OBJECTIVETo investigate pathologic and differential diagnostic features of pediatric Burkitt lymphoma (BL).

METHODSA total of 20 cases of pediatric BL were retrospectively reviewed for their clinical and pathologic profiles. Bone marrow aspiration specimens were available in all cases and bone marrow biopsies were available for immunohistochemical study in 18 cases. Flow cytometry study was available in 16 cases. MYC translocation by FISH method was performed in 11 cases.

RESULTSAtypical lymphocytes with cytoplasmic vacuoles were found in bone marrow smears in all 20 cases and peripheral blood films in all 19 available cases. The bone marrow biopsies showed infiltration by uniform medium-sized atypical lymphocytes with multiple small nucleoli but without the starry-sky pattern in all 18 cases. Immunohistochemistry showed the following results in all 18 cases: positive for CD20, PAX-5, CD10, CD34 and TdT, but negative for bcl-2 and CD3 with Ki-67 > 95%.Flow cytometry showed CD19+CD20+CD10+FMC7+CD22+TdT-CD3- in 16 cases, including κ+ in 8 cases, λ+ in 7 cases, and κ-λ- in 1 case. MYC gene rearrangement by FISH was observed in 10 of the 11 cases.

CONCLUSIONSThe histopathology of BL is distinct, including atypical lymphocytes with cytoplasmic vacuoles in bone marrow aspirate, lack of starry-sky patternin bone marrow biopsy. Generally, the diagnosis should be made with a combined immunophenotype and FISH approach. Pediatric BL must be distinguished from DLBCL and B-cell lymphoma, unclassifiable, which has intermediate features between DLBCL and Burkitt lymphoma.

Biopsy ; Bone Marrow ; pathology ; Burkitt Lymphoma ; genetics ; pathology ; Child ; Diagnosis, Differential ; Female ; Flow Cytometry ; Genes, myc ; Humans ; Immunohistochemistry ; Immunophenotyping ; In Situ Hybridization, Fluorescence ; Lymphocytes ; pathology ; Lymphoma, B-Cell ; pathology ; Lymphoma, Large B-Cell, Diffuse ; pathology ; Male ; Retrospective Studies ; Translocation, Genetic

OBJECTIVETo investigate the effects of eukaryotic translation initiation factor 5A2 (EIF5A2) down-regulation by small interfering RNA (siRNA) on aggressiveness of human gastric cancer cell and its potential mechanisms.

METHODSThe expressions of EIF5A2 in human gastric cancer cell lines (MKN28 and HGC27) and immortalized gastric mucosal epithelial cells (GES-1) were measured by real-time quantitative reverse transcription polymerase chain reaction (qRT-PCR) and Western blotting. EIF5A2 gene in MKN28 cells was silenced by RNA interference and the inhibitory effect was evaluated by both qRT-PCR and Western blotting. Cell proliferation was assessed by CCK-8 assay. Cell migration and invasion were assessed by Transwell assay. The possible downstream targets of EIF5A2, such as CyclinD1, CyclinD3, matrix metallopeptidase-9 (MMP-9), E-cadherin, vimintin, C-myc, and metastasis-associated protein 1 (MTA1) expression levels, were examined by Western blotting.

RESULTSHigh expressions of EIF5A2 were found in MKN28 cells and human gastric adenocarcinoma tissues. Both EIF5A2 mRNA and protein expression in MKN28 cells were significantly down-regulated by siRNA#1 and siRNA#2, especially siRNA#1. Knockdown of EIF5A2 caused an apparent suppression of MKN28 cell proliferation (all P<0.01), migration (P<0.001), and invasion (P<0.001). After the knockdown of EIF5A2 in MKN28 cells, E-cadherin levels were upregulated, whereas vimentin, Cyclin D1, Cyclin D3, C-myc and MTA1 levels were downregulated.

CONCLUSIONKnockdown of EIF5A2 may inhibit MKN28 cell proliferation by downregulating the CyclinD1 and CyclinD3 and suppressing the cell migration and invasion by inhibiting MTA1, C-myc and epithelial-mesenchymal transition.

