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PubMed1988

So-called primitive neuroectodermal tumor in aborted previable fetuses.

We have described the gross anatomic and histopathologic characteristics of 36 tumorlike lesions found in previable fetuses. Although these lesions appear to be invasive, metastasizing, and likely contributing to the death of the fetus, they represent a frequent finding only among severely macerated retained fetuses of 9-16 developmental weeks and have never been found in fresh nonretained fetuses. No family history of neurofibromatosis could be elicited in any of these cases to support the suggestion in the literature that these tumors may represent fetal manifestations of neurofibromatosis. The most likely explanation is that they represent an artifact owing to squeezing of brain tissue into the spinal canal and along the spinal nerves into retroperitoneal and retropleural spaces or the neck area. As this artifact appears to be confined to a specific developmental period (9-16 weeks), it may be related to certain developmental characteristics such as a very soft consistency of brain tissue or incomplete development of vertebral foramina. A higher incidence of these lesions among heteroploid fetuses remains unexplained.

Aneuploidy↗
PubMed1999

Molecular biology of the primitive neuroectodermal tumor: a review.

In terms of its molecular biology and molecular genetics, medulloblastoma is the most thoroughly studied of the pediatric brain tumors. Alterations in chromosome 17, usually an isochromosome 17q, are the most common cytogenetic abnormalities. Similarly, deletion of the short arm of one 17 chromosome, the result of formation of an iso17q, is the most common molecular biological abnormality found. The gene or genes important in the development of medulloblastoma found on chromsome 17 have not yet been identified. Both a tumor suppressor gene and an oncogene have been identified that may play a role in the development of this tumor type. The Patched (PTC) tumor suppressor gene is inactivated in approximately 15% of medulloblatomas; this alteration may be specific to the desmoplastic variant. Oncogenic mutations in the beta-catenin gene are found in a small subset of medulloblastomas. Both of these genes play central roles in developmental pathways. Prognosis in this tumor type has been related to the level of expression of the neurotrophin receptor trkC. In this review, these and other molecular biological and genetic findings are discussed with respect to the development of medulloblastoma.

Journal Article↗
PubMed1992

[Prognostic implications of the proliferation index (H3-TdR-labeling index) and ploidy in neuroectodermal tumors (astrocytomas and glioblastomas)].

Kinetic cellular methods were used in 53 cases of various sizes of astrocytomas and glioblastomas to obtain reliable prognostic information. Kinetic analysis revealed a wide variation of proliferative activity, with a gradual increase of the mean value from the most differentiated astrocytomas to glioblastomas. DNA content was significantly correlated with the degree of histological differentiation. Chromosomic patterns, which were detected in a few cases, were generally aspecific. The sole recurrent alteration in the karyotype was a small metacentric marker. The comparison of results obtained with the follow-up of patients showed that the labeling index offers a more accurate estimate of the proliferative potential of individual tumours, and thus of the probability of survival, than histological diagnosis and the evaluation of other biological parameters such as ploidy and karyotype.

Adolescent↗