Abstract
BackgroundMYCN gene amplification is related to risk stratification. Therefore it is important to identify accurately the level of the MYCN gene as early as possible in neuroblastoma (NB); however, for patients with bone marrow (BM) metastasis who need chemotherapy before surgery, timely detection of the MYCN gene is not possible due to the unavailability of primary tumors.MethodsMYCN gene status was evaluated in 81 BM metastases of NB by interphase fluorescence in situ hybridization (FISH) analysis of BM cells. The clinicobiological characteristics and prognostic impact of MYCN amplification in NB metastatic to BM were analyzed.ResultsMYCN amplification was found in 16% of patients with metastases, and the results were consistent with the primary tumors detected by pathological tissue FISH. MYCN amplification was associated with age, lactate dehydrogenase (LDH) levels and prognosis (P = 0.038, P < 0.001, P = 0.026). Clinical outcome was poorer in patients with MYCN amplification than in those without amplification (3-year EFS 28.8 ± 13.1 vs. 69.7 ± 5.7%, P = 0.005; 3-year OS 41.5 ± 14.7 vs. 76.7 ± 5.5%, P = 0.005).ConclusionsMYCN amplification predicts a poor outcome in NB metastatic to BM, and interphase FISH of bone marrow cells provides a timely direct and valid method to evaluate the MYCN gene status.
Highlights
MYCN gene amplification is related to risk stratification
Clinical and laboratory characteristics of patients with bone marrow (BM) metastases of NB The criteria for diagnosis and staging adhered to the international neuroblastoma staging system (INSS)
We found interphase fluorescence in situ hybridization (FISH) of BM cells was reliable in detecting MYCN gene status in BM metastases of NB
Summary
It is important to identify accurately the level of the MYCN gene as early as possible in neuroblastoma (NB); for patients with bone marrow (BM) metastasis who need chemotherapy before surgery, timely detection of the MYCN gene is not possible due to the unavailability of primary tumors. Neuroblastoma (NB),derived from the postganglionic sympathetic nervous system, is the most common extracranial malignancy in children [1] It represents 8–10% of pediatric tumors and accounts for >10% of all pediatric cancer mortality [2]. Because MYCN gene amplification is related to risk stratification, it is important to identify accurately the level of MYCN gene amplification as early as possible in order to avoid either under- or over-treating patients [9,10,11]. BM is the most common site of metastasis, and there are no reports on the status of the MYCN gene in BM cells in patients with NB metastatic to BM
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