2019
DOI: 10.5958/0976-5506.2019.01394.9
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Interplay between EBERS and P27 Tumor Suppressor Proteins in Molecular Transformation of Nasopharyngeal and Sinonasal Carcinomas

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Cited by 3 publications
(4 citation statements)
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“…Additionally, it was shown that the disease causes the accumulation of high quantities of the proteins p53 and retinoblastoma (Groves et al, 2021). This study's findings are consistent with those of , who found a high prevalence of cytomegalovirus infections in the sinonasal and nasopharyngeal malignant tumors of a cohort of Iraqi patients, and suggest that cytomegalovirus may play an oncomodulatory role in the development of these tumors (Jassim et al, 2020). CMV has been implicated in modifying cellular immune responses in cancer in both human and preclinical investigations (Erkes et al, 2017;Meng et al, 2018).…”
Section: Discussionsupporting
confidence: 90%
“…Additionally, it was shown that the disease causes the accumulation of high quantities of the proteins p53 and retinoblastoma (Groves et al, 2021). This study's findings are consistent with those of , who found a high prevalence of cytomegalovirus infections in the sinonasal and nasopharyngeal malignant tumors of a cohort of Iraqi patients, and suggest that cytomegalovirus may play an oncomodulatory role in the development of these tumors (Jassim et al, 2020). CMV has been implicated in modifying cellular immune responses in cancer in both human and preclinical investigations (Erkes et al, 2017;Meng et al, 2018).…”
Section: Discussionsupporting
confidence: 90%
“…e overall incidence of malnutrition in hospitalized malignant tumor patients in different countries is basically similar, such as 65.6% in Latin America, 69.2% in Argentina, 62.0% in Cuba, and 64.5% in China [4,5]. e literature used the actual body mass to ideal body mass ratio (IBW%) to evaluate the status malnutrition and found that different malignant tumors occur at different locations, and the incidence of malnutrition is different at different stages [6].…”
Section: Review Of the Literaturementioning
confidence: 99%
“…IE1-p72 transactivates the promoters of numerous HCMV early genes including gene products that facilitate the replication process. It also interacts with the p107 protein through a domain at the N-terminus of IE1-p72 and increase the p107-mediated repression of E2F promoters leading to the inhibition of p107-mediated growth suppression [97]. Therefore, it appears that IE1-p72 can induce E2F activity.…”
Section: Lytic Replicationmentioning
confidence: 99%
“…The expression of IE1-p72 can promote S phase entry only in cells lacking p53 or p21 [96]. Controversial to that, IE1-p72 expression causes wild-type cells to arrest, most likely in G1 due to increased levels of p53 protein, which results in a p53-dependent induction of p21 expression and subsequent growth arrest [96,97]. IE2-p86 is expressed from the UL122 ORF during the IE phase of the replication cycle and is essential for HCMV replication [98].…”
Section: Lytic Replicationmentioning
confidence: 99%