Cytogenetic studies of human brain tumors and their clinical significance

Latimer, F R; Al-Saadi, Abdul; Robbins, Thomas O.

doi:10.1007/bf00150618

Cited by 25 publications

(2 citation statements)

References 11 publications

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“…Whether or not amplification of this gene is a poor prognostic factor for the patient, as has been shown for MYCN gene amplification in neuroblastomas, remains to be determined. Approximately 50 cases of medulloblastoma have been evaluated cytogenetically using chromosomal banding (9)(10)(11)(12)(13). Tumours with abnormal stemlines in the near diploid, hyperdiploid and polyploid regions have been described.…”

Section: Malignant Gliomasmentioning

confidence: 99%

Cytogenetics and Molecular Genetics of Malignant Gliomas and Medulloblastoma

1990

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Malignant gliomas and medulloblastomas which are the most common primary malignant brain tumours of adult and children, respectively, resemble other neurogenic tumours as they frequently contain gene amplification and show non-random loss of specific chromosomal regions. In gliomas the gene which is most often amplified, is the epidermal growth factor receptor gene. In many cases the gene is rearranged as well, producing abnormally small epidermal growth factor receptor proteins. More than 80% of tumours have lost chromosome 10 and losses of 9p13, 17p and 22 occur in subgroups of cases. 17p loss is associated with point mutations of the p53 gene, but the relevant genes in the other chromosomal regions remain to be identified. For medulloblastoma the most frequent chromosomal abnormality is i(17q). Whether or not p53 gene mutations are the targets of 17p losses in these tumours remains to be determined. Approximately 5% of medulloblastoma biopsies contain gene amplification, although the incidence in medulloblastoma cell lines is more than 80%. c-myc is the gene which is most frequently amplified in this tumour type. The relationship of these various molecular genetic abnormalities to the biology of the tumours and the course of the patients remains largely unexplored.

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Section: Malignant Gliomasmentioning

confidence: 99%

Cytogenetics and Molecular Genetics of Malignant Gliomas and Medulloblastoma

1990

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“…These include age at the time of diagnosis, cellular differentiation within the tumor, metastatic disease at the time of diagnosis, and extent of surgical resection (Allen et al, 1982;Packer et al, 1985). Efforts to identify additional factors that could aid in determining the prognosis such as DNA aneuploidy or growth fraction as assessed by flow cytometry, as well as limited cytogenetic studies, have led to conflicting results (Latimer et al, 1987;Yasue et al, 1989).…”

Section: Introductionmentioning

confidence: 99%

Isochromosome 17q in primitive neuroectodermal tumors of the central nervous system

Biegel¹,

Rorke²,

Packer³

et al. 1989

Genes Chromosomes & Cancer

154

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We have prepared karyotypes from 22 primitive neuroectodermal tumors (PNETs) from pediatric patients ranging in age from 10 months to 16 years. Twenty-one cases were newly diagnosed, primary, posterior fossa tumors. One case was a recurrent tumor in a patient previously treated with radiation. Cytogenetic results were obtained from direct preparations and/or short-term (1-10 day) culture. Three tumors had apparently normal karyotypes. Nineteen tumors demonstrated numerical and/or structural abnormalities. The most frequent structural chromosomal changes were deletions and nonreciprocal translocations. Four tumors contained double minutes. Several chromosomes appear to be nonrandomly involved in PNETs. These include chromosomes 5, 6, 11, 16, 17, and a sex chromosome. The most consistent change, however, was an i(17q), present in one-third (8/22) of the cases. Strikingly, in three of these eight tumors, the i(17q) was the only structural abnormality observed. An i(17q) is not specific for pediatric PNETs, as it is also seen in leukemias and other solid tumors. However, in PNETs it may be a primary change related to tumor development and/or progression. Clinically, there was no correlation of the cytogenetic findings with histologic features of the tumors, size of the tumor, extent of metastasis, or surgical resection.

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Flow cytometric DNA analysis of medulloblastoma.Prognostic implication of aneuploidy

Tomita

Yasue

Engelhard

et al. 1988

Cancer

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Paraffin-embedded surgical specimens from 26 infants and children with medulloblastomas treated between 1972 and 1981 were examined for DNA ploidy by flow cytometry (FCM). All patients received a standard treatment (a combination of maximum debulking of medulloblastoma and postoperative craniospinal irradiation with a posterior fossa boost of 5000 rad or more). They were studied to correlate the results of the findings of FCM DNA analysis with their final outcome, DNA ploidy, and extent of tumor resection. All seven patients with totally resected aneuploid medulloblastoma are alive, whereas only one of six patients with subtotally resected diploid medulloblastoma is alive (P = 0.0047). The current study suggests both DNA ploidy and extent of surgical resection are the most important determinant of patients' prognosis. Patients in selected group, particularly those with subtotally resected diploid tumor, are advised to undergo aggressive adjuvant chemotherapy.

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Cytogenetic studies of human brain tumors and their clinical significance

Cited by 25 publications

References 11 publications

Cytogenetics and Molecular Genetics of Malignant Gliomas and Medulloblastoma

Cytogenetics and Molecular Genetics of Malignant Gliomas and Medulloblastoma

Isochromosome 17q in primitive neuroectodermal tumors of the central nervous system

Flow cytometric DNA analysis of medulloblastoma.Prognostic implication of aneuploidy

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