Correlation of DNA ploidy and morphological features of human glioma cell cultures with the establishment of cell lines

Onda, Kiyoshi; Tanaka, Ryuichi; Washiyama, Kazuo; Takeda, Nobutaka; Kumanishi, Toshiro

doi:10.1007/bf00686381

Cited by 18 publications

(8 citation statements)

References 13 publications

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“…The finding with flow cytometry of an aneuploid peak in all four tested high-grade gliomas and diploid peak in one high-grade and one low-grade glioma agrees with the distribution found by others (Onda et al, 1988;Spaar & Spaar, 1990).…”

Section: Specificity Of the Measured Inhibitionsupporting

confidence: 91%

“…On the other hand, it should be considered that it is most likely that even the early passage populations represent a selection of the original tumour heterogeneity (Shapiro et al, 1981). In addition the findings with cytogenetic and flow cytometric studies in the near-diploid range may be of nontumorous origin, and aneuploid findings may be generated in vitro, as we did not make direct preparations in order to identify original tumour characteristics (Shapiro et al, 1981;Onda et al, 1988).…”

Section: Specificity Of the Measured Inhibitionmentioning

confidence: 99%

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Growth of cultured human glioma tumour cells can be regulated with histamine and histamine antagonists

Ven¹,

Prinsen²,

Jansen³

et al. 1993

Br J Cancer

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Summary The 50% survival time for low grade astrocytomas is 50 months and for high grade astrocytomas it is 13 months, underlining the need for new therapies. Several reports show that in vivo histamine antagonists cause retardation of tumour growth in some animal models and prolonged survival in cancer patients. Therefore we have tested the growth modulating effects of histamine and histamine antagonists on human glioma cultures.Twelve freshly excised human gliomas were cultured and tested for their in vitro sensitivity to histamine and histamine antagonists. Four continuous glioma cell lines were used to confirm the glioma-specificity of the effects observed in the primary cell lines. In low serum concentration (0 or 1%) the growth of 5/9 primary glioma-derived cultures could be stimulated with 0.2 mm histamine, and in 4/5 cases with 0.2 tLM histamine. One mm of the histamine H2-receptor antagonist cimetidine could inhibit the growth of 4/5 primary glioma cultures when tested in 1% human AB serum, and of 6/13 cases when tested in 1% FCS. Lower concentrations (down to I fLM) were less effective. The histamine HI-receptor antagonist pyrilamine gave variable results.The specificity of the effects is indicated by the absence of a generalised toxic effect, by the observation that the antagonist-induced inhibition could be reversed with histamine, and by the correlation of the obtained cimetidine-induced growth inhibition with the maximal growth rate of the primary cell lines in 10% FCS.The observed cimetidine-induced inhibition of the in vitro proliferation of gliomas suggests that cimetidine is a relevant candidate for the in vivo growth inhibition of these tumours.

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Section: Specificity Of the Measured Inhibitionsupporting

confidence: 91%

Section: Specificity Of the Measured Inhibitionmentioning

confidence: 99%

Growth of cultured human glioma tumour cells can be regulated with histamine and histamine antagonists

Ven¹,

Prinsen²,

Jansen³

et al. 1993

Br J Cancer

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“…Nine (cases 1-6 and 8-10) had been established in our institute [25][26][27][28] and the other was U-251MG (case 7).…”

Section: Glioma Cell Linesmentioning

confidence: 99%

“…Nine (cases 1-6 and 8-10) had been established in our institute [25][26][27][28] and the other was U-251MG (case 7). 29) The pathological diagnosis of the primary tumors from which the cell lines were established was anaplastic glioma (WHO grade III) in 8 cases and glioblastoma (WHO grade IV) in 2 cases.…”

Section: Glioma Cell Linesmentioning

confidence: 99%

“…In analysis of the MMAC1 gene, exons 1 to 9 were PCR-amplified using the primers described by Liaw et al 31) and Wang et al, 7) which corresponded to intronic sequences except for the sense primer for exon 1 and the antisense primer for exon 9, which corresponded to the 5′ [25][26][27][28] Among them, cases 3, 6 and 10 are Onda 11, 10 and 9 cell lines, respectively. 26,27) b) Pa Dx, pathological diagnosis; F, frontal; P, parietal; T, temporal.…”

