scholarly journals The Very Low Frequency of Epstein-Barr JC and BK Viruses DNA in Colorectal Cancer Tissues in Shiraz, Southwest Iran

2018 ◽  
Vol 67 (1) ◽  
pp. 73-79 ◽  
Author(s):  
Jamal Sarvari ◽  
Shahab Mahmoudvand ◽  
Neda Pirbonyeh ◽  
Akbar Safaei ◽  
Seyed Younes Hosseini
Keyword(s):  
Colorectal Cancer ◽  
Dna Sequences ◽  
Low Frequency ◽  
Normal Tissues ◽  
Barr Virus ◽  
Total Dna ◽  
Epstein Barr ◽  
Tissue Specimens ◽  
Cancer Tissues ◽  
Southwest Iran

Viruses including Epstein-Barr virus (EBV), JCV and BKV have been reported to be associated with some cancers. The association of these viruses with colorectal cancers remains controversial. Our objective was to investigate their infections association with adenocarcinoma and adenomatous polyps of the colon. Totally, 210 paraffin-embedded tissue specimens encompassing 70 colorectal adenocarcinoma, 70 colorectal adenomatous and 70 colorectal normal tissues were included. The total DNA was extracted, then qualified samples introduced to polymerase chain reaction (PCR). The EBV, JCV and BKV genome sequences were detected using specific primers by 3 different in-house PCR assays. Out of 210 subjects, 98 cases were female and the rest were male. The mean age of the participants was 52 ± 1.64 years. EBV and JCV DNA was detected just in one (1.42%) out of seventy adenocarcinoma colorectal tissues. All adenomatous polyp and normal colorectal tissues were negative for EBV and JCV DNA sequences. Moreover, all the patients and healthy subjects were negative for BKV DNA sequences. The results suggested that EBV and JCV genomes were not detectable in the colorectal tissue of patients with colorectal cancer in our population. Hence, BKV might not be necessitated for the development of colorectal cancer. The findings merit more investigations.

Comparison of Co-Presence of Epstein-Barr Virus and High-Risk Human Papillomaviruses in Colorectal Cancers in the Middle East Region

2020 ◽  
Author(s):  
Karim Nagi ◽  
Ishita Gupta ◽  
Hamda A Al-Thawadi ◽  
Ayesha Jabeen ◽  
Mohammed I. Malk ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
High Risk ◽  
Epstein Barr Virus ◽  
Human Papillomaviruses ◽  
Colorectal Cancers ◽  
Barr Virus ◽  
Human Carcinomas ◽  
Epstein Barr ◽  
Invasive Carcinomas ◽  
High Risk Hpv

Background: Several studies have shown the presence of onco viral DNA in colorectal tumor tissues. Viral infection by onco-viruses such as Human papillomaviruses (HPVs) and Epstein–Barr virus (EBV) are well-known to be involved in the onset and/or progression of numerous human carcinomas. Methods: We explored the co-presence of high-risk HPVs and EBV in a cohort of colorectal cancer samples from Lebanon (94) and Syria (102) by PCR, immunohistochemistry and tissue microarray. Results: The results of the study point out that 54% of colorectal cancer cases in Syria are positive for high-risk HPVs, while 30% of the cases in Lebanon are positive for these viruses; the most frequent high-risk HPV types in these populations are 16, 18, 31, 33 and 35. Analysis of LMP1 showed similar results in both populations; 36% of Syrian and 31% of Lebanese samples. Additionally, we report that EBV and high-risk HPVs are co-present in these samples. In Syrian samples, EBV and HPVs are co-present in 16% of the population, however, in the Lebanese samples, 20% of the cases are positive for both EBV and HPVs; their co-presence is associated with high/intermediate grade invasive carcinomas. Conclusion: These data suggest that EBV and high-risk HPVs are co-present in human colorectal cancers where they can cooperate in the progression of these cancers. Nevertheless, further studies are needed to elucidate the role of those oncoviruses in the development of human colorectal carcinomas.

scholarly journals Presence of Human Papillomavirus DNA in Colorectal Cancer Tissues in Shiraz, Southwest Iran

2015 ◽  
Vol 16 (17) ◽  
pp. 7883-7887 ◽  
Author(s):  
Shahab Mahmoudvand ◽  
Akbar Safaei ◽  
Nasrollah Erfani ◽  
Jamal Sarvari
Keyword(s):  
Colorectal Cancer ◽  
Human Papillomavirus ◽  
Cancer Tissues ◽  
Southwest Iran ◽  
Papillomavirus Dna

scholarly journals A putative origin of replication of plasmids derived from Epstein-Barr virus is composed of two cis-acting components.

