Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0012872 (DNA marker)
929 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A molecular genetic approach employing polymorphic DNA markers has been used to investigate the role of chromosomal aberrations in meningioma, one of the most common tumors of the human nervous system. Comparison of the alleles detected by DNA markers in tumor DNA versus DNA from normal tissue revealed chromosomal alterations present in primary surgical specimens. In agreement with cytogenetic studies of cultured meningiomas, the most frequent alteration detected was loss of heterozygosity on chromosome 22. Forty of 51 patients were constitutionally heterozygous for at least one chromosome 22 DNA marker. Seventeen of the 40 constitutionally heterozygotic patients (43%) displayed hemizygosity for the corresponding marker in their meningioma tumor tissues. Loss of heterozygosity was also detected at a significantly lower frequency for markers on several other autosomes. In view of the striking association between acoustic neuroma and meningioma in bilateral acoustic neurofibromatosis and the discovery that acoustic neuromas display specific loss of genes on chromosome 22, we propose that a common mechanism involving chromosome 22 is operative in the development of both tumor types. Fine-structure mapping to reveal partial deletions in meningiomas may provide the means to clone and characterize a gene (or genes) of importance for tumorigenesis in this and possibly other clinically associated tumors of the human nervous system.
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PMID:Molecular genetic approach to human meningioma: loss of genes on chromosome 22. 303 50

Cytogenetic and molecular analyses of human breast cancer cells have identified consistent losses of specific chromosomal regions in these tumors, suggesting that such regions harbor tumor suppressor genes whose homozygous loss or inactivation directly contributes to tumorigenesis. To date, deletions of chromosome 8 sequences have been described infrequently and only in low percentages of breast carcinomas. We report the identification of a new DNA marker on chromosome 8p that is deleted in 6 (75%) of 8 breast carcinoma cell lines and in 1 primary breast carcinoma examined. No deletion of this marker was detected in any normal or nonbreast carcinoma cell lines analyzed. Southern blot and fluorescence in situ hybridization studies indicate that this clone maps to chromosome 8 between bands p12 and p21. These observations suggest that a new gene, whose loss or inactivation may foster breast carcinoma tumorigenesis, may reside in this chromosome 8p region.
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PMID:Loss of chromosome 8p sequences in human breast carcinoma cell lines. 807 45

The mitotic activity astrocytes in the adult central nervous system (CNS) is of interest due to their roles in gliosis and tumorigenesis, and their potential in aiding recovery of function following injury or disease. The posterior pituitary offers a potentially powerful model to study proliferation in vivo, since its resident astrocytes, called pituicytes, have been reported to divide concurrently with hormone release from the neurosecretory terminals there. our aim in this study was to confirm and characterize this proliferative response during dehydration and rehydration in fully adult animals using contemporary techniques. Adult male rats were given 2% saline in substitution for water for 0-9 days. Proliferation of pituicytes was quantified in tissue sections triple-labeled with the proliferation marker, 5-bromodeoxyuridine (BrdU), the astrocyte marker glial fibrillary acidic protein (GFAP), and the DNA marker 4,6,diamidino-2-phenylindole, HCL(DAPI). A robust proliferative response began within three days of dehydration and continued at a constant rate thereafter. In animals allowed to rehydrate, this response continued. After 9 days of dehydration, approximately 35% of pituicytes had participated in mitosis. While cell density remained constant across conditions, a reversible increase in posterior pituitary area was seen, suggesting that some cell death also occurs simultaneously. A significant proportion of non-pituicytes also underwent similar changes. These results indicate that pituicytes in the adult posterior pituitary retain characteristics necessary for reentering the cell cycle in response to local factors present during neurosecretory activity. We hypothesize that this proliferative response is directly related to the morphological changes previously reported for these cells under activating conditions.
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PMID:Dehydration-induced proliferation of identified pituicytes in fully adult rats. 884 2