Section: )mentioning

confidence: 99%

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Rare‐type Mutations of MMAC1 Tumor Suppressor Gene in Human Glioma Cell Lines and Their Tumors of Origin

Zhang¹,

Endo²,

Ichikawa³

et al. 1999

Japanese Journal of Cancer Research

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A total of 10 glioma cell lines were examined to evaluate the status of the MMAC1 gene, a candidate tumor suppressor gene. Six cell lines showed mutations with presumed loss of heterozygosity and 1 cell line showed no mRNA expression. The 6 mutations consisted of 3 3-bp deletions (codons 17, 101 or 199), 1 missense mutation (codon 252) and 2 truncation mutations (1 nonsense mutation at codon 233 and 1 2-bp insertion at codon 241). Among them, the 3-bp deletions, which are a rare type of mutation in MMAC1 gene, were located in the N-terminal half (codons 1-212) of the coding region, which is considered important in MMAC1 function. The missense mutation was located unusually in the C-terminal half (codons 212-403), but it was in a small region in which some other reported missense mutations are clustered. Thus, these 4 mutations were suggested to have functional effects on the MMAC1 activity, like the other 2 mutations with predicted protein truncations. By sequence analysis of cDNA clones, we confirmed that all the mutations including these 4 rare ones were in the MMAC1 gene, not in the PTH2 pseudogene. In 2 cases, we also examined the primary glioma tissues from which the cell lines had been derived and found the same mutations as in the cell lines in both cases. This suggested that the mutations in these cell lines were derived from the primary glioma tissues, but not from artifacts arising during long-term in vitro cultivation. Key words: MMAC1 -PTEN -Tumor suppressor gene -Pseudogene -GliomaThe MMAC1 gene (also called PTEN and TEP1), a candidate tumor suppressor gene which is located on chromosome 10q23, contains 9 exons and encodes 403 amino acids.1-3) The proximal half of the protein is homologous to phosphatases and cytoskeleton-associated proteins, tensin and auxilin, [1][2][3] and its phosphatase activity has been demonstrated in in vitro assays.3-6) MMAC1 gene alterations have already been examined in various tumors including malignant glioma, prostate carcinoma and endometrial carcinoma.1, 2, 7-19) Among them, malignant gliomas have revealed frequent alterations in both primary tumor tissues and cell lines, 1, 2, 7-14) consistent with the previous LOH (loss of heterozygosity) studies that showed frequent deletion of regions of chromosome 10 in malignant gliomas. [20][21][22] MMAC1 gene alterations in malignant gliomas included small deletions, small insertions, splicing mutations, nonsense mutations and missense mutations. However, despite the considerable number of MMAC1 gene alterations reported, the entire profile of the alterations in malignant gliomas and other tumors as well has not been fully detailed.In this study, we examined a total of 10 glioma cell lines for alterations of the MMAC1 gene and its mRNA and found mutations in 6 cell lines and no mRNA expression in 1 cell line. All the mutations, which included 4 rarely reported ones, were confirmed to be in the MMAC1 gene itself, but not in the PTH2 pseudogene (also called ψPTEN), 23,24) and were analyzed in connection with previous results in...

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Models for CNS Malignancies

Crotty

Sampson

Archer

et al. 2005

The Cancer Handbook

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Correlation of DNA ploidy and morphological features of human glioma cell cultures with the establishment of cell lines

Cited by 18 publications

References 13 publications

Growth of cultured human glioma tumour cells can be regulated with histamine and histamine antagonists

Growth of cultured human glioma tumour cells can be regulated with histamine and histamine antagonists

Rare‐type Mutations of MMAC1 Tumor Suppressor Gene in Human Glioma Cell Lines and Their Tumors of Origin

Models for CNS Malignancies

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