N-Myc oncogene plays an important role in the process of hematopoietic cell proliferation and differentiation in embryos. Once the body suffers from hematologic malignancies, the expression of N-Myc would increase and significantly associate with disease progression. In this article the structure of N-Myc, the regulatory mechanism in the different hematopoietic lineages, the interaction in each signal pathways, the transgenic animal model of overexpression, and intervention by drugs are reviewed.
Hematologic Neoplasms ; Hematopoiesis ; Humans ; Proto-Oncogene Proteins c-myc ; metabolism

The Proto-oncogene c-myc and c-myb has been shown to be crucial in the development of the hematopoietic system. The changes in the expression of c-myc are concerned the cell proliferation and differentiation, the expression products of which play an important regulatory role in cell growth, differentiation or malignant transformation. The c-myb involves in transcription and affects cell proliferation, differentiation, apoptosis. More recently, the researches on proto-oncogene c-myc, c-myb in hematopoietic regulation have gradually increased along with development of molecular biology, molecular immunology and cell biology. Scientists point out that the directive differentiation of erythroid and megakaryocytic progenitors, and platelet abnormalities all relate to the level of their expressions. The most common thrombocytopathy includes thrombocytopenia, thrombocytosis and so on. The etiology and the mechanism of these diseases are unknown. This article reviews the structure, function and the expression of c-myc and c-myb in platelet diseases and their significance.
Blood Platelet Disorders ; genetics ; metabolism ; Humans ; Proto-Oncogene Proteins c-myb ; genetics ; metabolism ; Proto-Oncogene Proteins c-myc ; genetics ; metabolism

OBJECTIVETo investigate the correlation between the expression of key proto-oncogenes playing major roles in tumorigenic process and abnormal sarring.

METHODSImmunohistochemical technique was performed to detect the expressions of c-myc, c-fos and ras p21 proteins on hypertrophic scars, keloids and normal skin. Image analysis was used to compare their quantitative difference of expression.

RESULTSC-myc and c-fos expressions on the nucleus of fibroblasts of hypertrophic and keloid scars were significantly higher than normal skin controls, and there was no difference between the two lesions. Ras p21 expression was not detected on the fibroblasts of hypertrophic and keloid scars.

CONCLUSION1. c-myc and c-fos oncogenes are activated on hypertrophic and keloid scars, which may contribute to proliferation and differentiation of fibroblasts, synthesis and degradation of collagen and regulation of cytokines and induce abnormal scarring, the mechanisms of their effects remain to be further studied. 2. Ras gene may not mutate or its mutations may not play a major role in the process of abnormal scarring. 3. Only part of proto-oncogenes moderately expressed on abnormal scars. The expression of multiple oncogenes does not coexist in abnormal scars may be the cause of their less chances to induce malignant transformation.

Cicatrix, Hypertrophic ; metabolism ; Humans ; Immunohistochemistry ; Proto-Oncogene Proteins c-fos ; analysis ; Proto-Oncogene Proteins c-myc ; analysis ; Proto-Oncogene Proteins p21(ras) ; analysis ; Proto-Oncogenes

OBJECTIVETo study the oncogene transcriptor c-myc, stimulatory protein 1 (SP1) expression in ameloblastoma (AB) and their relation with telomerase reverse transcripase (hTERT), and to investigate the clinical biological characteristics of AB.

METHODSThe expression was observed in AB by in situ hybridization and SP method.

RESULTSThe positive rates of c-myc mRNA, hTERT mRNA and SP1 protein were 81.5% (44/54), 94.4% (51/54) and 83.3% (45/54), respectively. Their positive rates increased as AB recurred and transformed malignantly. A strong correlation was found between hTERT and c-myc, hTERT and SP1 (rs = 0.853, P < 0.001; rs = 0.900, P < 0.001).

CONCLUSIONActivity of telomerase plays an important role in the tumorigenesis development of AB. Increasing of hTERT expression may be related to c-myc and SP1. The expression of these three parameters has a significant correlation with the clinical biological characteristics of AB.

Ameloblastoma ; metabolism ; Humans ; Proto-Oncogene Proteins c-myc ; metabolism ; Sp1 Transcription Factor ; metabolism ; Telomerase ; metabolism

Cell Transformation, Neoplastic ; metabolism ; Humans ; Proto-Oncogene Proteins c-myc ; metabolism

OBJECTIVETo study the effects of polychlorinated biphenyl (PCB) on the phenotype of the testis tissue and the testis tissue and the expression c-fos, c-Myc and beta-catenin in the rat testis.

METHODSForty-five Wistar male rats were divided into a control and three perimental groups, the former fed normally, and the latter with PCB at 0.1, 1 and 10 mg/kg respectively for 90 days. Then the effects of PCB on the phenotype of the testis tissue and the expressions of c-fos, c-Myc and p-catenin were determined by histopathology and immunohistochemistry.

RESULTSHistopathological examinations revealed testis edema, damage of the mesenchymal phenotype, morphological changes of the contorted seminiferous tubules, absence of stromal cells, spermiocytes and prespermatids, and decreased number of sperm. The expressions of c-fos and c-Myc were significantly higher in the 1 and 10 mg/kg PCB groups than in the control and 0.1 mg/kg PCB groups (P < 0.01). The expression of beta-catenin was downregulated in the 0.1 mg/kg PCB group, with significant differences from the other groups (P < 0.01), but it was higher in the 1 mg/kg PCB than in the control and 10 mg/kg PCB groups (P < 0.01).

CONCLUSIONPCB causes changes in the phenotype of the testis tissue, and the abnormal expressions of c-fos, c-Myc and beta-catenin are closely related to the PCB-induced testis injury.