1985 ◽  
Vol 5 (8) ◽  
pp. 1822-1832 ◽  
Author(s):  
D Reisman ◽  
J Yates ◽  
B Sugden
Keyword(s):  
Dna Sequences ◽  
Epstein Barr Virus ◽  
Simian Virus 40 ◽  
Repeated Sequence ◽  
Simian Virus ◽  
Nuclear Antigen ◽  
Barr Virus ◽  
Early Promoter ◽  
The Family ◽  
Epstein Barr

A genetic element of Epstein-Barr virus, oriP, when present on recombinant plasmids allows those plasmids to replicate and to be maintained in cells that express the Epstein-Barr virus-encoded nuclear antigen EBNA-1. Here we define the DNA sequences required for oriP activity. Two noncontiguous regions of oriP are required in cis for activity. One consists of approximately 20 tandem, imperfect copies of a 30-base-pair (bp) sequence. The other required region, approximately 1,000 bp away, is at most 114 bp in length and contains a 65-bp region of dyad symmetry. When present together on a plasmid, these two components supported plasmid replication even when the distance between them was varied or their relative orientation was altered, or both. When present alone on a plasmid that expresses a selectable marker, the family of 30-bp repeats efficiently conferred a transient drug-resistant phenotype in human 143 cells that is dependent on the presence of EBNA-1. This result leads us to suggest that EBNA-1 interacts with the 30-bp repeated sequence to activate oriP. To test whether the 30-bp repeats might cause the increased transient expression of drug resistance by enhancing transcription, the family of 30-bp repeats was tested for the ability to activate the simian virus 40 early promoter present in plasmid pA10CAT2 (Laimins, et al., Proc. Natl. Acad. Sci. U.S.A. 79:6453-6457). In this assay, the 30-bp repeats could activate the simian virus 40 early promoter in Raji cells, an EBNA-positive Burkitt's lymphoma cell line, but not detectably an EBNA-positive 143 cells in which oriP also functions.

Evidence of c-myc gene abnormalities in mediastinal large B-cell lymphoma of young adult age [see comments]

Blood ◽  
1991 ◽  
Vol 78 (3) ◽  
pp. 780-788
Author(s):  
A Scarpa ◽  
L Borgato ◽  
M Chilosi ◽  
P Capelli ◽  
F Menestrina ◽  
...  
Keyword(s):  
B Cell ◽  
Dna Sequences ◽  
Epstein Barr Virus ◽  
Cell Lymphoma ◽  
B Cell Lymphoma ◽  
Barr Virus ◽  
Large B Cell Lymphoma ◽  
Myc Gene ◽  
Epstein Barr ◽  
Large B Cell

Six cases of mediastinal large B-cell lymphoma (MLCL) with sclerosis were analyzed for the presence and patterns of c-myc and bcl-2 loci rearrangements, and for the presence of Epstein-Barr virus DNA sequences by Southern blot hybridization, c-myc gene alterations were found in three of six cases. Two cases showed the presence of mutations or small rearrangements at the 3′ end of the first exon. The c-myc gene abnormalities found in these two cases are similar to those observed in the translocation 8;14 of the endemic Burkitt's lymphomas or in its variants t(2;8) and t(8;22). A third case showed a major rearrangement of c-myc gene, with truncation within its first intron, similar to those observed in sporadic Burkitt's and in acquired immunodeficiency- associated lymphomas. None of the cases displayed bcl-2 gene rearrangements or contained viral sequences. Our data suggest a possible role for a translocation-mediated c-myc activation in the pathogenesis of MLCL. Conversely, bcl-2 gene and Epstein-Barr virus do not appear to be involved in the pathogenesis of these peculiar lymphomas. The association between c-myc structural modifications and MLCL also seems to be of relevance in light of the peculiar tendency of this tumor to involve unusual extranodal site (eg, kidney), reminiscent of the spreading attitude of Burkitt's limphomas.

Identification of epigenetic silencing of GCNT2 expression by comprehensive real-time PCR screening in colorectal cancer.

2014 ◽  
Vol 32 (3_suppl) ◽  
pp. 506-506
Author(s):  
Kazunorii Nakamura ◽  
Horomichi Sawaki ◽  
Keishi Yamashita ◽  
Masahiko Watanabe ◽  
Hisashi Narimatsu
Keyword(s):  
Colorectal Cancer ◽  
Dna Methylation ◽  
Real Time ◽  
Cell Lines ◽  
Real Time Pcr ◽  
Critical Role ◽  
Normal Mucosa ◽  
Primary Cancer ◽  
Normal Tissues ◽  
Cancer Tissues

