Frequent loss of heterozygosity on chromosome 14q in neuroblastoma. 1989

T Suzuki, and J Yokota, and H Mugishima, and I Okabe, and M Ookuni, and T Sugimura, and M Terada
National Cancer Center Research Institute, Tokyo, Japan.

Using 29 polymorphic DNA markers which detect allelic deletion of genes at specific loci on 19 different chromosomes, we analyzed 14 neuroblastomas for possible loss of chromosomal heterozygosity. The incidence of loss of heterozygosity was high at the D14S1 locus on chromosome 14q, being detected in six of 12 patients (50%). In spite of the cytogenetic finding suggesting high frequency of chromosome 1p deletion, loss of heterozygosity at the MYCL locus on 1p32 was detected only in two of nine patients (22%). It was also found in two of 11 patients (18%) on 13q, but not on chromosomes 2, 3, 5, 6, 7, 8, 9, 10, 11, 12, 15, 16, 17, 18, 19, and 20. The present results indicate that recessive genetic changes involving sequences on chromosome 14q may play an important role in the development of neuroblastoma.

UI MeSH Term Description Entries
D008297 Male Males
D009447 Neuroblastoma A common neoplasm of early childhood arising from neural crest cells in the sympathetic nervous system, and characterized by diverse clinical behavior, ranging from spontaneous remission to rapid metastatic progression and death. This tumor is the most common intraabdominal malignancy of childhood, but it may also arise from thorax, neck, or rarely occur in the central nervous system. Histologic features include uniform round cells with hyperchromatic nuclei arranged in nests and separated by fibrovascular septa. Neuroblastomas may be associated with the opsoclonus-myoclonus syndrome. (From DeVita et al., Cancer: Principles and Practice of Oncology, 5th ed, pp2099-2101; Curr Opin Oncol 1998 Jan;10(1):43-51) Neuroblastomas
D011519 Proto-Oncogenes Normal cellular genes homologous to viral oncogenes. The products of proto-oncogenes are important regulators of biological processes and appear to be involved in the events that serve to maintain the ordered procession through the cell cycle. Proto-oncogenes have names of the form c-onc. Proto-Oncogene,Proto Oncogene,Proto Oncogenes
D012150 Polymorphism, Restriction Fragment Length Variation occurring within a species in the presence or length of DNA fragment generated by a specific endonuclease at a specific site in the genome. Such variations are generated by mutations that create or abolish recognition sites for these enzymes or change the length of the fragment. RFLP,Restriction Fragment Length Polymorphism,RFLPs,Restriction Fragment Length Polymorphisms
D002872 Chromosome Deletion Actual loss of portion of a chromosome. Monosomy, Partial,Partial Monosomy,Deletion, Chromosome,Deletions, Chromosome,Monosomies, Partial,Partial Monosomies
D002878 Chromosomes, Human, Pair 1 A specific pair of human chromosomes in group A (CHROMOSOMES, HUMAN, 1-3) of the human chromosome classification. Chromosome 1
D002882 Chromosomes, Human, Pair 13 A specific pair of GROUP D CHROMOSOMES of the human chromosome classification. Chromosome 13
D002883 Chromosomes, Human, Pair 14 A specific pair of GROUP D CHROMOSOMES of the human chromosome classification. Chromosome 14
D005260 Female Females
D005784 Gene Amplification A selective increase in the number of copies of a gene coding for a specific protein without a proportional increase in other genes. It occurs naturally via the excision of a copy of the repeating sequence from the chromosome and its extrachromosomal replication in a plasmid, or via the production of an RNA transcript of the entire repeating sequence of ribosomal RNA followed by the reverse transcription of the molecule to produce an additional copy of the original DNA sequence. Laboratory techniques have been introduced for inducing disproportional replication by unequal crossing over, uptake of DNA from lysed cells, or generation of extrachromosomal sequences from rolling circle replication. Amplification, Gene

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