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MYC Gene (myc + gene)
Selected AbstractsLevel of MYC overexpression in pediatric Burkitt's lymphoma is strongly dependent on genomic breakpoint location within the MYC locusGENES, CHROMOSOMES AND CANCER, Issue 2 2004Monika Wilda Increased transcriptional activity of the MYC gene is a characteristic feature of Burkitt's lymphoma. Aberrant MYC expression is caused by (1) chromosomal translocation to one of the loci carrying an immunoglobulin gene, (2) mutation within the translocated allele, (3) loss of the block to transcription elongation, or (4) promoter shift. To investigate the influence of breakpoint locations within the MYC gene on MYC transcript levels, we determined both the precise genomic MYC/IGH breakpoints and the amount of MYC mRNA in 25 samples of pediatric Burkitt's lymphoma with translocation t(8;14)(q24;q32). Patients with breakpoints that were 5, from MYC exon 1 had significantly lower expression of MYC than did patients who had a breakpoint within exon 1 or intron 1 (P < 0.05 and 0.005, respectively). The highest mRNA level of MYC (1,006 copies per 100 copies ABL1) was detected in patients with loss of the first exon and transcription initiation from a cryptic P3 promoter within the first intron of the MYC gene. In contrast, there was no obvious correlation between breakpoint locations within the IgH locus and the amount of MYC mRNA. © 2004 Wiley-Liss, Inc. [source] Genomic imbalances in CML blast crisis: 8q24.12,q24.13 Segment identified as a common region of over-representationGENES, CHROMOSOMES AND CANCER, Issue 4 2003Susan M. Gribble The acute phase of chronic myeloid leukemia (CML) is accompanied by secondary chromosomal changes. The additional changes have a non-random pattern; however, highly abnormal (marker) chromosomes are reported in some 20% of abnormal karyotypes. These marker chromosomes have proved to be beyond the resolution of conventional G-banding analysis. We used molecular cytogenetic techniques to determine the structure of complex chromosome markers in 10 CML-derived cell lines after our investigations of CML patients in blast crisis. Multicolor fluorescence in situ hybridization identified a multitude of structural chromosome aberrations. In addition, genomic gains identified by comparative genomic hybridization (CGH) were mapped to highly complex marker chromosomes in more than one cell line. The most common genomic loss detected by CGH affected chromosome 9, whereas the most common genomic gains affected, in order of frequency, the sequences of 8q, 6, and 13q. The smallest discrete amplification on 8q was identified in cell line MEG-01. This amplicon contains sequences represented by the marker D8S263/RMC08P029 but did not contain the proximal MYC gene or a more distal marker, D8S256/RMC08P025. We determined the size of the amplicon to be less than the chromosome segment 8q24.12,q24.13. The use of region- and locus-specific probes to analyze the organization of highly complex marker structures aided the identification of preferentially amplified genomic regions. The resultant amplifications could harbor gene(s) driving disease progression. © 2003 Wiley-Liss, Inc. [source] Burkitt lymphoma versus diffuse large B-cell lymphoma: a practical approachHEMATOLOGICAL ONCOLOGY, Issue 4 2009Cristiana Bellan Abstract Burkitt Lymphoma (BL) is listed in the World Health Organization (WHO) classification of lymphoid tumours as an "aggressive B-cell non-Hodgkin's lymphoma", characterized by a high degree of proliferation of the malignant cells and deregulation of the c- MYC gene. The main diagnostic challenge in BL is to distinguish it from diffuse large B-cell lymphoma (DLBCL). While in children BL and DLBCL types probably do not differ clinically, and the differential diagnosis between BL and DLBCL may theoretically appear clear-cut, in adults daily practice shows the existence of cases that have morphological features, immunophenotypic and cytogenetics intermediate between DLBCL and BL, and cannot be classified with certainty in these categories. Distinguishing between BL and DLBCL is critical, as the two diseases require different management. This review summarizes the current practical approach, including the use of a large panel of antibodies, and cytogenetic and molecular diagnostic techniques, to distinguish between BL, DLBCL and the provisional category of "B-cell lymphoma, unclassificable, with features intermediate between diffuse large B-cell lymphoma and Burkitt lymphoma", now listed in the updated WHO classification. Copyright © 2009 John Wiley & Sons, Ltd. [source] Chromosome-mediated alterations of the MYC gene in human cancerJOURNAL OF CELLULAR AND MOLECULAR MEDICINE, Issue 2 2002N. C. Popescu Abstract The step-wise accumulation of genetic and epigenetic alterations in cancer development includes chromosome rearrangements and viral integration-mediated genetic alterations that frequently involve proto-oncogenes. Protooncogenes deregulation lead to unlimited, self-sufficient cell growth and ultimately generates invasive and destructive tumors. C-MYC gene, the cellular homologue of the avian myelocitic leukemia virus, is implicated in a large number of human solid tumors, leukemias and lymphomas as well as in a variety of animal neoplasias. Deregulated MYC expression is a common denominator in cancer. Chromosomal rearrangements and integration of oncogenic viruses frequently target MYC locus, causing structural or functional alterations of the gene. In this article, we illustrate how genomic rearrangements and viruses integration affect MYC locus in certain human lymphomas and solid