Correlation of modified Shimada classification with MYCN and 1p36 status detected by fluorescence in situ hybridization in neuroblastoma

被引:23
|
作者
Altungoz, Oguz [1 ]
Aygun, Nevim
Tumer, Sait
Ozer, Erdener
Olgun, Nur
Sakizli, Meral
机构
[1] Dokuz Eylul Univ, Sch Med, Dept Med Biol & Genet, TR-35340 Izmir, Turkey
[2] Dokuz Eylul Univ, Sch Med, Dept Pathol, TR-35340 Izmir, Turkey
[3] Dokuz Eylul Univ, Sch Med, Dept Pediat Oncol, TR-35340 Izmir, Turkey
关键词
D O I
10.1016/j.cancergencyto.2006.10.005
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Neuroblastoma (NB) is a childhood cancer derived from neural crest cells, with a highly variable clinical course and biologic behavior. NB cells harbor complex genetic changes. Also, MYCN amplification is a well-known Molecular marker for aggressive progression, and deletion of the short arm of chromosome I is frequently observed in NB. The aim of this study was to investigate the correlation between genetic markers and prognostic morphological parameters to address the biology and underlying the clinical complexity of NB. Therefore, we perforated fluorescence in Situ hybridization analyses of chromosome band 1p36 and MYCN in a series of tumors from 43 cases classified according to the recommendation of International Neuroblastoma pathology Committee (modification of Shimada classification). The correlations of MYCN amplification status and two distinct types of 1p36 alterations (deletion and imbalance) with Shimada classification and histologic prognostic factors were statistically analyzed. Amplification of MYCN and 1p36 deletion was present in 14 (32.6%) and 18 (41.9%) cases, respectively. Sixteen cases (37.2%) displayed a favorable histology, while 27 (62.8%) had an unfavorable histology. The lp36 deletion was found to be an independent predictor Of Unfavorable histology by multivariate analysis (logistic regression test, P = 0.03), but the 1p36 imbalance did not show any significance. Both lp36 deletion and MYCN amplification showed significant correlation With Undifferentiated tumors (chi-square test, P = 0.002 and 0.03, respectively). Highly significant correlation was found between the higher mitotic karyorrhectic index (MKI) and MYCN amplification (chi-square test, P < 0.001). whereas neither 1p36 deletion nor 1p36 imbalance significantly correlated with a higher MKI (chi-square test, P > 0.05). We conclude that 1p36 deletion may be a reliable parameter in determining unfavorable histology and predicting prognosis in NB. Further Studies with prognostic data are needed to highlight its clinical significance. (c) 2007 Elsevier Inc. All rights reserved.
引用
收藏
页码:113 / 119
页数:7
相关论文
共 42 条
  • [21] Correlation of ROS1 Immunohistochemistry With ROS1 Fusion Status Determined by Fluorescence In Situ Hybridization
    Huang, Richard S. P.
    Smith, Derek
    Le, Catherine H.
    Liu, Wen-Wei
    Ordinario, Ellen
    Manohar, Chitra
    Lee, Michael
    Rajamani, Jaya
    Truong, Huan
    Li, Jing
    Choi, Cindy
    Li, Jingchuan
    Pati, Amrita
    Bubendorf, Lukas
    Buettner, Reinhard
    Kerr, Keith M.
    Lopez-Rios, Fernando
    Marchetti, Antonio
    Marondel, Ivonne
    Nicholson, Andrew G.
    Oz, Aysim Buge
    Pauwels, Patrick
    Penault-Llorca, Frederique
    Rossi, Giulio
    Thunnissen, Erik
    Newell, Amy Hanlon
    Pate, Greg
    Menzl, Ina
    ARCHIVES OF PATHOLOGY & LABORATORY MEDICINE, 2020, 144 (06) : 735 - 741
  • [22] Aberrations of chromosome 9 detected by fluorescence in situ hybridization in urothelial carcinoma in situ:: Correlation with p16INK4 immunohistochemical expression
    Yin, M.
    Cieply, K.
    Cumbie, K.
    Bastacky, S.
    Dhir, R.
    LABORATORY INVESTIGATION, 2007, 87 : 185A - 185A
  • [23] Aberrations of chromosome 9 detected by fluorescence in situ hybridization in urothelial carcinoma in situ:: Correlation with p16INK4 immunohistochemical expression
    Yin, M.
    Cieply, K.
    Cumbie, K.
    Bastacky, S.
    Dhir, R.
    MODERN PATHOLOGY, 2007, 20 : 185A - 185A
  • [24] Fluorescence in situ hybridization for 1p, 19q status in a cohort of glial neoplasms
    Singh, Vandita Y.
    Chacko, Geeta
    Chacko, Ari G.
    Rajshekhar, Vedantam
    NEUROLOGY INDIA, 2014, 62 (01) : 32 - 36
  • [25] Detection of deletions in 1q25, 1p36 and 1pTEL and chromosome 17 aneuploidy in oral epithelial dysplasia and oral squamous cell carcinoma by fluorescence in situ hybridization (FISH)
    Barem Rabenhorst, Silvia Helena
    Verde Osterne, Rafael Lima
    Weege Nonaka, Cassiano Francisco
    Sales Rodrigues, Andre Montezuma
    Maia Nogueira, Renato Luiz
    Rodriguez Burbano, Rommel Mario
    Cavalcante, Roberta Barroso
    ORAL ONCOLOGY, 2021, 116
  • [26] Allelic losses at 1p36 and 19q13 in gliomas:: Correlation with histologic classification, definition of a 150-kb minimal deleted region on 1p36, and evaluation of CAMTA1 as a candidate tumor suppressor gene
    Barbashina, V
    Salazar, P
    Holland, EC
    Rosenblum, MK
    Ladanyi, M
    CLINICAL CANCER RESEARCH, 2005, 11 (03) : 1119 - 1128
  • [27] Assignment of the ovine uroporphyrinogen decarboxylase (UROD) gene to chromosome 1p34→p36 by fluorescence in situ hybridization
    Nezamzadeh, R
    Habermann, J
    Fries, R
    Brenig, B
    CYTOGENETIC AND GENOME RESEARCH, 2004, 106 (01) : 142B - U2
  • [28] LARGE-SCALE ISOLATION OF HUMAN 1P36-SPECIFIC P1 CLONES AND THEIR USE FOR FLUORESCENCE IN-SITU HYBRIDIZATION
    LENGAUER, C
    HENN, T
    ONYANGO, P
    FRANCIS, F
    LEHRACH, H
    WEITH, A
    GENETIC ANALYSIS-BIOMOLECULAR ENGINEERING, 1994, 11 (5-6): : 140 - 147
  • [29] Assignment of the genes encoding the human chloride channels, CLCNKA and CLCNKB, to 1p36 and of CLCN3 to 4q32-q33 by in situ hybridization
    SaitoOhara, F
    Uchida, S
    Takeuchi, Y
    Sasaki, S
    Hayashi, A
    Marumo, F
    Ikeuchi, T
    GENOMICS, 1996, 36 (02) : 372 - 374
  • [30] Comparison of 1p and 19q status of glioblastoma by whole exome sequencing, array-comparative genomic hybridization, and fluorescence in situ hybridization
    Sim, Jongmin
    Nam, Do-Hyun
    Kim, Yuil
    Lee, In-Hee
    Choi, Jung Won
    Sa, Jason K.
    Suh, Yeon-Lim
    MEDICAL ONCOLOGY, 2018, 35 (05)