scholarly journals BCL2 Gene Translocation

2020 ◽  
Author(s):  
Keyword(s):  
Gene Translocation ◽  
Bcl2 Gene

CD10−MUM1+ follicular lymphoma lacks BCL2 gene translocation and shows characteristic biologic and clinical features

Blood ◽  
2006 ◽  
Vol 109 (7) ◽  
pp. 3076-3079 ◽  
Author(s):  
Kennosuke Karube ◽  
Ying Guo ◽  
Junji Suzumiya ◽  
Yasuo Sugita ◽  
Yuko Nomura ◽  
...  
Keyword(s):  
Follicular Lymphoma ◽  
Clinical Features ◽  
Somatic Hypermutation ◽  
The Elderly ◽  
High Rate ◽  
High Grade ◽  
B Cell Differentiation ◽  
Differentiation Markers ◽  
Gene Translocation ◽  
Bcl2 Gene

Abstract CD10 and MUM1 are representative B cell differentiation markers. Follicular lymphoma (FL) is usually positive for CD10 and negative for MUM1. In this study, however, we compared 22 FLs with peculiar phenotype CD10−MUM1+ with 119 typical CD10+MUM1− FLs. All CD10−MUM1+ FL patients exhibited follicular structure with follicular dendritic meshwork, and a high rate of somatic hypermutation and ongoing mutation, similar to typical FL. However, CD10−MUM1+ FLs were encountered frequently in the elderly compared with CD10+MUM1− typical FLs (67.0 versus 58.7 years, P < .01), showed high grade (grade 3A or 3B) morphology (91% versus 17%, P < .001), diffuse proliferation (59% vs 19%, P < .001), and lacked BCL2/IGH translocation (5% versus 92.5%, P < .001), which is the most characteristic aberration in FL, and 88% showed BCL6 gene abnormalities (translocation or amplification). Our results indicate that CD10−MUM1+ FL is different from typical FL with respect to biologic and clinical features.

Hypoxia induced chemo-resistance of central giant cell granulomas and their treatment options based on cytogenetic analysis of Bcl2 gene

2018 ◽  
Vol 1 (1) ◽  
Author(s):  
Mohamed I Mourad ◽  
Lyla Tharwat ◽  
Rehab Allah Ahmed ◽  
Laila E Amin ◽  
Mona Denawar ◽  
...  
Keyword(s):  
Giant Cell ◽  
Cytogenetic Analysis ◽  
Treatment Options ◽  
Bcl2 Gene

scholarly journals Frequent tRNA gene translocation towards the boundaries with control regions contributes to the highly dynamic mitochondrial genome organization of the parasitic lice of mammals

BMC Genomics ◽  
2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Wen-Ge Dong ◽  
Yalun Dong ◽  
Xian-Guo Guo ◽  
Renfu Shao
Keyword(s):  
Mitochondrial Genome ◽  
Control Region ◽  
Genome Organization ◽  
Trna Gene ◽  
Trna Genes ◽  
Single Chromosome ◽  
Gene Translocation ◽  
Sucking Lice ◽  
Different Types ◽  
Mt Genome

Abstract Background The typical single-chromosome mitochondrial (mt) genome of animals has fragmented into multiple minichromosomes in the lineage Mitodivisia, which contains most of the parasitic lice of eutherian mammals. These parasitic lice differ from each other even among congeneric species in mt karyotype, i.e. the number of minichromosomes, and the gene content and gene order in each minichromosome, which is in stark contrast to the extremely conserved single-chromosome mt genomes across most animal lineages. How fragmented mt genomes evolved is still poorly understood. We use Polyplax sucking lice as a model to investigate how tRNA gene translocation shapes the dynamic mt karyotypes. Results We sequenced the full mt genome of the Asian grey shrew louse, Polyplax reclinata. We then inferred the ancestral mt karyotype for Polyplax lice and compared it with the mt karyotypes of the three Polyplax species sequenced to date. We found that tRNA genes were entirely responsible for mt karyotype variation among these three species of Polyplax lice. Furthermore, tRNA gene translocation observed in Polyplax lice was only between different types of minichromosomes and towards the boundaries with the control region. A similar pattern of tRNA gene translocation can also been seen in other sucking lice with fragmented mt genomes. Conclusions We conclude that inter-minichromosomal tRNA gene translocation orientated towards the boundaries with the control region is a major contributing factor to the highly dynamic mitochondrial genome organization in the parasitic lice of mammals.

scholarly journals Impact of Adenosine A2 Receptor Ligands on BCL2 Expression in Skeletal Muscle Cells

