Genes, myc ; Humans ; Lymphoma ; genetics

No abstract available.
Genes, myc* ; Neuroblastoma* ; Polymerase Chain Reaction*

Multiple myeloma(MM) as one of the most common tumors of hmatologic system, is characterized by malignant proliferation of plasma cells, and the chemotherapy is the main therapeutic method. MM is an incurable disease because of drug-resistance of MM cells. Although the pathogenesis of MM remains unknown, the chromosome abnormalities exit in half of the patients, particularly the highly expressed gene C-MYC. Furthermore, plenty of clinical researches indicated a high expression level of C-MYC implied worse progression and/or poor prognosis of MM. Recently, the work exploiting the compounds targeting MYC has made substantial progress, even in the MM therapy. In this article, briefly the recent advances of the research on C-MYC proto-oncogene in multiple myeloma are reviewed.
Chromosome Aberrations ; Genes, myc ; Humans ; Multiple Myeloma ; Plasma Cells ; Proto-Oncogene Proteins c-myc

OBJECTIVE: The chemotherapeutic agent Cisplatin (cis-diammminedichloroplatinum (II)) is particularly effective against ovarian carcinoma, however, its clinical success is limited by recurrent drug resistant tumors. It is mandatory to reveal the mechanism of cisplatin resistance for the ovarian cancer treatment or prognosis. This study assessed the expression of p53, p16, PTEN, and c-myc genes with cisplatin treatment in human ovarian cancer cell lines; cisplatin-sensitive (A2780) and cisplatin-resistant (A2780/CP70) ovarian cancer cell line to elucidate the mechanism of cisplatin resistance. METHODS: Cytotoxic assay for cisplatin was performed in cisplatin-sensitive ovarian cancer cell line, A2780 and cisplatin-resistant ovarian cancer cell line, A2780/CP70. After cisplatin treatment, expression of p53, p16, PTEN, c-myc was analyzed by Western blot analysis. RESULTS: PTEN expression was significantly about 30% higher in A2780 than in A2780/CP70. p16 expression was defective in both cell lines. p53 and c-myc expression was no difference in cancer cell lines. After cisplatin treatment, the expression of p53, PTEN, c-myc genes increased 2-3 times in both cell lines. CONCLUSION: Relatively lower expression of PTEN was detected in A2780/CP70 suggesting that PTEN expression might play a role in the development of cisplatin resistance in ovarian cancer cell line, A2780/ CP70.
Blotting, Western ; Cell Line* ; Cisplatin* ; Genes, myc* ; Humans ; Ovarian Neoplasms* ; Prognosis

OBJECTIVE: The aim of this investigation was to analyze the association between a single nucleotide polymorphism (SNP) in L-myc gene (T3109G) and ovarian cancer risk or prognosis in Korean women. METHODS: The blood samples of 98 ovarian cancer patients and 332 non-cancer control subjects who managed at Seoul National University Hospital from 1999 to 2002 were collected. Polymorphism in L-myc (T3109G) was determined using TaqMan method. Allele frequency and genotype distribution in the ovarian cancer group were compared with those of the control group to determine whether this polymorphism elevates the susceptibility of Korean women to ovarian cancer. The relationship between this SNP and cancer invasiveness or prognosis were also evaluated by collating clinicopathologic data of those in the cancer group, such as surgical stage, stromal invasion, histologic type, and survival. RESULTS: In the ovarian cancer group, the allele frequency of G was 51.0%, in the control group 48.5%, showing no significant difference (p=0.569). Similarly the genotypes with TG or GG showed no increased risk for ovarian cancer susceptibility compared with TT genotype. A subgroup analysis of the clinicopathologic parameters in cancer group also showed no significant difference suggesting the lack of an association between SNP of the L-myc and ovarian cancer invasiveness and survival. CONCLUSION: This study shows that Korean women with specific polymorphism in L-myc are neither more susceptible to develop ovarian cancer nor more vulnerable for cancer progression.
Female ; Gene Frequency ; Genes, myc ; Genotype ; Humans ; Ovarian Neoplasms* ; Polymorphism, Single Nucleotide* ; Prognosis* ; Seoul

OBJECTIVETo investigate the effect and possible mechanism of bromo-domain inhibitors (JQ1) on proliferation inhibition and inducing apoptosis of acute T lymphocyte leukemia cell line (Jurkat) .

METHODSJurkat cell line was treated by JQ1 at different concentrations. MTT was used to detect the cell proliferation inhibition rate. The flow cytometry with AnnexinV-FITC/PI fluorescence staining was used to detect the changes of apoptosis rate, and real-time fluorescent quantitative PCR was used to detect c-Myc/Notch1 gene expression levels.

RESULTSWith the increasing of drug concentration and prolonging of time, the inhibitory rate of Jurkat cell growth was enhanced in time-dose dependent manner; Jurkat cells was treated by 0.8, 1.6, and 4 µ mol/LJQ1 for 48 h and 72 h, the cell apoptosis rate was enhanced with the increase of drug concentration and prolonging of time, and the difference was statistically different in comparison with the control group(P<0.05); PCR detection indicated that Notch1 and c-Myc mRNA expression was reduced in 48 h after JQ1 treatment, which was statistically different from the control group,(P<0.05) .

