Molecular Genetics in Epstein–Barr Virus-Associated Malignancies

Umakanthan, Srikanth; Bukelo, Maryann M

doi:10.3390/life11070593

Cited by 7 publications

(11 citation statements)

References 90 publications

(111 reference statements)

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“…Another set of EBV-latent gene products, EBNA2 and EBNA-LP , were found in a recent study to alter the alternative splicing regulation of genes NUMB and BCL-X , which are involved in cell survival and proliferation after EBV infection [ 18 ]. Other EBV gene products that act as BCL-2 homologs provide anti-apoptotic function and are also involved in oncogenesis [ 3 ].…”

Section: Direct Carcinogenesis: Ebv Infectious Cycle and Related Onco...mentioning

confidence: 99%

“…EBV is an oncogenic virus; the global burden of EBV-associated malignancies is 1.5%, and the virus is responsible for 1.8% of cancer-related deaths [ 2 ]. EBV plays a role in the pathogenesis of multiple lymphoid and epithelial cancers, including Burkitt Lymphoma (BL), Hodgkin’s Lymphoma (HL), NK/T Cell Lymphoma (NKTCL), Nasopharyngeal Carcinoma (NPC), EBV Related Breast Cancer (EBVrBCa), and EBV-Associated Gastric Cancer (EBVaGC) [ 3 ]. The oncogenic properties of EBV have been thoroughly studied, with the hopes that by elucidating them, we can develop therapeutic strategies to target them.…”

Section: Introductionmentioning

confidence: 99%

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Tumor Molecular and Microenvironment Characteristics in EBV-Associated Malignancies as Potential Therapeutic Targets: Focus on Gastric Cancer

Atri-Schuller

Abushukair

Cavalcante

et al. 2022

CIMB

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Although most people are infected with Epstein-Barr Virus (EBV) during their lifetime, only a minority of them develop an EBV-associated malignancy. EBV acts in both direct and indirect ways to transform infected cells into tumor cells. There are multiple ways in which the EBV, host, and tumor environment interact to promote malignant transformation. This paper focuses on some of the mechanisms that EBV uses to transform the tumor microenvironment (TME) of EBV-associated gastric cancer (EBVaGC) for its benefit, including overexpression of Indoleamine 2,3-Dioxygenase 1 (IDO1), synergism between H. pylori and EBV co-infection, and M1 to M2 switch. In this review, we expand on different modalities and combinatorial approaches to therapeutically target this mechanism.

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Section: Direct Carcinogenesis: Ebv Infectious Cycle and Related Onco...mentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Tumor Molecular and Microenvironment Characteristics in EBV-Associated Malignancies as Potential Therapeutic Targets: Focus on Gastric Cancer

Atri-Schuller

Abushukair

Cavalcante

et al. 2022

CIMB

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show abstract

“…Other EBV gene products that act as BCL-2 homologs provide anti-apoptotic function and are also involved in oncogenesis [3].…”

Section: Ebv Cell-cycle Dysregulationmentioning

confidence: 99%

Tumor Molecular and Microenvironment Characteristics in EBV-Associated Malignancies as Potential Therapeutic Targets: Focus on Gastric Cancer

Schuller¹,

Abushukair²,

Cavalcante³

et al. 2022

Preprint

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Although most people are infected with Epstein-Barr Virus (EBV) during their lifetime, only a minority of them develop an EBV-associated malignancy. EBV acts in both direct and indirect ways to transform infected cells into tumor cells. There are multiple ways in which the EBV, host, and tumor environment interact to promote malignant transformation. This paper focuses on some of the mechanisms that EBV uses to transform the tumor microenvironment (TME) of EBV-associated gastric cancer (EBVaGC) for its benefit, including overexpression of IDO1, synergism between H pylori and EBV coinfection, and M1 to M2 switch. In this review, we expand on different modalities and combinatorial approaches to therapeutically target this mechanism.

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“…Similarly, the alterations in the gene expression of c-Myc, BCL-2, TP53, MDM-2, Rb, BRCA-1, BRCA-2, CDKN-1B, CDKN-1A , and CDKN-1B have shown to be associated with PCa progression 14 , 15 , and EBV has been shown to modulate several of these genes in other cancer types 4 , 16 , however, the EBV-associated dysregulation of gene expression in PCa has not been explored. In addition, certain prostate-specific miRNAs (oncomiRs) reportedly regulate a wide array of prostatic functions, ranging from proliferation to apoptosis.…”

Section: Introductionmentioning

confidence: 99%

Differential analysis of histopathological and genetic markers of cancer aggressiveness, and survival difference in EBV-positive and EBV-negative prostate carcinoma

Ahmed,

Sheikh,

Fatima

et al. 2024

Sci Rep

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Several studies have shown an association between prostate carcinoma (PCa) and Epstein-Barr virus (EBV); however, none of the studies so far have identified the histopathological and genetic markers of cancer aggressiveness associated with EBV in PCa tissues. In this study, we used previously characterized EBV-PCR-positive (n = 39) and EBV-negative (n = 60) PCa tissues to perform an IHC-based assessment of key histopathological and molecular markers of PCa aggressiveness (EMT markers, AR expression, perineural invasion, and lymphocytic infiltration characterization). Additionally, we investigated the differential expression of key oncogenes, EMT-associated genes, and PCa-specific oncomiRs, in EBV-positive and -negative tissues, using the qPCR array. Finally, survival benefit analysis was also performed in EBV-positive and EBV-negative PCa patients. The EBV-positive PCa exhibited a higher percentage (80%) of perineural invasion (PNI) compared to EBV-negative PCa (67.3%) samples. Similarly, a higher lymphocytic infiltration was observed in EBV-LMP1-positive PCa samples. The subset characterization of T and B cell lymphocytic infiltration showed a trend of higher intratumoral and tumor stromal lymphocytic infiltration in EBV-negative tissues compared with EBV-positive tissues. The logistic regression analysis showed that EBV-positive status was associated with decreased odds (OR = 0.07; p-value < 0.019) of CD3 intratumoral lymphocytic infiltration in PCa tissues. The analysis of IHC-based expression patterns of EMT markers showed comparable expression of all EMT markers, except vimentin, which showed higher expression in EBV-positive PCa tissues compared to EBV-negative PCa tissues. Furthermore, gene expression analysis showed a statistically significant difference (p < 0.05) in the expression of CDH1, AR, CHEK-2, CDKN-1B, and CDC-20 and oncomiRs miR-126, miR-152-3p, miR-452, miR-145-3p, miR-196a, miR-183-3p, and miR-146b in EBV-positive PCa tissues compared to EBV-negative PCa tissues. Overall, the survival proportion was comparable in both groups. The presence of EBV in the PCa tissues results in an increased expression of certain oncogenes, oncomiRs, and EMT marker (vimentin) and a decrease in CD3 ITL, which may be associated with the aggressive forms of PCa.

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Molecular Genetics in Epstein–Barr Virus-Associated Malignancies

Cited by 7 publications

References 90 publications

Tumor Molecular and Microenvironment Characteristics in EBV-Associated Malignancies as Potential Therapeutic Targets: Focus on Gastric Cancer

Tumor Molecular and Microenvironment Characteristics in EBV-Associated Malignancies as Potential Therapeutic Targets: Focus on Gastric Cancer

Tumor Molecular and Microenvironment Characteristics in EBV-Associated Malignancies as Potential Therapeutic Targets: Focus on Gastric Cancer

Differential analysis of histopathological and genetic markers of cancer aggressiveness, and survival difference in EBV-positive and EBV-negative prostate carcinoma

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