Enhanced Expression of the c-myc Oncogenes in Human Brain Tumors

Kazumoto, Kiyoshi; Matsumoto, Masahiro; Tamada, Junpei; Handa, Ichiro; Tamura, Masahito; Yuasa, Yasuhito

doi:10.1007/978-4-431-68150-2_46

Cited by 6 publications

(9 citation statements)

References 9 publications

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“…Human meningiomas are marked by enhanced expression of the c-sis and cmyc oncogenes. 13,36,82 Similarly, the rare Ha-ras and c-mos oncogenes have a higher activation in individuals with intracranial tumors, including meningiomas, than in healthy patients.…”

Section: Oncogene Expression In Meningiomasmentioning

confidence: 99%

Molecular genetics of meningiomas

Ragel¹,

Jensen²

2005

FOC

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In this article the authors provide a brief description of the current understanding of meningioma genetics. Chromosome 22 abnormalities, especially in the Neurofibromatosis Type 2 (NF2) gene, have been associated with meningioma development. Loss of heterozygosity of chromosome 22 occurs in approximately 60% of meningiomas; however, loss of NF2 gene function occurs in only one third of these lesions. This discrepancy supports the theory that a second tumor suppressor gene exists on chromosome 22, and the authors introduce several possible gene candidates, including BAM22, LARGE, INI1, and MN1 genes. Deletions of 1p have also been shown to correlate with meningioma progression. The genetic similarities and differences among sporadic, NF2-associated, pediatric, and radiation-induced meningiomas are discussed, with the observation that the nonsporadic meningiomas have a higher incidence of multiple chromosomal abnormalities at presentation. Ultimately, a better understanding of the molecular pathways of meningioma tumorigenesis will lead to new, successful treatments.

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Section: Oncogene Expression In Meningiomasmentioning

confidence: 99%

Molecular genetics of meningiomas

Ragel¹,

Jensen²

2005

FOC

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“…The discovery of recombination of PDGF B with NF-2 ruled out c-sis as thc sitc of thc primary defect in this disordcr (Roulcau et al, 1990). Studies on meningiomas addressed the same question by checking the structure of the c-sis gene (Press et ul., 1989), but so far only one casc of c-sis rearrangement has been reported (Kazumoto et al, 1990). A deletion in an Alu repetitive sequence in the 5th intron of c-sis has also bcen described in meningioma patients, but a pathogenetic role for such an alteration has been excluded (Smidt et ul., 1991).…”

mentioning

confidence: 95%

Expression of c‐sis and c‐fos genes in human meningiomas and neurinomas

Riva

Larizza

1992

Intl Journal of Cancer

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The HindIII c-sis RFLP was analyzed in constitutional and tumor DNAs of 19 meningioma patients. Loss of a c-sis allele (allele I in all cases) was observed in 6 out of 10 tumors from heterozygous patients. No alteration in the structure or dosage of the c-sis gene was detected in any tumor sample. Northern analysis of c-sis evidenced sis transcripts in 7 out of 8 meningiomas which were amenable to analysis. All tumors expressing c-sis also expressed c-fos, suggesting that the autocrine loop elicited by sis activation may have c-fos as its nuclear target. Co-expression of c-sis and c-fos was also observed in 5 neuromas out of 7 analyzed. Very high levels of fos-mRNA were observed in 2 neuromas, but were not found to be caused by apparent alteration or amplification of the c-fos gene.

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“…Furthermore, using Northern bIot and immunocytochemical analyses, others have demonstrated c-sis mRNA and PDGF immunoreactivity in meningioma tumour cells but not in surrounding normal brain tissue. Moreover, P D G F receptor mRNA and protein were also detected, an essential requisite if the secreted PDGF were to act in an autocrine manner (Kazumoto et aL, 1990;Maxwell et aL, 1990). Significantly, the estimated molecular weight of 28 kDa of the major peak of mitogenic activity eluting from a Sephadex gel exclusion column in the present studies (Fig.…”

Section: Discussionmentioning

confidence: 75%

Autocrine control of human meningioma proliferation: Secretion of platelet‐derived growth‐factor‐like molecules

Adams

Todo

Schrell

et al. 1991

Intl Journal of Cancer

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We have used cell-culture techniques to investigate growth-factor production by human meningioma cells. Meningioma tissue was dispersed with collagenase and the cells grown to high density in tissue-culture flasks. The cultures were used to generate conditioned medium (MEN-CM), which was used to cultivate IMR32 cells (a human neuroblastoma line) and freshly dispersed primary meningioma cells. MEN-CM profoundly stimulated the in vitro growth of both IMR32 and meningioma cells. In addition, H3-thymidine uptake by cultured meningioma cells was increased in a dose-dependent manner by varying concentrations of MEN-CM. A neutralizing anti-body against platelet-derived growth factor (PDGF) completely abolished the stimulatory effects of MEN-CM, whereas an antibody against TGF-alpha was without effect. The mitogenic activity of MEN-CM, as assayed by promotion of H3-thymidine uptake by cultured meningioma cells, eluted from a Sephadex G-100 column in 3 peaks corresponding to molecular weights of greater than or equal to 150, 56 and 28 kDa. Our results show that proliferation of human meningiomas may be under autocrine control via secretion of PDGF-like molecules.

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Enhanced Expression of the c-myc Oncogenes in Human Brain Tumors

Cited by 6 publications

References 9 publications

Molecular genetics of meningiomas

Molecular genetics of meningiomas

Expression of c‐sis and c‐fos genes in human meningiomas and neurinomas

Autocrine control of human meningioma proliferation: Secretion of platelet‐derived growth‐factor‐like molecules

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