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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cytogenetic findings in a squamous cell carcinoma (SCC) of the penis in a 60-year-old patient was observed for the first time. The stemline karyotype of the tumor was 46,XY,del(2) (q33q36),der(4)t(4;?)(p16;?),der(5;15)(q10;q10),der(8)t(8;?13)(p21 ;?),-13,- 13,-15,+3mar.
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PMID:Cytogenetic abnormalities in a squamous cell carcinoma of the penis. 148 62

Wilms' tumor has been associated with deletions in two loci on chromosome 11, and the introduction of a translocated human chromosome [t(X;11)] into a Wilms' tumor cell line (G401.6TG.6) by microcell hybridization suppresses tumor formation in nude mice. The tumorigenic phenotype is restored in segregants of these microcell hybrids, in which the introduced chromosome is lost. We have used ultrahigh-resolution 'giant' two-dimensional gel electrophoresis of metabolically labeled cellular proteins and in vitro translation products of isolated mRNA to identify changes in cellular gene expression that occur in these cell lines. The changes in gene expression associated with these chromosomal manipulations per se are quite minimal. However, we have identified two proteins (p16 and p28) whose synthesis is consistently decreased in three non-tumorigenic (suppressed) microcell hybrid clones relative to parental and segregant tumorigenic lines. They are also decreased at the level of mRNA in at least two of the non-tumorigenic clones. The decrease of these proteins represents markers of the suppressed phenotype, and their down-regulation may conceivably mediate the suppression of tumorigenicity.
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PMID:Suppression of tumorigenicity of a Wilms' tumor cell line is associated with a decrease in synthesis of two proteins. 165 66

Cytogenetic analysis of short-term cultures from ten giant cell tumors of bone revealed clonal and nonclonal chromosome abnormalities in three tumors and nonclonal changes only in seven. None of the clonal aberrations, inv(21)(p11q21) in one tumor, +5 in another, and t(15q22q), dic(4;22)(p16;p1?), double minutes, dicentrics, and ring chromosomes present in three separate clones in the third tumor, were identical to previously reported clonal changes in giant cell tumors. Telomeric associations were found in five tumors. The telomeres of chromosome arms 19q and 15p were particularly frequently involved.
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PMID:Chromosomal abnormalities in giant cell tumors of bone. 175 93

Cytogenetic analysis of meningioma cells from one particular patient (MN32) displayed the stem-line karyo-type 45, XY, -1, 4p+, 22q-, 22q+, which thus had rearrangements of both chromosomes 22. The 22q+ marker appeared as a dicentric: 22 pter----q11::1p11----qter. The reciprocal product of this translocation has presumably been lost because it lacked a centromere. The 22q- chromosome also appeared to have lost sequences distal to band q11. We assumed that this marker could have been the result of a reciprocal translocation between chromosomes 4 and 22. To investigate the 4p+ and 22q- chromosomes in more detail, human-hamster somatic cell hybrids were constructed that segregated the 22q- and 4p+ chromosomes. Southern blot analysis with DNA from these hybrids showed that sequences from 22q were indeed translocated to 4p+ and that reciprocally sequences from 4p were translocated to 22q-, demonstrating a balanced t(4;22)(p16;q11). On the basis of these results we presume that in this tumor a tumor-suppressor gene is deleted in the case of the 22q+ marker and that the t(4;22) disrupts the second allele of this gene. The latter translocation was mapped between D22S1 and D22S15, a distance of 1 cM on the linkage map of this chromosome. The area in which we have located the translocation is within the region where the gene predisposing to neurofibromatosis 2 has been mapped.
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PMID:A t(4;22) in a meningioma points to the localization of a putative tumor-suppressor gene. 201 1

Fresh tumor cells from pleural effusion of a patient with Hodgkin's disease were analyzed cytogenetically, immunologically and enzymocytochemically. They were characterized by the presence of alpha-naphthyl butyrate esterase activity, Fc gamma-receptor, HLA-DR antigen and No. 9 antigen which has been shown to be present in Hodgkin's cells and granulocytes, and the absence of definite T-, B- and myeloid cell markers. The karyotype analysis of these tumor cells revealed chromosome instability, but the clonality was confirmed by the many common abnormalities such as -4, -6, -10, -12, -13, -14, +21, del(X) (q22,q26), del(7) (q32q36), and +der(19)t(19;?). In addition, there were more duplicated tetraploid clones than near-diploid clones. The karyotype of the near-diploid clone was interpreted as: 48, X, del(X) (q22q26), -4, -6, -10, -12, -13, -14, +20, +21, +der(4)t(4;?) (p16;?), del(7) (q32q36), +der(19)t(19;?) (p13;?), +mar1, +mar2, +mar3. The karyotype abnormalities characteristic of lymphomas or leukemias were not found. These results indicate that the tumor cells are not of lymphoid or myeloid lineage. Further studies are needed to determine the cellular origin of the tumor cells of Hodgkin's disease.
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PMID:Karyotype aberrations and surface marker analyses of the tumor cells of Hodgkin's disease: a case report and review of literature. 243 93