Animals ; Male ; Polychlorinated Biphenyls ; adverse effects ; Proto-Oncogene Proteins c-fos ; metabolism ; Proto-Oncogene Proteins c-myc ; metabolism ; Rats ; Rats, Wistar ; Testis ; metabolism ; pathology ; beta Catenin ; metabolism

OBJECTIVE: To analyze the prognostic value of BCL-2, BCL-6 and MYC in patients with diffuse large B cell lymphoma (DLBCL). METHODS: One hundred and sixty three cases of DLBCL in our hospital from March 2012 to March 2015 were selected. The specimens of lymphoma tissue of patients were collected. The expression of BCL-2, BCL-6 and MYC was detected by immunohistochemical method. The fusion of IGH/BCL-2, the gene breakage of BCL-6 and MYC were detected by interphase fluorescence in situ hybridization. The correlation of the expression levels of BCL-2, BCL-6 and MYC with the clinicopathological features and prognosis in the patients with DLBCL was further analyzed. RESULTS: MYC, BCL-2 and BCL-6 showed pale brown or reddish brown positive signals, among them MYC mainly positively expressed on the cell membrane, and BCL-2 mainly expressed on the cytoplasm and local cell membrane, and BCL-6 mainly expressed in the nucleus. The expression level of BCL-2 in ECOG physical status score 2 was higher than that in patients with ＜2 scores, and the expression level of BCL-2 in CD5 and germinal center B-cell-like (GCB) was significantly higher than that in patients with non-GCB (P＜0.05), and the international prognostic index (IPI) for 3-5 scores at the MYC expression level was significantly higher than that of the 0-2 score (P＜0.05); the expression level of BCL-6 in immune subtype CD5 and GCB was significantly lower than that in non-GCB (P＜0.05). The results of Cox multivariate analysis showed that the expression level of BCL-2, BCL-6 and MYC significant correlate with the overall survival and progression-free survival (P＜0.05) of the patients with DLBCL. CONCLUSION BCL-2, BCL-6 and MYC as important molecular markers are of high value for evaluating the prognosis of patients with DLBCL.
Humans ; In Situ Hybridization, Fluorescence ; Lymphoma, Large B-Cell, Diffuse ; Prognosis ; Proto-Oncogene Proteins c-bcl-2 ; metabolism ; Proto-Oncogene Proteins c-bcl-6 ; metabolism ; Proto-Oncogene Proteins c-myc ; metabolism

Animals ; Gene Amplification ; Genes, myc ; Humans ; Lymphoma, B-Cell ; genetics ; metabolism ; pathology ; Mutagenesis, Insertional ; Proto-Oncogene Proteins c-myc ; metabolism ; Translocation, Genetic

OBJECTIVETo study the clinical significance of P53, C-MYC and BCL-6 abnormality in the patients with diffuse large B cell lymphoma (DLBCL).

METHODSFrom July 2011 to January 2013, 80 patients with DLBCL were admitted in our hospital and were chosen as study objects, their clinical data were collected. The abnormality of P53, C-MYC and BCL-6 was examined by using I-FISH for all the patients. The correlation of abnormality of P53, C-MYC and BCL-6 with clinical staging, curative efficacy and prognosis of the patients were analyzed.

RESULTSOut of 80 patients 27 patients (33.75%) had P53 deletion, 24 patients (30.00%) had C-MYC rearrangement/amplification, and 46 patients (57.50%) had BCL-6 rearrangement. The P53 deletion, C-MYC rearrangement/amplification and BCL-6 rearrangement significantly correlated with staging, curative effect and prognosis of the patients (P < 0.05).

CONCLUSIONThe curative efficacy and prognosis of the DLBCL patients with abnormality of P53, C-MYC and BCL-6 have been confirmed to be unsatisfactory.

DNA-Binding Proteins ; genetics ; metabolism ; Humans ; In Situ Hybridization, Fluorescence ; Lymphoma, Large B-Cell, Diffuse ; diagnosis ; genetics ; metabolism ; Prognosis ; Proto-Oncogene Proteins c-bcl-6 ; Proto-Oncogene Proteins c-myc ; genetics ; metabolism ; Tumor Suppressor Protein p53 ; genetics ; metabolism

This study was aimed to investigate the effect of SU11248 on proliferation and apoptosis of leukemia cell line K562 in vitro and its mechanism. The inhibitory effect of 3.2 µg/ml SU11248 on K562 proliferation was tested by MTT assay. The ability of SU11248 to induce apoptosis of K562 cells was examined by TUNEL and DNA ladder. The expression of C-MYC, hTERT and BCR-ABL mRNA in K562 cells was detected by RT-PCR. The protein expression of Akt and p-Akt in K562 cells was detected by Western blot. The results showed that the proliferation of K562 cells was obviously inhibited by 3.2 µg/ml SU11248 in a time-dependent manner. SU11248 could induce K562 cells apoptosis in dose-and time-dependent manner. The mRNA expression of C-MYC, hTERT and BCR-ABL was reduced significantly by SU11248 in a time-dependent manner (P < 0.05). Western blot detection showed that the expression of p-Akt protein in K562 cells decreased in dose-and time-dependent manner after SU11248 treatment, but the expression of Akt was not significantly changed. It is concluded that SU11248 can inhibit the growth of K562 cells efficiently through inducing apoptosis, its mechanism may be closely relate with the expression down-regulation of C-MYC, hTERT, BCR-ABL and the inhibition of Akt phosphorylation.
Apoptosis ; drug effects ; Cell Proliferation ; drug effects ; Fusion Proteins, bcr-abl ; metabolism ; Humans ; Indoles ; pharmacology ; K562 Cells ; Proto-Oncogene Proteins c-akt ; metabolism ; Proto-Oncogene Proteins c-myc ; metabolism ; Pyrroles ; pharmacology ; RNA, Messenger ; genetics ; Telomerase ; metabolism