Prognostic value of cytogenetic analysis in human cerebral astrocytomas

Kimmel, David W.; O’Fallon, Judith R.; Scheithauer, Bernd W.; Kelly, Patrick J.; Dewald, Gordon W.; Jenkins, Robert B.

doi:10.1002/ana.410310512

Cited by 44 publications

(23 citation statements)

References 23 publications

(7 reference statements)

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“…Both of these lines were derived from high grade tumours. The association between complex karyotypic changes and high malignancy in brain tumours has been reported recently by Kimmel et al (1992). Of particular note is the presence of structural abnormalities involving the short arm of chromosome 9 in cell lines G47 and G223.…”

Section: Specificity Of the Measured Inhibitionmentioning

confidence: 86%

“…Of particular note is the presence of structural abnormalities involving the short arm of chromosome 9 in cell lines G47 and G223. Kimmel et al (1992) also demonstrated that aberrations of 9p appear to be continued to brain tumours of high malignancy. Molecular studies using a range of probes for this region of sent an important step in the progression of these tumours (Olufunmilayo et al, 1992).…”

Section: Specificity Of the Measured Inhibitionmentioning

confidence: 90%

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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 Inhibitionmentioning

confidence: 86%

Section: Specificity Of the Measured Inhibitionmentioning

confidence: 90%

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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“…108 m in Astrocytomas sizes and proliferative rates than neoplastic cells, factors that could potentially affect the number of signals identified. Chromosome 3 was chosen over other chromosomes as a suitable control chromosome marker because it has remained disomic in most published karyotypes of diffuse astrocytomas, including GBM, [2][3][4][5][6][7] and because the probe produced strong discrete signals in our cases.…”

Section: Positive Controlsmentioning

confidence: 99%

“…[2][3][4][5][6][7] The two most common numeric abnormalities have been the gain of chromosome 7 in 24% to 52% and loss of an entire chromosome 10 in 27% to 46%. The results of our in situ hybridization studies reveal similar frequencies.…”

Section: Dna In Situ Hybridizationmentioning

confidence: 99%

Interphase Cytogenetic (In Situ Hybridization) Analysis of Astrocytomas Using Archival, Formalin-Fixed, Paraffin-Embedded Tissue and Nonfluorescent Light Microscopy

et al. 1997

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Astrocytomas contain nonrandom chromosomal abnormalities that recently have been correlated with shortened patient survival. Two frequently reported aberrations are trisomy 7 and monosomy 10.We assessed the numerical complement of chromosomes 7 and 10 in formalin-fixed, paraffin-embedded brain biopsy tissue from 28 diffuse astrocytomas by in situ hybridization using a nonfluorescent enzymatic detection system. Clinical follow-up of at least 5 years was available in 26 cases (93%).Monosomy 10 was identified in 7 cases (25%): astrocytoma, 1 case; anaplastic astrocytoma, 1 case; and glioblastoma, 5 cases.Cytogenetic studies have revealed consistent nonrandom numerical and structural chromosomal abnormalities in astrocytic neoplasms. Two recent studies at the Mayo Clinic (Rochester, Minn) have demonstrated prolonged survival of patients with a normal tumor karyotype compared with those exhibiting clonal aberrations, 1 ' 2 suggesting that cytogenetic analysis may provide useful diagnostic and prognostic information for patients with central nervous system malignancies. Common numerical changes in diffuse astrocytomas include gains of chromosome 7 and losses of chromosomes 10, 22, X, and Y, whereas structural abnormalities most frequently involve chromosomes 1 and 9.2-7 Furthermore, molecular genetic and cytogenetic studies provide evidence for an orderly M a n u s c r i p t received A u g u s t 6, 1996; revision accepted December 11,1996.Address reprint requests to Dr White: Department of Pathology, Division of Neuropathology, University of Texas Southwestern Medical Center, 5323 Harry Hines Blvd., Dallas, Dr Tonk is now with the Department of Pediatrics, Texas Tech University Health Science Center, Lubbock, Texas.Trisomy 7 was identified in 11 cases (39%): astrocytoma, 5 cases; glioblastoma, 6 cases. Multivariate analysis revealed that monosomy 10 was the most statistically significant negative predictor of patient survival.Numerical chromosomal abnormalities are detectable in astrocytomas in archival tissue using interphase cytogenetics and nonfluorescent light microscopy. Although larger studies are required, our data suggest that potentially useful prognostic information may be obtained with this approach.

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“…For astrocytomas of all grades, it appears that certain genetic changes are associated with an unfavourable clinical course. Astrocytomas with chromosomal abnormalities as detected by karyotyping lead to a shorter survival as compared to astrocytomas without these abnormalities (Kimmel et al, 1992). An ISH study showed that monosomy for chromosome 10, harbouring the tumour suppressor gene PTEN/MMAC1, results in shorter survival (Cianciulli et al, 2000).…”

Section: Discussionmentioning

confidence: 99%

Proliferation and aneusomy predict survival of young patients with astrocytoma grade II

Wessels¹,

Hopman²,

Kubat³

et al. 2003

Br J Cancer

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The clinical course of astrocytoma grade II (AII) is highly variable and not reflected by histological characteristics. As one of the best prognostic factors, higher age identifies rapid progressive A II. For patients over 35 years of age, an aggressive treatment is normally propagated. For patients under 35 years, there is no clear guidance for treatment choices, and therefore also the necessity of histopathological diagnosis is often questioned. We studied the additional prognostic value of the proliferation index and the detection of genetic aberrations for patients with A II. The tumour samples were obtained by stereotactic biopsy or tumour resection and divided into two age groups, that is 18 -34 years (n ¼ 19) and X35 years (n ¼ 28). Factors tested included the proliferation (Ki-67) index, and numerical aberrations for chromosomes 1, 7, and 10, as detected by in situ hybridisation (ISH). The results show that age is a prognostic indicator when studied in the total patient group, with patients above 35 years showing a relatively poor prognosis. Increased proliferation index in the presence of aneusomy appears to identify a subgroup of patients with poor prognosis more accurately than predicted by proliferation index alone. We conclude that histologically classified cases of A II comprise a heterogeneous group of tumours with different biological and genetic constitution, which exhibit a highly variable clinical course. Immunostaining for Ki-67 in combination with the detection of aneusomy by ISH allows the identification of a subgroup of patients with rapidly progressive A II. This is an extra argument not to defer stereotactic biopsy in young patients with radiological suspicion of A II.

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Prognostic value of cytogenetic analysis in human cerebral astrocytomas

Cited by 44 publications

References 23 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

Interphase Cytogenetic (In Situ Hybridization) Analysis of Astrocytomas Using Archival, Formalin-Fixed, Paraffin-Embedded Tissue and Nonfluorescent Light Microscopy

Proliferation and aneusomy predict survival of young patients with astrocytoma grade II

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