Characterization of homogeneously staining regions in a small cell lung cancer cell line, using in situ hybridization with an <i>MYCN</i> probe

Dietzsch, E.; Lukeis, Robyn; Vrazas, Vickie; Hasthorpe, Suzanne; Garson, O. Margaret

doi:10.1002/gcc.2870100312

Cited by 7 publications

(3 citation statements)

References 10 publications

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“…MYCN encodes N-Myc, a basic helix-loop-helix protein that binds with other basic helix-loop-helix protein proteins, acting as a transcription factor to control the expression of cell cycle genes that promote proliferation. 54 It is frequently amplified in tumours of neuroectodermal origin, including neuroblastoma, retinoblastoma, glioblastoma, medulloblastoma, rhabdomyosarcoma and small cell lung carcinoma, [54][55][56][57][58][59][60][61] and is associated with poor prognosis in neuroblastoma. 62 MYCN is also amplified in the archetypal retinoblastoma cell line Y79 34 and has been reported amplified in approximately 3% of primary retinoblastomas.…”

Section: Mycn -V-myc Myelocytomatosis Viral-related Oncogene Neuroblmentioning

confidence: 99%

The genomic landscape of retinoblastoma: a review

Thériault

Dimaras

Gallie

et al. 2013

Clinical Exper Ophthalmology

166

131

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Retinoblastoma is a paediatric ocular tumour that continues to reveal much about the genetic basis of cancer development. Study of genomic aberrations in retinoblastoma tumours has exposed important mechanisms of cancer development, and identified oncogenes and tumour suppressors that offer potential points of therapeutic intervention. The recent development of next-generation genomic technologies has allowed further refinement of the genomic landscape of retinoblastoma at high resolution. In a relatively short period of time, a wealth of genetic and epigenetic data has emerged on a small number of tumour samples. These data highlight the inherent molecular complexity of this cancer, despite the fact that most retinoblastomas are initiated by the inactivation of a single tumour suppressor gene. Here, we review the current understanding of the genomic, genetic and epigenetic changes in retinoblastoma, highlighting recent genome-wide analyses that have identified exciting candidate genes worthy of further validation as potential prognostic and therapeutic targets.

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Section: Mycn -V-myc Myelocytomatosis Viral-related Oncogene Neuroblmentioning

confidence: 99%

The genomic landscape of retinoblastoma: a review

Thériault

Dimaras

Gallie

et al. 2013

Clinical Exper Ophthalmology

166

131

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“…However, in some cases, chromosome 7 or 17 was either over-or underrepresented compared with the DNA index. Fluorescence ISH (FISH) analysis of a SCLC cell line elucidated the origin of homogeneously staining regions (HSRs; Dietzsch et al 1994). These authors found the amplified region to contain the N-myc gene.…”

Section: Lung Cancermentioning

confidence: 99%

Interphase cytogenetics and comparative genomic hybridization of human epithelial cancers and precursor lesions

Dekken

Rosenberg

Krijtenburg

et al. 1997

Histochemistry and Cell Biology

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The accuracy of cytogenetic analyses of human solid cancers has improved enormously over the past decade by the introduction and refinement of DNA in situ hybridization (ISH) techniques. This methodology can be applied to cells in the interphase state, thereby making it an excellent tool for the delineation of chromosomal aberrations in solid tumors. The use of non-isotopic ISH to intact and disaggregated cancer specimens will be discussed, as well as comparative genomic hybridization (CGH) with tumor-derived DNAs. In this review we will focus on hybridocytochemical interphase approaches for the detection of chromosomal changes in frequently occurring human epithelial malignancies, e.g., breast, lung, and prostate carcinomas. We will further discuss the use of ISH procedures for the genetic analysis of precursor conditions leading to invasive carcinomas. Knowledge concerning these precancerous conditions is increasing, and its importance in cancer prevention has been recognized. Interphase cytogenetics by ISH, as well as CGH, with DNAs derived from microdissected, precancerous, dysplastic tissue areas will increase our understanding of these lesions, both at the investigative and diagnostic levels.

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“…MYCN has been found to be amplified and overexpressed in small cell lung cancer (SCLC) [73][74][75][76][77][78][79][80][81][82], a frequently occurring and highly aggressive (and frequently lethal) human tumor with primitive neuroendocrine features. An analysis of 336 patients [77][78][79][80][81][82] reported MYCN amplification in approximately 10% of cases, and the increased MYCN expression is strongly associated with poor response to chemotherapy, rapid tumor growth, and short survival [80].…”

Section: Small Cell Lung Cancermentioning

confidence: 99%

The MYCN Oncogene as a Specific and Selective Drug Target for Peripheral and Central Nervous System Tumors

Pession

Tonelli

2005

CCDT

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MYCN belongs to the MYC family of proto-oncogenes, which encode for transcription factors of the basic-helix-loop-helix-zipper (bHLHZ) class and is fundamental in the development of the peripheral and central nervous systems (PNS and CNS). While Myc is ubiquitous, MYCN has a very restricted expression pattern: it is mainly expressed during embryonic development, but then becomes downregulated, while in adults it is usually detected in B-cell development. Identification of selective inhibitors of MYCN and its mRNA and protein could be important for the development of more specific, effective and less toxic therapeutic agents for tumors of the PNS and CNS. In children, the most common tumors of the PNS and CNS are neuroblastomas and medulloblastomas, respectively. About 30% of neuroblastoma (NB) tumors present MYCN amplification/over-expression, which is associated with rapid progression and poor prognosis. N-Myc is essential during neurogenesis for the rapid expansion of progenitor cells in the brain. MYCN amplification and over-expression has been reported in medulloblastoma, and especially in the desmoplastic type. Other tumors associated with MYCN overexpression include retinoblastoma, small cell lung carcinoma, glioblastoma and certain embryonal tumors. A cell-based, N-Myc-dependent luciferase reporter gene assay to identify specific N-Myc small-molecule inhibitors has allowed identification of five compounds showing significant activity. Antisense oligodeoxynucleotides have been shown to inhibit N-Myc production and anti-tumoral activity in vitro and in vivo for NB. Peptide nucleic acids (PNA), which belong to the most recent (third) generation of nucleic acid therapeutics, form highly stable duplexes with DNA and RNA, and are resistant to degradation by nucleases and proteases. Encouraging results have been reported utilizing a PNA-based antisense strategy for inhibition of N-Myc expression in neuroblastoma.

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Characterization of homogeneously staining regions in a small cell lung cancer cell line, using in situ hybridization with an MYCN probe

Cited by 7 publications

References 10 publications

The genomic landscape of retinoblastoma: a review

The genomic landscape of retinoblastoma: a review

Interphase cytogenetics and comparative genomic hybridization of human epithelial cancers and precursor lesions

The MYCN Oncogene as a Specific and Selective Drug Target for Peripheral and Central Nervous System Tumors

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