To evaluate the role of p16 multiple tumor suppressor (MTS1) and p53 protein in human radiation-induced skin cancer, we examined the expression of p16 and p53 in eight cases using immunohistochemistry. An abnormal location of p16 expression in the cytoplasm was found in seven of eight cases, but the expression of p53 in nuclei was noted in only three of eight cases. These findings suggest that the inactivation of p16 might be related to its binding with another unknown oncoprotein in the cytoplasm and thus lead to carcinogenesis.
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PMID:Abnormal location of p16 protein and overexpression of p53 protein in human radiation-induced skin cancer. 747 71

P16 was originally discovered by its ability to interact with CDK4 and to specifically inhibit the catalytic activity of the CDK4/D1 kinase. Increased attention has focused on the p16 gene because of its location on chromosome 9p21, a region involved in chromosomal rearrangements in a large number of tumor types. The p16 gene is also mutated in a large number of tumor cell lines and primary tumor cells. Furthermore, linkage analysis studies suggest that the p16 gene is involved in familial melanoma susceptibility. Due to the oncogenic potential of mutations in this tumor suppressor, it is important to identify and characterize those mutations which alter p16 activity. We have performed a systematic analysis of melanoma associated p16 mutants and of mutants generated in charge to Ala mutagenesis. Using microtiter plate assays to measure both p16-cdk4 binding and cdk4/D1 kinase activity, we show here that the melanoma associated mutants are defective, as are some of the Ala mutants. These results support the idea that p16 mutation, via its deregulation of the cdk4/D1 pathway, is of biological significance in the development of melanoma. Furthermore, we have defined a region within the p16 molecule in which changes are likely to result in a defective protein.
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PMID:Biochemical and mutagenic analysis of the melanoma tumor suppressor gene product/p16. 747 20

Cyclins and cyclin-dependent kinases (cdk) have been identified as important regulators of cell replication. Molecular alteration in the cdk pathways appear to be important in cancer with some cyclins (eg cyclin D and E) proposed to be oncogenes and some inhibitors of cdk (eg p16) proposed to be tumor suppressor genes. In human breast carcinoma cell line MDA361 both cyclin D and E are overexpressed and cdk 4 and 6 are the predominate kinases which phosphorylate retinoblastoma protein and to a greater extent a novel 88 kDa protein. This 88 kDa protein was detected as a significant substrate in five of seven breast carcinoma cell lines, three lung carcinoma cell lines as well as in primary breast and lung epithelium. Normal human and murine T lymphocytes and established lymphoid cell lines are devoid of this protein and minimal amounts were detected in normal human fibroblast. In contrast to retinoblastoma protein, the 88 kDa protein appears to be more prevalent in the cytosolic than the nuclear subfraction. The phosphorylation of this 88 kDa protein by the G1 associated cdks suggest that this protein may represent another targeted substrate regulating the G1 phase of the cell cycle.
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PMID:A novel cytoplasmic substrate for cdk4 and cdk6 in normal and malignant epithelial derived cells. 747 27

Loci on chromosome 9p are frequently deleted in several malignant tumors, suggesting the presence of putative tumor suppressor genes. The MTS1/p16 and MTS2/p15 genes on 9p are considered to be candidates. Binding of p15 and p16 cell cycle-regulatory proteins to the cyclin dependent protein kinase CDK4 inhibits CDK4/cyclin D dependent phosphorylation of retinoblastoma protein. We analysed the DNAs from 37 gliomas of several grades of malignancy for allelic loss of chromosome 9p and aberrations of the MTS1/p16 and MTS2/p15 genes. We detected losses of one allele and homozygous deletions at loci, including those of the MTS1/p16 and MTS2/p15 genes, in 10 and 3 tumors, respectively. However, we did not detect any tumor-specific mutation in the two genes. The CDK4 gene was amplified in two malignant gliomas without homozygous deletion of the MTS1/p16 and MTS2/p15 genes and one malignant glioma with an allelic loss of the genes. These data suggest that aberrations of the genes coding for components of the cell cycle-regulatory system occurred in at least 15 of 37 gliomas.
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PMID:Homozygous deletion of the MTS1/p16 and MTS2/p15 genes and amplification of the CDK4 gene in glioma. 747 35

We used PCR amplification of tandem repeats to study the pattern of allelic loss in borderline and invasive ovarian epithelial tumors using 12 primer pairs to generate a detailed deletion map of chromosome 9p. In the invasive ovarian carcinomas, there were three regions displaying high frequency of loss of heterozygosity (LOH) ranging from 31-38%. In contrast, LOH was a rare event among the borderline ovarian tumors, with one region revealing a rate of 20% and the remaining regions only 0-8% LOH. Therefore, allelic loss does not seem to be important for the development of borderline ovarian tumors. We also examined p16 gene expression and mutations in ovarian cancer cell lines and invasive and borderline ovarian tumor tissues. Southern blot analysis revealed no losses of the p16 gene in either the invasive or borderline ovarian tumors. However, the ovarian carcinoma cell lines showed a 50% homozygous deletion rate. SSCP analysis detected a mobility shift in only one (borderline) tumor. Since the primary invasive ovarian tumors did not show any deletions or mutations, it appears that p16 does not play a role in the pathogenesis of these tumors.
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PMID:Detailed deletion mapping of chromosome 9p and p16 gene alterations in human borderline and invasive epithelial ovarian tumors. 747 44


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