Allelic status on 1p and 11p15 in neuroblastoma and benign ganglioneuroma

Hiroki Kurahashi, T. Oue, K. Akagi, M. Fukuzawa, A. Okada, A. Tawa, S. Okada, I. Nishisho

Research output: Contribution to journalArticle

5 Citations (Scopus)

Abstract

A tumor suppressor gene responsible for neuroblastoma (NB) is thought to be located on 1p, while a gene(s) commonly involved in embryonal tumors in childhood is(are) located on 11p15. To determine whether and how those putative genes affect tumorigenesis of NB, a total of 25 NBs and two benign ganglioneuromas (GNs) were examined by Southern technique with polymorphic markers on chromosomes 1 and 11 for analysis of the loss of heterozygosity at these loci. Because NB often features an increased number of chromosomes, we performed a detailed examination of allelic status and then compared it with their prognostic factors. While allelic loss on 1p was observed in only four cases (16%), eight additional cases showed allelic imbalance on a portion of 1p, indicating that these cases featured 1p deletions, so that the total number of cases with a 1p deletion was 12 out of 25 NBs (48%). A 1p deletion was observed not only in disseminated cases (8/14 of stage III or IV), but also in several cases with localized tumors (4/11 of stage I or II, p = 0.529). Moreover, one GN case showed a 1p deletion. However, allelic loss or imbalance on 11p15 was observed in only two NBs (8%). These data suggest that 1p deletion is an initial event of NB tumorigenesis rather than a later event associated with tumor progression, while deletion of 11p15 is related to the development of a small proportion of NBs. Cases with 1p deletion do not always follow an aggressive clinical course and may differentiate into GN.

Original languageEnglish
Pages (from-to)669-674
Number of pages6
JournalInternational Journal of Oncology
Volume6
Issue number3
Publication statusPublished - 01-01-1995
Externally publishedYes

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Ganglioneuroma
Neuroblastoma
Loss of Heterozygosity
Allelic Imbalance
Carcinogenesis
Neoplasms
Chromosomes, Human, Pair 11
Chromosomes, Human, Pair 1
Tumor Suppressor Genes
Genes
Monosomy 1p Chromosome 1
Chromosomes

All Science Journal Classification (ASJC) codes

  • Cancer Research
  • Oncology

Cite this

Kurahashi, H., Oue, T., Akagi, K., Fukuzawa, M., Okada, A., Tawa, A., ... Nishisho, I. (1995). Allelic status on 1p and 11p15 in neuroblastoma and benign ganglioneuroma. International Journal of Oncology, 6(3), 669-674.
Kurahashi, Hiroki ; Oue, T. ; Akagi, K. ; Fukuzawa, M. ; Okada, A. ; Tawa, A. ; Okada, S. ; Nishisho, I. / Allelic status on 1p and 11p15 in neuroblastoma and benign ganglioneuroma. In: International Journal of Oncology. 1995 ; Vol. 6, No. 3. pp. 669-674.
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abstract = "A tumor suppressor gene responsible for neuroblastoma (NB) is thought to be located on 1p, while a gene(s) commonly involved in embryonal tumors in childhood is(are) located on 11p15. To determine whether and how those putative genes affect tumorigenesis of NB, a total of 25 NBs and two benign ganglioneuromas (GNs) were examined by Southern technique with polymorphic markers on chromosomes 1 and 11 for analysis of the loss of heterozygosity at these loci. Because NB often features an increased number of chromosomes, we performed a detailed examination of allelic status and then compared it with their prognostic factors. While allelic loss on 1p was observed in only four cases (16{\%}), eight additional cases showed allelic imbalance on a portion of 1p, indicating that these cases featured 1p deletions, so that the total number of cases with a 1p deletion was 12 out of 25 NBs (48{\%}). A 1p deletion was observed not only in disseminated cases (8/14 of stage III or IV), but also in several cases with localized tumors (4/11 of stage I or II, p = 0.529). Moreover, one GN case showed a 1p deletion. However, allelic loss or imbalance on 11p15 was observed in only two NBs (8{\%}). These data suggest that 1p deletion is an initial event of NB tumorigenesis rather than a later event associated with tumor progression, while deletion of 11p15 is related to the development of a small proportion of NBs. Cases with 1p deletion do not always follow an aggressive clinical course and may differentiate into GN.",
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Kurahashi, H, Oue, T, Akagi, K, Fukuzawa, M, Okada, A, Tawa, A, Okada, S & Nishisho, I 1995, 'Allelic status on 1p and 11p15 in neuroblastoma and benign ganglioneuroma', International Journal of Oncology, vol. 6, no. 3, pp. 669-674.

