standardized molecular data for the prognostic assessment of primary neuroblasomas and for the detection of tumor cells in the bone marrow and the screening of peripheral stem cell harvests. Primary tumors will be evaluated for two clinically proven prognostic markers : N-myc proto-oncogene amplification and TrkA gene expression. We also demonstrate in the present proposal the heterogeneity of TrkA expression in neuroblastomas and propose that tissue-inappropriate splicing of TrkA transcripts is correlated with poor prognosis. Preliminary data are presented showing the predominant expression of TrkA I (non-neuronal isoform) in patients older than 1.5 yrs at diagnosis whereas younger patients express predominantly TrkA II (neuronal isoform) in a subgroup of histopathologically indistinguishable tumors comprising the stroma-poor, undifferentiated, low MKI Shimada class. In addition, bone marrow metastases will be detected and the tumor burden quantitated using multiple expression markers (including tyrosine hydroxylase and PGP 9.5) labeled with distinguishable fluorescent tags a multiplex RT-PCR format.

Report

(4 results)
  • 1999 Annual Research Report   Final Research Report Summary
  • 1998 Annual Research Report
  • 1997 Annual Research Report

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Published: 1997-04-01   Modified: 2016-04-21  

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