506 Background: Glycoprotein expression profile has been proved to be dramatically altered in human cancers, however specific glycogenes which are aberrant in expression in cancer cells has not been fully identified. Recent accumulated evidence supported notion that the reduced expression of tumor suppressor genes is explained by DNA promoter methylation in human cancer. Methods: We used Comprehensive Real time PCR system (CRPS) for glycogenes (189 genes) to identify genes aberrantly expressed in colorectal cancer tissues (CRC) as compared to the corresponding normal mucosa tissues. GCNT2 was of particular interest among the identified genes in CRC. Results: (1) GCNT2 harbors 3 isoforms which have different promoter regions. (2) All of the 3 isoforms of GCNT2 genes were remarkably decreased in CRC as compared to the corresponding normal mucosa, and each isoform expression was strongly associated with other 2 isoforms in primary cancer tissues by TaqMan real time PCR (R = 0.99-995, p < 0.0001). (3) Among the 5 CRC cell lines (DLD1, HCT116, CACO2, LOVO), those which were silenced in expression were reactivated by demethylating agents such as 5-aza-2’ deoxycytidine and trichostatin A. (4) Promoter region of the variant 2 of GCNT2 was consistent with its silenced expression in CRC cell lines by cloned sequence, so we examined DNA methylation status of the promoter of the GCNT2 variant 2 in 50 primary cancer tissues and the corresponding normal tissues. Quantitative MSP revealed that almost half of normal tissues have methylation as high as tumor tissues, while, in the primary CRC with less methylation in the corresponding normal tissues, DNA methylation was higher in primary CRC tissues than in the corresponding normal tissues. Finally, GCNT2 variant 2 stable transfection induced expression of other 2 isoform variants. Conclusions: We identified novel methylation gene GCNT2 among the glycoenes. Glycoenes that were altered in genomic or epigenetic manner have been few, so GCNT2 may play a critical role in cancer progression through glycan change.

scholarly journals Marked Variation in Response of Consensus Binding Elements for the Rta Protein of Epstein-Barr Virus

2005 ◽  
Vol 79 (15) ◽  
pp. 9635-9650 ◽  
Author(s):  
Lee-Wen Chen ◽  
Pey-Jium Chang ◽  
Henri-Jacques Delecluse ◽  
George Miller
Keyword(s):  
Dna Sequences ◽  
Transcriptional Activation ◽  
Mammalian Cells ◽  
Epstein Barr Virus ◽  
Lytic Cycle ◽  
Maximal Response ◽  
Binding Affinities ◽  
Barr Virus ◽  
Epstein Barr

ABSTRACT The R transactivator (Rta) protein activates Epstein-Barr virus (EBV) lytic-cycle genes by several distinct mechanisms that include direct binding to viral promoters, synergy with BamHI Z EBV replication activator (ZEBRA), and activation of cellular signaling pathways. In the direct and synergistic mechanisms of action, Rta binds to specific DNA sequences that are present in the promoters of responsive genes. It has been difficult to demonstrate the capacity of Rta expressed in mammalian cells to bind DNA in vitro in order to study the relative affinities of Rta binding elements. We discovered that a short C-terminal region of Rta inhibits the ability of Rta to bind DNA in vitro. C-terminally truncated versions of Rta bind DNA efficiently and thus facilitate a comparison of consensus Rta binding elements (CRBEs) found in promoters of five Rta-responsive genes: BMLF1, BHLF1, BMRF1, BaRF1, and BLRF2. All CRBEs in the promoters of the five genes conform to the proposed recognition sequence GNCCN9GGNG, where N is any nucleotide and N9 represents a sequence of nine nucleotides. Nonetheless, CRBEs varied markedly in their abilities to bind Rta in electrophoretic mobility shift assays. Not all CRBEs bound or responded to Rta. Binding affinities of the CRBEs and the capacity to be activated by Rta in reporter assays were strongly correlated. The CRBEs from the BMLF1 and BHLF1 promoters conferred the greatest response. The response of the BMRF1, BaRF1, and BLRF2 CRBEs was less robust. By creation of chimeras, inversions, and point mutations, differences in binding affinities and transcriptional activation levels could be attributed to N9 sequence variation. The length of N9 was also critical for a maximal response. In Raji and BZLF1-knockout cells, the mRNAs of the five Rta-responsive lytic-cycle genes differed dramatically in kinetics of expression, abundance, and synergistic responses to ZEBRA and Rta. Affinities of Rta response elements for Rta are likely to play an important role in temporal regulation and the level of lytic-cycle EBV gene expression.

scholarly journals Low frequency of HLA-A*0201 allele in patients with Epstein-Barr virus-positive nasal lymphomas with polymorphic reticulosis morphology

2000 ◽  
Vol 87 (2) ◽  
pp. 195-199 ◽  
Author(s):  
Hiroyuki Kanno ◽  
Shizuo Kojya ◽  
Ting Li ◽  
Masahiko Ohsawa ◽  
Shin-ichi Nakatsuka ◽  
...  
Keyword(s):  
Epstein Barr Virus ◽  
Low Frequency ◽  
Barr Virus ◽  
Epstein Barr
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