Allelic status on 1p and 11p15 in neuroblastoma and benign ganglioneuroma. / Kurahashi, Hiroki; Oue, T.; Akagi, K.; Fukuzawa, M.; Okada, A.; Tawa, A.; Okada, S.; Nishisho, I.

In: International Journal of Oncology, Vol. 6, No. 3, 01.01.1995, p. 669-674.

Research output: Contribution to journalArticle

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T1 - Allelic status on 1p and 11p15 in neuroblastoma and benign ganglioneuroma

AU - Kurahashi, Hiroki

AU - Oue, T.

AU - Akagi, K.

AU - Fukuzawa, M.

AU - Okada, A.

AU - Tawa, A.

AU - Okada, S.

AU - Nishisho, I.

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N2 - A tumor suppressor gene responsible for neuroblastoma (NB) is thought to be located on 1p, while a gene(s) commonly involved in embryonal tumors in childhood is(are) located on 11p15. To determine whether and how those putative genes affect tumorigenesis of NB, a total of 25 NBs and two benign ganglioneuromas (GNs) were examined by Southern technique with polymorphic markers on chromosomes 1 and 11 for analysis of the loss of heterozygosity at these loci. Because NB often features an increased number of chromosomes, we performed a detailed examination of allelic status and then compared it with their prognostic factors. While allelic loss on 1p was observed in only four cases (16%), eight additional cases showed allelic imbalance on a portion of 1p, indicating that these cases featured 1p deletions, so that the total number of cases with a 1p deletion was 12 out of 25 NBs (48%). A 1p deletion was observed not only in disseminated cases (8/14 of stage III or IV), but also in several cases with localized tumors (4/11 of stage I or II, p = 0.529). Moreover, one GN case showed a 1p deletion. However, allelic loss or imbalance on 11p15 was observed in only two NBs (8%). These data suggest that 1p deletion is an initial event of NB tumorigenesis rather than a later event associated with tumor progression, while deletion of 11p15 is related to the development of a small proportion of NBs. Cases with 1p deletion do not always follow an aggressive clinical course and may differentiate into GN.

AB - A tumor suppressor gene responsible for neuroblastoma (NB) is thought to be located on 1p, while a gene(s) commonly involved in embryonal tumors in childhood is(are) located on 11p15. To determine whether and how those putative genes affect tumorigenesis of NB, a total of 25 NBs and two benign ganglioneuromas (GNs) were examined by Southern technique with polymorphic markers on chromosomes 1 and 11 for analysis of the loss of heterozygosity at these loci. Because NB often features an increased number of chromosomes, we performed a detailed examination of allelic status and then compared it with their prognostic factors. While allelic loss on 1p was observed in only four cases (16%), eight additional cases showed allelic imbalance on a portion of 1p, indicating that these cases featured 1p deletions, so that the total number of cases with a 1p deletion was 12 out of 25 NBs (48%). A 1p deletion was observed not only in disseminated cases (8/14 of stage III or IV), but also in several cases with localized tumors (4/11 of stage I or II, p = 0.529). Moreover, one GN case showed a 1p deletion. However, allelic loss or imbalance on 11p15 was observed in only two NBs (8%). These data suggest that 1p deletion is an initial event of NB tumorigenesis rather than a later event associated with tumor progression, while deletion of 11p15 is related to the development of a small proportion of NBs. Cases with 1p deletion do not always follow an aggressive clinical course and may differentiate into GN.

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Kurahashi H, Oue T, Akagi K, Fukuzawa M, Okada A, Tawa A et al. Allelic status on 1p and 11p15 in neuroblastoma and benign ganglioneuroma. International Journal of Oncology. 1995 Jan 1;6(3):669-674.