Cell Line, Tumor ; Cell Movement ; Cell Proliferation ; Cyclin D1 ; metabolism ; Cyclin D3 ; metabolism ; Down-Regulation ; Gene Expression Regulation, Neoplastic ; Genes, myc ; Histone Deacetylases ; metabolism ; Humans ; Peptide Initiation Factors ; genetics ; RNA Interference ; RNA, Small Interfering ; genetics ; RNA-Binding Proteins ; genetics ; Repressor Proteins ; metabolism ; Stomach Neoplasms ; pathology

Genes, myc ; Humans ; Lymphoma ; genetics

OBJECTIVETo investigate c-myc and CCNE2 gene amplifications and their relationship in breast cancer.

METHODSSixty-six infiltrating ductal breast carcinomas with foci of ductal carcinoma in situ components collected from January 2005 to December 2007 were selected for tissue microarray and quantitative multi-gene FISH for c-myc and CCNE2 gene amplification, and the relationship with the clinicopathologic features was analyzed.

RESULTSOf the 66 cases, 18 (27.3%) showed c-myc amplification and 23 (34.8%) showed CCNE2 amplification. A strong correlation was found between c-myc and CCNE2 amplification (P < 0.01). The breast cancers showing c-myc and CCNE2 amplifications were all aneuploidy, and were HER2 positive (P < 0.05). Tumors with c-myc amplification also showed higher Ki-67 index (P < 0.05).

CONCLUSIONSC-myc and CCNE2 amplifications are common events in breast cancer, and they often coexist. C-myc and CCNE2 genes may play critical roles in the pathogenesis and development of breast cancer through unique and overlapping signaling pathways.

Aneuploidy ; Breast Neoplasms ; genetics ; Carcinoma in Situ ; genetics ; Carcinoma, Ductal, Breast ; genetics ; Carcinoma, Intraductal, Noninfiltrating ; genetics ; Cyclins ; genetics ; Female ; Gene Amplification ; Genes, myc ; Humans ; In Situ Hybridization, Fluorescence ; methods ; Tissue Array Analysis

Adult ; Aged ; Female ; Genes, myc ; genetics ; Humans ; In Situ Hybridization, Fluorescence ; Lymphoma, Large B-Cell, Diffuse ; diagnosis ; genetics ; Male ; Middle Aged ; Retrospective Studies ; Young Adult

OBJECTIVETo study the effect of astragalus injection on U937 leukemia cells proliferation and apoptosis and relevant molecular mechanisms.

METHODSLeukemia cell line U937 cells were treated with different concentrations of astragalus (62.5, 125, 250, 500, 1 000 μg/mL). The U937 cells without astragalus treatment were used as the control group. The ability of cell proliferation was measured by MTT method. Flow cytometry was used to explore cell apoptosis. The cell morphology changes were observed under a fluorescent microscope by dyeing Hoechst33258. mRNA expression of c-myc and p27 in U937 cells which was exposed in 1 000 μg/mL astragalus after 0, 12, 24 and 48 hours was detected by reverse transcription polymerase chain reaction (RT-PCR).

RESULTSVarious concentrations of astragalus injection inhibited U937 cell proliferation effectively compared with the control group (P<0.05). They also induced U937 cells apoptosis and the apoptosis rate reached to (63 ± 4)% in the 1 000 μg/mL astragalus treatment group. mRNA expression level of c-myc was gradually declined and p27 mRNA expression was gradually increased with astragalus treatment time (P<0.01).

CONCLUSIONSAstragalus injection may inhibit proliferation and induce apoptosis of leukemia cell line U937 in vitro. This contributes to down-regulation of c-myc expression and up-regulation of p27 expression.