tumors. [source] MYC gene amplification reveals clinical association with head and neck squamous cell carcinoma in Indian patientsJOURNAL OF ORAL PATHOLOGY & MEDICINE, Issue 10 2009N. Bhattacharya Background:, Amplification of the MYC gene is reported to be associated with the development of head and neck squamous cell carcinoma (HNSCC). This study is focused to analyze the correlation between MYC gene amplification and various clinicopathological features and outcome in a cohort of 49 dysplastic and 187 primary head and neck lesions. Methods:,MYC gene amplification was assessed by differential polymerase chain reaction using primer sets from the MYC gene as target locus and DRD2 gene as the control locus. Result:, The MYC gene amplification was detected in a total of 23.7% (56/236) head and neck lesions comprising 14.2% (7/49) dysplastic lesions and 26% (49/187) HNSCC samples. The clinicopathological association study between MYC gene amplification with the different clinical parameters like sex, tumor stage, tumor differentiation, lymph node status, tobacco habit and HPV 16/18 status determined significant association of MYC amplification with tumor progression (P = 0.009). Kaplan Meier analysis revealed MYC gene has no prognostic significance on survival in HNSCC. Conclusion: , In conclusion, our results suggest that MYC gene amplification is associated with tumor progression in HNSCC. [source] The effect of dichloroacetic acid and trichloroacetic acid on DNA methylation and cell proliferation in B6C3F1 miceJOURNAL OF BIOCHEMICAL AND MOLECULAR TOXICOLOGY, Issue 2 2001Rongrong Ge Abstract The chlorine disinfection by-products, dichloroacetic acid (DCA) and trichloroacetic acid (TCA), are carcinogenic in mouse liver. We have previously reported that DCA and TCA induced DNA hypomethylation in mouse liver. In the present study, we determined the temporal association for DNA hypomethylation and cell proliferation. Female B6C3F1 mice were administered daily doses of 500 mg/kg DCA or TCA by gavage and sacrificed at 24, 36, 48, 72, and 96 hours after the first dose. The proliferating cell nuclear antigen-labeling index in the liver was increased at 72 and 96 hours by both DCA and TCA, that is, at 72 hours the index was 1.00 ± 0.21, 0.51 ± 0.11, and 0.095 ± 0.016 for DCA, TCA, and the vehicle control, respectively. The mitotic index was also significantly increased at 96 hours. The promoter region for the c- myc gene was hypomethylated only at 72 and 96 hours and not at the earlier sacrifices. Similarly, the methylation of the c- myc gene in the kidney and urinary bladder was decreased only at 72 and 96 hours. In summary, enhancement of cell proliferation and decreased methylation of the c- myc gene were first observed simultaneously at 72 hours after the start of exposure. Thus, the results support the hypothesis that DCA and TCA induce DNA hypomethylation by inducing DNA replication and preventing the methylation of the newly synthesized strands of DNA. © 2001 John Wiley & Sons, Inc. J Biochem Mol Toxicol 15:100,106, 2001 [source] Clades within the ‘higher land birds’, evaluated by nuclear DNA sequencesJOURNAL OF ZOOLOGICAL SYSTEMATICS AND EVOLUTIONARY RESEARCH, Issue 1-2 2001Johansson In this study we investigated the phylogenetic relationships within the ‘higher land birds’ by parsimony analysis of nucleotide DNA sequences obtained from the two nuclear, protein-coding genes, c- myc and RAG-1. Nuclear genes have not previously been used to address this phylogenetic question. The results include high jackknife support for a monophyletic Apodiformes (including the Trochilidae). This arrangement was further supported by the observation of an insertion of four amino acids in the c- myc gene in all apodiform taxa. Monophyly was also inferred for each of the two piciform groups Galbulae and Pici. Within Pici, the Capitonidae was found to be paraphyletic, with the New World barbets more closely related to the Ramphastidae than to the Old World barbets. Another clade with high jackknife support consists of the Upupidae, Phoeniculidae and Bucerotidae. The families Momotidae and Todidae, and Coraciidae and Brachypteraciidae, respectively, also form well supported monophyletic clades. The results are inconclusive regarding the monophyly of the orders Coraciiformes and Piciformes, respectively. Die von nuklearen DNA-Sequenzen abgeleiten Kladen bei den ‘Höheren and vögeln’ Es wurde eine Studie über die phylogenetischen Beziehungen bei den ‘höheren Landvögeln’ mit Hilfe einer Parsimonie-Analyse von DNA-Kernsequenzen zweier proteincodierender Genen, c-myc und RAG-1, durchgeführt. Kerngene wurden bisher noch nicht für die Untersuchung dieser phylogentischen Frage eingesetzt. Die Ergebnisse unterstützen mit hohen Jackknife-Werten eine Monophylie der Apodiformes (einschließlich der Trochilidae). Eine solche Einordnung wird auch durch die Beobachtung einer Einfüngung von vier Aminosäuren im c-myc -Gen bei allen apodiformen Taxa unterstützt. Eine Monophylie konnte ebenso für die beiden picidiformen Gruppen, Glabulae und Pici, bestätigt werden. Bei den Pici erweisen sich die Capitonidae als paraphyletisch, wobei die Bartvögel der NeuenWelt näher mit den Ramphistidae verwandt sind als mit den Bartvögeln der Alten Welt. Eine weitere Klade, die durch hohe Jackknife-Werte unterstützt wird, besteht aus den Upupidae, Phoeniculidae und Bucerotidae. Die Familien Momotidae und Todidae bzw. Coraciidae und Brachypteraciidae bilden ebenfalls gut unterstützte Kladen. Über die Monophylie der Ordnungen Coraciiformes und Piciformes können die Ergebnisse jedoch keine Entscheidung herbeiführen. [source] | ||||||||||