5 methylcytosine/sarkom

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Cytotoxicity of platinum (II) dinuclear complexes with 1-alkylthymine ligands against mouse sarcoma 180 cells.

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We synthesized five platinum (II) dinuclear complexes containing 1-alkylated thymines. Two of the 1-alkylated thymine, 1-MeThy and 1-EtThy, complexes afforded good crystals. The X-ray structures of these complexes were determined. The 1-MeThy complexes has a head-to-head (H-H) arrangement, while the

A study on DNA hydroxymethylation in Kaposi sarcoma and cutaneous angiosarcoma.

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Hydroxymethylation studies on cutaneous vascular tumours, such as classic Kaposi sarcoma (CKS) and cutaneous angiosarcoma (CAS), have not been reported yet. We aimed to investigate the expression of 5-methylcytosine (5-mc), 5-hydroxymethylcytosine (5-hmc), ten-eleven translocation enzyme 2 (TET-2)

The rat XC sarcoma cell line: ribosomal RNA gene amplification and banded karyotype.

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Ribosomal RNA gene amplification has been demonstrated in the rat XC sarcoma cell line. Cells of this rat line have a fairly stable karyotype with several unusual features, which have been clarified by in situ hybridization, silver staining, and binding of antibodies to 5-methylcytosine. There are

Modification of avian sarcoma proviral DNA sequences in nonpermissive XC cells but not in permissive chicken cells.

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For the first time, we present evidence with restriction enzymes HpaII and MspI which indicates that the proviral DNA sequence of avian sarcoma virus is modified by methylation in a nonpermissive rat cell line but not in permissive chicken cells. Some of the endogenous viral sequences in the

Decrease of TET2 expression and increase of 5-hmC levels in myeloid sarcomas.

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BACKGROUND Myeloid sarcoma is a tumor mass that consists of myeloblasts or immature myeloid cells at an extramedullary site. Pathological diagnosis is very difficult based on morphology if systemic signs of disease are absent. The subtype of myeloid sarcoma is also minimally identifiable in the

[Structural characteristics of DNA from sarcoma 45].

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It is shown that thermodynamical parameters of thermal melting and the content of 5-methylcytosine for tumor DNA of sarcoma 45 differ from DNA in the norm. The reason of such difference is the presence of regions with changed DNA structure in sarcoma 45, which occurs apparently owing to

Ubiquitous and tenacious methylation of the CpG site in codon 248 of the p53 gene may explain its frequent appearance as a mutational hot spot in human cancer.

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Cytosine methylation at CpG dinucleotides is thought to cause more than one-third of all transition mutations responsible for human genetic diseases and cancer. We investigated the methylation status of the CpG dinucleotide at codon 248 in exon 7 of the p53 gene because this codon is a hot spot for

Effect of cytostatic proline rich polypeptide-1 on tumor suppressors of inflammation pathway signaling in chondrosarcoma.

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Cytokines produced in the tumour microenvironment exert an important role in cancer pathogenesis and in the inhibition of disease progression. Cancer of the cartilage is termed metastatic chondrosarcoma; however, the signaling events resulting in mesenchymal cell transformation to sarcoma have yet

[Comparative study of three antineoplastic alkylating agents on DNA].

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The influence of three alkylating anticancer preparations phosphamide, sarcolysine, cyclophosphane on content of the 5-methylcytosine and parameters of the melting DNA of the liver healthy animals and tumor sarcoma 45 was investigated. It was shown, that among the investigated preparations

Mutational Hotspot of TET2, IDH1, IDH2, SRSF2, SF3B1, KRAS, and NRAS from Human Systemic Mastocytosis Are Not Conserved in Canine Mast Cell Tumors.

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BACKGROUND Both canine cutaneous mast cell tumor (MCT) and human systemic mastocytosis (SM) are characterized by abnormal proliferation and accumulation of mast cells in tissues and, frequently, by the presence of activating mutations in the receptor tyrosine kinase V-Kit Hardy-Zuckerman 4 Feline

Tumors associated with p53 germline mutations: a synopsis of 91 families.

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Although inherited p53 mutations are present in all somatic cells, malignant transformation is limited to certain organs and target cells. The analysis of 475 tumors in 91 families with p53 germline mutations reported since 1990 shows that breast carcinomas are most frequent (24.0%), followed by

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