SPOTS: A Model for the Creation of Sustainable, Population-Based, Occupational Therapy Fieldwork Sites.

This paper describes a model for the creation of sustainable, population-based, occupational therapy fieldwork sites (SPOTS). An example of a population-based fieldwork site was created with Appalachian Mountain People in Kentucky and its outcomes are presented. Outcomes were gathered using a wide variety of evaluation feedback forms.

Identification of regulatory regions of the putative tumor suppressor gene DMBT1.

The lack of expression of the putative tumor suppressor gene DMBT1 has been described in gliomas, lung carcinomas, and other malignancies. To investigate the mechanisms regulating DMBT1 expression we have screened a human genomic library with a 5' cDNA probe and identified a fragment of approximately 3 kb upstream of the proposed coding sequence of DMBT1. This fragment contains subregions that may up- or down-regulate the expression of a reporter gene.

Identification of PTEN-related sequences in glioma cells and in non-neoplastic cell lines.

The PTEN gene, which encodes a tumor suppressor with phosphatase activity, is located on chromosome 10q23 and is mutated in different tumors, including glioblastomas (GBM). We found evidence for a PTEN-related sequence (PTEN-rs) on genomic DNA of GBM and non-neoplastic cells. PTEN-rs does not contain introns and presents several conserved missense mutations, including a T to G transversion at the initiation codon.

A recurrent 19q11-12 breakpoint suggested by cytogenetic and fluorescence in situ hybridization analysis of three glioblastoma cell lines.

Loss of genetic material at chromosome 19 is a rather frequent finding in malignant gliomas. Loss of heterozygosity at region 19q13.3 is common in oligodendrogliomas and is also present, together with other genetic alterations on the same chromosome, in glioblastoma multiforme (GBM).

PTEN/MMAC1 mutations in primary glioblastomas and short-term cultures of malignant gliomas.

A novel tumor suppressor, PTEN/MMAC1, was recently found on chromosome 10q23 and mutations of this gene were described in about 20% of primary glioblastomas (GBM) and 60% of GBM cell lines. To define further the relevance of PTEN/MMAC1 mutations in GBM we investigated by SSCP analysis its coding sequence in 44 gliomas, including 41 GBM, and in 21 short-term cultures (15 GBM and six malignant astrocytomas). Loss of heterozygosity (LOH) at 10q23 was present in at least one marker in the vicinity of the PTEN/MMAC1 locus in 59% of the informative GBM (primary tumors and cell cultures).