CONCLUSIONJQ1 can effectively inhibit the growth of Jurkat cell line, and potentially induce apoptosis through Notch1 and c-Myc gene. Hence JQ1 may be one of new methods used to treat T-ALL.

Apoptosis ; Azepines ; Cell Proliferation ; Flow Cytometry ; Genes, myc ; Humans ; Jurkat Cells ; Nuclear Proteins ; Transcription Factors ; Triazoles

Pterygium, a disease of unknown origin and pathogennesis, is a chronic condition characterized by the encroachment of triangular portion of the bulbar conjunctiva onto the cornea. We have studied the expression of extracellular matrix genes and oncogenes in cultured pterygium using Northernm dot, and slot blot hybridizations. Northern hybridization with total RNA isolated from passaged (4-8 passages) cultures demonstrated expression of genes for alpha1(I) and alpha1(III) procollagen, fibronectin, and c-Ha-ras, but no expression of gene for c-myc was observed. The pterygium exhibited significantly increased expression of alpha1(I) and alphal(III) procollagen genes when compared with normal control cells(p<0.01). And We observed there were no differences between pterygium and normal control cells in the expression of genes for fibronectin and c-Ha-ras. According to these results we thought that the causes of pterygium may be related to the increased expression of alpha1(I) and alphal(III) procollagen genes but may not be related to c-Ha-ras, c-myc, and fibronectin genes.
Conjunctiva ; Cornea ; Extracellular Matrix* ; Fibroblasts* ; Fibronectins ; Genes, myc* ; Oncogenes ; Procollagen ; Pterygium ; RNA

The amplification of c-myc oncogene was evaluated in 42 cases of ovarian carcinomas to correlate with clinical parameters. Using oligonucleotide primers, sequences from the c-myc exon-3 gene and from a control gene, tissue plasminogen activator (tPA), were amplified simultaneously by polymerase chain reaction (PCR). After the products of differential PCR (d-PCR) were electrophoresed, slot blot hybridization was performed, and hybridized with P32 dATP-labeled myc and tPA oligonucleotide probes and then autoradiographed. The signal intensities of the two products were quantitated by densitometry and the ratios of two products (c-myc/tPA) were measured. The ovarian carcinomas showed significantly increased amplification of c-myc oncogene Oligonucleoti compared to normal control group (p<0.05). 15 of 42 cases (35.7%) showed various degrees of the MYC gene amplification up to 27 folds in various histologic types of ovarian carcinomas. No significant differences of the MYC gene amplification according to histologic subtypes, tumor action) grades and clinical stages of ovarian carcinomas were present.
Densitometry ; DNA Primers ; Genes, myc ; Oligonucleotide Probes ; Oncogenes* ; Polymerase Chain Reaction* ; Tissue Plasminogen Activator

OBJECTIVE: To carry out combined genetic analysis on two patients suspected for Burkitt lymphoma to facilitate their diagnosis and treatment. METHODS: G banded karyotyping and interphase and metaphase fluorescence in situ hybridization (FISH) were used to detect the specific sites of chromosomes by using separate and fusion probes. RESULTS: The separate probe showed no presence of MYC gene abnormality, while fusion probe confirmed the IGH::MYC translocation in the samples. Combined with the clinical features and pathological characteristics, the two patients were finally diagnosed with Burkitt lymphoma, which was confirmed by targeted capture next generation sequencing. CONCLUSION The separate probe for the MYC gene has some shortcomings and should be used together with dual fusion probe to improve the accuracy of diagnosis.
Humans ; Burkitt Lymphoma/pathology* ; In Situ Hybridization, Fluorescence ; Genes, myc ; Translocation, Genetic ; Karyotyping

OBJECTIVE: Comparative genomic hybridization was performed to evaluate DNA sequence copy number changes in human ovarian carcinomas from paraffin-embedded tissue blocks. PATIENTS AND METHODS: DNA from 20 cases of primary ovarian carcinomas underwent comparative genomic hybridization to evaluate the extent of genetic gains or losses in a test sample. RESULTS: In thirteen cases of 20 samples, varying degree of genetic imbalances was observed. Of the remaining 7 cases, two revealed normal, five failed to yield a result. Most common genetic imbalances are 8q22.2-q24 site amplification and 12p site amplification, where c-myc gene and k-ras gene respectively are included. Second most common site of genetic imbalance is 7p21-pter site deletion. CONCLUSION: Our results have shown many chromosomal alterations in human ovarian carcinomas, and these sites are known previously as oncogene or tumor-suppression gene, and some sites are not known specific cancer associated sites. Our data can be useful for screening chromosomal changes and molecular mechanism of human ovarian carcinogenesis.
Base Sequence ; Carcinogenesis ; Comparative Genomic Hybridization* ; DNA ; Genes, myc ; Genes, ras ; Humans ; Mass Screening ; Oncogenes ; Ovarian Neoplasms