Apoptosis ; drug effects ; Astragalus Plant ; Cell Proliferation ; drug effects ; Cyclin-Dependent Kinase Inhibitor p27 ; genetics ; Genes, myc ; Humans ; Injections ; U937 Cells

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

Animals ; Antibodies, Monoclonal, Murine-Derived ; therapeutic use ; Antineoplastic Combined Chemotherapy Protocols ; therapeutic use ; Cyclophosphamide ; therapeutic use ; Doxorubicin ; therapeutic use ; Gene Rearrangement ; Genes, myc ; Humans ; Immunohistochemistry ; In Situ Hybridization, Fluorescence ; Lymphoma, Large B-Cell, Diffuse ; drug therapy ; genetics ; Prednisone ; therapeutic use ; Proto-Oncogene Proteins c-bcl-2 ; genetics ; metabolism ; Proto-Oncogene Proteins c-bcl-6 ; genetics ; metabolism ; Proto-Oncogene Proteins c-myc ; genetics ; metabolism ; Translocation, Genetic ; Vincristine ; therapeutic use

Animals ; Carcinogenesis ; Cell Cycle Proteins ; genetics ; metabolism ; Cyclin E ; metabolism ; F-Box Proteins ; genetics ; metabolism ; F-Box-WD Repeat-Containing Protein 7 ; Gene Silencing ; Genes, Tumor Suppressor ; Humans ; Mutation ; Myeloid Cell Leukemia Sequence 1 Protein ; metabolism ; Neoplasms ; genetics ; metabolism ; pathology ; Proto-Oncogene Proteins c-myc ; metabolism ; Receptors, Notch ; metabolism ; Signal Transduction ; TOR Serine-Threonine Kinases ; metabolism ; Ubiquitin-Protein Ligases ; genetics ; metabolism

OBJECTIVETo study the clinicopathologic features and possible molecular mechanisms of adenoid cystic carcinoma with high-grade transformation.

METHODSFour cases of adenoid cystic carcinoma with high-grade transformation were enrolled into the study. Immunohistochemical study for smooth muscle actin, p63, p53 and Ki-67 was carried out. C-myc gene status was analyzed by fluorescence in-situ hybridization.

RESULTSThere were altogether 3 males and 1 female. The mean age of the patients was 55.5 years. Two patients died 17 months and 29 months after operation, respectively. One patient had distant metastasis 23 months after operation and was still alive at 26-month follow up. The remaining patient remained tumor free at 3-month follow up. High-grade transformation in adenoid cystic carcinoma presented either as poorly differentiated adenocarcinoma or undifferentiated carcinoma. Histologic examination showed sheets of pleomorphic tumor cells occupying more than one low-power field. The high-grade carcinoma cells showed increased nuclear-cytoplasmic ratio, prominent eosinophilic nucleoli and active mitosis (ranging from 8 to 25 per high-power field). Comedo necrosis was observed in 2 cases and multiple foci of calcifications in 3 cases. Immunohistochemical study demonstrated loss of myoepithelial differentiation, overexpression of p53 and high proliferative index by Ki-67. No c-myc translocation or copy-number changes were observed.

CONCLUSIONSHigh-grade transformation in adenoid cystic carcinoma is rare. The histopathologic features are rather distinctive and the biologic behavior is aggressive. C-myc gene mutation does not seem to play a key role in the pathogenesis.

Actins ; metabolism ; Adenocarcinoma ; genetics ; metabolism ; pathology ; Adult ; Aged ; Carcinoma ; genetics ; metabolism ; pathology ; Carcinoma, Adenoid Cystic ; genetics ; metabolism ; pathology ; Cell Transformation, Neoplastic ; Eye Neoplasms ; genetics ; metabolism ; pathology ; Female ; Follow-Up Studies ; Genes, myc ; Humans ; Ki-67 Antigen ; metabolism ; Lacrimal Apparatus ; Lacrimal Apparatus Diseases ; genetics ; metabolism ; pathology ; Lung Neoplasms ; genetics ; metabolism ; pathology ; Male ; Maxillary Sinus Neoplasms ; genetics ; metabolism ; pathology ; Membrane Proteins ; metabolism ; Middle Aged ; Mutation ; Parotid Neoplasms ; genetics ; metabolism ; pathology ; Survival Rate ; Tumor Suppressor Protein p53 ; metabolism