Prevention and treatment of cervical cancer by a single administration of human papillomavirus peptide vaccine with CpG oligodeoxynucleotides as an adjuvant in vivo

2019 ◽  
Vol 69 ◽  
pp. 279-288 ◽  
Author(s):  
Yang Yang ◽  
Yuxin Che ◽  
Yan Zhao ◽  
Xuelian Wang
Keyword(s):  
Cervical Cancer ◽  
Human Papillomavirus ◽  
Peptide Vaccine ◽  
Single Administration ◽  
Cpg Oligodeoxynucleotides ◽  
Prevention And Treatment

The role of human papillomavirus vaccines in cervical cancer: Prevention and treatment

2018 ◽  
Vol 122 ◽  
pp. 92-97 ◽  
Author(s):  
Giorgio Bogani ◽  
Umberto Leone Roberti Maggiore ◽  
Mauro Signorelli ◽  
Fabio Martinelli ◽  
Antonino Ditto ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Human Papillomavirus ◽  
Cancer Prevention ◽  
Cervical Cancer Prevention ◽  
Papillomavirus Vaccines ◽  
Human Papillomavirus Vaccines ◽  
Prevention And Treatment

scholarly journals Immunoinformatics Study on Early 4 Protein of Human Papillomavirus Type 16 for Cervical Cancer Vaccine Peptide Candidate

2019 ◽  
Vol 4 (2) ◽  
pp. 252-262
Author(s):  
Yani Suryani ◽  
Opik Taupiqurrohman ◽  
Muhammad Yusuf ◽  
Toto Subroto ◽  
Sukma Nuswantara
Keyword(s):  
Cervical Cancer ◽  
Human Papillomavirus ◽  
Amino Acid ◽  
Cancer Vaccine ◽  
Vaccine Candidate ◽  
Peptide Vaccine ◽  
Human Papillomavirus Type 16 ◽  
Cervical Cancer Vaccine ◽  
Peptide Candidate

 The aims of this study were to carry out testing of the early 4 protein of type 16 HPV through immunoinformatics meth-ods in an effort to get the peptide vaccine candidate for cervical cancer. The software used are IEDB-AR, CABSdock and Accelrys Discovery Study 4.5. Based on the analysis that sequence of ami-no acid lysine, leucine, leucine, glycine, serine, threonine, tryp-tophan, proline and threonine (KLLGSTWPT) and the sequence of amino acid tyrosine, tyrosine, valine, leucine, histidine, leucine, cysteine, leucine, alanine, alanine, threonine, lysine, tyrosine, pro-line and leucine (YYVLHLCLAATKYPL) are peptide vaccine can-didate for cervical cancer from the early 4 protein of HPV type 16 

scholarly journals The Interaction between Human Papillomavirus Type 16 and FADD Is Mediated by a Novel E6 Binding Domain

2008 ◽  
Vol 82 (19) ◽  
pp. 9600-9614 ◽  
Author(s):  
Sandy S. Tungteakkhun ◽  
Maria Filippova ◽  
Jonathan W. Neidigh ◽  
Nadja Fodor ◽  
Penelope J. Duerksen-Hughes
Keyword(s):  
Cervical Cancer ◽  
Human Papillomavirus ◽  
Tumor Necrosis Factor Receptor ◽  
Binding Domain ◽  
Death Domain ◽  
Infected Cells ◽  
E6 And E7 ◽  
Cancer Tissues

ABSTRACT High-risk strains of human papillomavirus, such as types 16 and 18, have been etiologically linked to cervical cancer. Most cervical cancer tissues are positive for both the E6 and E7 oncoproteins, since it is their cooperation that results in successful transformation and immortalization of infected cells. We have reported that E6 binds to tumor necrosis factor receptor 1 and to Fas-associated death domain (FADD) and, in doing so, prevents E6-expressing cells from responding to apoptotic stimuli. The binding site of E6 to FADD localizes to the first 23 amino acids of FADD and has now been further characterized by the use of deletion and site-directed mutants of FADD in pull-down and functional assays. The results from these experiments revealed that mutations of serine 16, serine 18, and leucine 20 obstruct FADD binding to E6, suggesting that these residues are part of the E6 binding domain on FADD. Because FADD does not contain the two previously identified E6 binding motifs, the LxxφLsh motif, and the PDZ motif, a novel binding domain for E6 has been identified on FADD. Furthermore, peptides that correspond to this region can block E6/FADD binding in vitro and can resensitize E6-expressing cells to apoptotic stimuli in vivo. These results demonstrate the existence of a novel E6 binding domain.

In Vivo Expression of Immunosuppressive Cytokines in Human Papillomavirus-Transformed Cervical Cancer Cells

2006 ◽  
Vol 19 (3) ◽  
pp. 481-491 ◽  
Author(s):  
Juan Manuel Alcocer-González ◽  
Jaime Berumen ◽  
Reyes Taméz-Guerra ◽  
Víctor Bermúdez-Morales ◽  
Oscar Peralta-Zaragoza ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Human Papillomavirus ◽  
Cancer Cells ◽  
In Vivo Expression ◽  
Cervical Cancer Cells ◽  
Immunosuppressive Cytokines

Differential splicing of E6 within human papillomavirus type 18 variants and functional consequences

2005 ◽  
Vol 86 (9) ◽  
pp. 2459-2468 ◽  
Author(s):  
Erick De la Cruz-Hernández ◽  
Alejandro García-Carrancá ◽  
Alejandro Mohar-Betancourt ◽  
Alfonso Dueñas-González ◽  
Adriana Contreras-Paredes ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Human Papillomavirus ◽  
Molecular Mechanisms ◽  
P53 Protein ◽  
Direct Consequence ◽  
Early Gene ◽  
Persistent Infections ◽  
Low Levels ◽  
Cervical Cancer Development

Persistent infections of the uterine cervix with ‘high-risk’ human papillomavirus (HPV) are now recognized as necessary for the development of cervical cancer. Among them, HPV types 16 and 18 exhibit numerous variants associated with different risks for cervical cancer development. In this study, the questions of whether different HPV type 18 variants exhibit changes in early gene transcription and the molecular mechanisms underlying these differences were investigated. It was shown that, indeed, type 18 variants exhibited singular differences in E6 transcripts in vivo. Higher levels of the E6*I transcript were detected regularly in clones harbouring the African variant, as opposed to low levels of this transcript detected in clones containing the reference clone (Asian–Amerindian), where significantly higher levels of full-length E6 transcript were usually observed. As a direct consequence, higher levels of p53 protein were found in the presence of African E6, as opposed to the low levels of p53 observed with the Asian–Amerindian E6. These variations in consequence affected the levels of cellular proteins regulated by p53, such as Bax. Similar changes in the relative levels of E6 transcripts were observed when tumours containing type 18 E6 variants were analysed. The different ability of cells containing variant E6 genes to form tumours in nude mice was suggested by the fact that tumour volumes were considerably higher when cells expressed the Asian–Amerindian E6. Mutagenesis analysis of the reference clone showed that a C491A change reverts the phenotype. These results suggest that different splicing patterns of E6 within HPV type 18 variants may possibly have biological implications in viral tumorigenesis.

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