2021 ◽  
Vol 11 (5) ◽  
pp. 2272
Author(s):  
Mansour Haddad
Keyword(s):  
Gene Expression ◽  
Skeletal Muscle ◽  
Adenosine Receptors ◽  
Muscle Cells ◽  
Skeletal Muscle Cells ◽  
Qrt Pcr ◽  
A2a Receptor ◽  
Adenosine A2a ◽  
Bcl2 Expression ◽  
Bcl2 Gene

Background: Adenosine plays the role of regulating cell differentiation, proliferation, and apoptosis in various kinds of cells through the B-cell lymphoma 2 (BCL2) pathway. Objectives: Since anti-apoptotic (BCL2) expression plays a role in controlling apoptosis in some cell lines, this study was designed to investigate whether adenosine analogue, NECA (non-selective adenosine receptors agonist), selective adenosine A2B receptor antagonist, PSB 603, and a selective adenosine A2A receptor agonist, CG21680, affect BCL2-gene expression in the skeletal muscle cells of rats. The purpose of this investigation was to test the hypothesis that CG21680 treatment would significantly intensify BCL2 gene expression in rat skeletal muscle. Methods: Flasks measuring 25 cm2 were employed in culturing the rat L6 skeletal muscle cells. After treating these differential cells, the relative mRNA expression level for the BCL2 gene, at varying conditions of treatment, was measured using quantitative reverse transcription-polymerase chain reaction (qRT-PCR). Results: From the qRT-PCR analysis results, it was concluded that BCL2 expression was markedly amplified after selective adenosine A2A receptor agonist, CGS21680 (p < 0.01) treatment. More prospective validation for the adenosine receptors’ contribution in modulating apoptosis by NECA was delivered by the outcomes from the combined pre-treatment of the cells with NECA and PSB 603. These outcomes show that when starved skeletal muscle cells are treated with a combination of NECA and 100 nM PSB 603, there was a substantial decrease in comparison to either treatment used on its own. Conclusions: This study’s results showed, for the first time, an increase in BCL2 gene expression within skeletal muscle after CGS21680 treatment. Hence, the prospective escalation in BCL2 protein expression might have a protective role to play against apoptosis and avert damage to the skeletal muscle.

Association between telomere length and BCL2 gene rearrangements in low- and high-grade non-Hodgkin lymphomas

2006 ◽  
Vol 171 (1) ◽  
pp. 1-8 ◽  
Author(s):  
Alejandra Silvina Haydeé Cottliar ◽  
María Fernanda Noriega ◽  
Marina Narbaitz ◽  
Andrea Rodríguez ◽  
Irma Rosa Slavutsky
Keyword(s):  
Telomere Length ◽  
Gene Rearrangements ◽  
High Grade ◽  
Bcl2 Gene

The oncogenic role of both lncRNA PANDA and BCL2 gene in glioblastoma

Gene Reports ◽  
2021 ◽  
pp. 101160
Author(s):  
Mahshid Sadat Hosseini ◽  
Nader Mansour Samaei ◽  
Sayyed Mohammad Hossein Ghaderian ◽  
Romina Dastmalchi ◽  
Sadegh Rajabi
Keyword(s):  
Bcl2 Gene

An antisense promoter of the murine c-myc gene is localized within intron 2

1992 ◽  
Vol 12 (3) ◽  
pp. 1324-1329
Author(s):  
D B Spicer ◽  
G E Sonenshein
Keyword(s):  
Antisense Transcription ◽  
In Vitro Transcription ◽  
Region Gene ◽  
S1 Nuclease ◽  
Gene Translocation ◽  
Antisense Orientation ◽  
Nuclear Extracts ◽  
Myc Gene ◽  
Intron 2

Previously we have demonstrated the existence of stable transcripts from the noncoding strand of a rearranged c-myc gene in murine plasmacytomas in which the oncogene has translocated to an immunoglobulin constant-region gene element (M. Dean, R. B. Kent, and G. E. Sonenshein, Nature [London] 305:443-446, 1983). The resulting RNAs are chimeric, containing c-myc antisense and immunoglobulin sense sequences. A normal unrearranged murine c-myc gene is transcribed in the antisense orientation throughout much of the gene; however, stable transcripts have not been detected. In this study, using Northern (RNA) blot, S1 nuclease, and primer extension analyses, we have mapped the 5' end of the stable chimeric transcripts to a site 175 bp from the start of exon 3, within intron 2 of the c-myc gene. In vitro transcription assays with constructs containing this site and 400 bp upstream, in the antisense orientation, and nuclear extracts from plasmacytoma cells, as well as a number of cell lines with normal unrearranged c-myc genes, indicated that this promoter was functional. This finding was confirmed in transient transfection assays using the antisense promoter linked to the chloramphenicol acetyltransferase reporter gene. These results suggest that a normal promoter of antisense transcription is used following c-myc gene translocation.

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