Relevant bibliographies by topics / HPV16 E7

Academic literature on the topic 'HPV16 E7'

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Published: 10 March 2023

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Journal articles on the topic "HPV16 E7"

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Alsanea, Madain, Asma Alsaleh, Dalia Obeid, Faten Alhadeq, Basma Alahideb, and Fatimah Alhamlan. "Genetic Variability in the E6, E7, and L1 Genes of Human Papillomavirus Types 16 and 18 among Women in Saudi Arabia." Viruses 15, no. 1 (December 30, 2022): 109. http://dx.doi.org/10.3390/v15010109.

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Cervical cancer is the eighth most frequent cancer in Saudi Arabia, and most cases are associated with human papillomavirus (HPV) types 16 and 18. HPV-induced carcinogenesis may be associated with the intra-type variant, genetic mutation, or the continuous expression of viral oncogenes E6 and E7. Infection efficiency and virus antigenicity may be affected by changes in the L1 gene. Thus, this retrospective cohort study analyzed E6, E7, and L1 gene mutations in cervical specimens collected from Saudi women positive for HPV16 or HPV18 infection. HPV16 and HPV18 lineages in these specimens were predominantly from Europe. The L83V mutation in the E6 gene of HPV16 showed sufficient oncogenic potential for progression to cervical cancer. By contrast, the L28F mutation in the E7 gene of HPV16 was associated with a low risk of cervical cancer. Other specific HPV16 and HPV18 mutations were associated with an increased risk of cancer, cancer progression, viral load, and age. Four novel mutations, K53T, K53N, R365P, and K443N, were identified in the L1 gene of HPV16. These findings for HPV16 and HPV18 lineages and mutations in the E6, E7, and L1 genes among women in Saudi Arabia may inform the design and development of effective molecular diagnostic tests and vaccination strategies for the Saudi population.
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Giarrè, Marianna, Sandra Caldeira, Ilaria Malanchi, Francesca Ciccolini, Maria João Leão, and Massimo Tommasino. "Induction of pRb Degradation by the Human Papillomavirus Type 16 E7 Protein Is Essential To Efficiently Overcome p16INK4a-Imposed G1 Cell Cycle Arrest." Journal of Virology 75, no. 10 (May 15, 2001): 4705–12. http://dx.doi.org/10.1128/jvi.75.10.4705-4712.2001.

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ABSTRACT It has previously been shown that the E7 protein from the cutaneous human papillomavirus type 1 (HPV1), which is associated with benign skin lesions, binds the product of the tumor suppressor gene retinoblastoma (pRb) with an efficiency similar to that of the E7 protein from the oncogenic HPV type 16. Despite this ability, HPV1 E7 does not display any activity in transforming primary cells. In addition, the two viral proteins differ in their mechanisms of targeting pRb. HPV16 E7 promotes pRb destabilization, while cells expressing HPV1 E7 do not show any decrease in pRb levels. In this study, we show that HPV1 E7, in contrast to HPV16 E7, has only a weak activity to neutralize the effect of cyclin-dependent kinase inhibitor p16INK4a. By generation of HPV1/16 E7 chimeric proteins, we have identified a central motif in the two E7 proteins, which determines their different abilities to overcome the p16INK4a-mediated cell cycle arrest. This motif is located downstream of the pRb-binding domain and comprises only three amino acids in HPV16 E7. Swapping this central motif in the two viral proteins causes an exchange of their activities involved in circumventing the inhibitory function of p16INK4a. Most importantly, our data show that the efficiency of the E7 proteins in neutralizing the inhibitory effect of p16INK4a correlates with their ability to promote pRb degradation.
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Ma, Yunyan, LV Xiaoyan, Xiaojiang Jia, Jingzhen Zhou, Zhenbo Ouyang, Zhen Gao, Wenjuan Qiao, Xin Liu, and Ninghu Zhu. "The Role and Mechanism of Human Papillomavirus16 E7 (HPV16 E7) in the Proliferation and Invasion of Cervical Cancer Cells Through Regulating Forkhead Box Protein A1." Journal of Biomaterials and Tissue Engineering 10, no. 8 (August 1, 2020): 1206–12. http://dx.doi.org/10.1166/jbt.2020.2481.

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High-risk HPV16 is an important factor for cervical cancer. HPV16 E7 can promote the malignant transformation of cervical epithelial cells. Forkhead box protein A1 (FOXA1) is abnormally expressed in several tumors. Our study assessed HPV16 E7's effect on cervical cancer cells. Hela cells were divided into control group; HPV16 E7 group; and siFOXA1+ HPV16 E7 group followed by analysis of HPV16 E7 and FOXA1 expression by Real-time PCR and Western blot, cell proliferation by MTT assay, Caspase 3 activity, Bax and Bcl-2 expression by Real-time PCR as well as cell invasion by Transwell assay. In HPV16 E7 group, HPV16 E7 and HOXA1 expression was significantly increased, cell proliferation was promoted, invasive ability was increased, Caspase 3 activity and Bax expression was decreased, and Bcl-2 expression was increased compared to control group (P < 0 05). Conversely, inhibition of FOXA1 expression in Hela cells overexpressing HPV16 E7 can significantly inhibit cell proliferation and invasion, and promote apoptosis (P < 0 05). HPV16 E7 protein can up-regulate FOXA1 in host cells, and promote cervical cancer cell growth, proliferation and invasion, indicating that it is one of the key factors contributing to cervical cancer.
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Wulandari, Dwi, Lisnawati Rachmadi, and Tjahjani M. Sudiro. "Phylogenetic analysis and predicted functional effect of protein mutations of E6 and E7 HPV16 strains isolated in Indonesia." Medical Journal of Indonesia 24, no. 4 (December 31, 2015): 197–205. http://dx.doi.org/10.13181/mji.v24i4.1197.

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Background: E6 and E7 are oncoproteins of HPV16. Natural amino acid variation in HPV16 E6 can alter its carcinogenic potential. The aim of this study was to analyze phylogenetically E6 and E7 genes and proteins of HPV16 from Indonesia and predict the effects of single amino acid substitution on protein function. This analysis could be used to reduce time, effort, and research cost as initial screening in selection of protein or isolates to be tested in vitro or in vivo.Methods: In this study, E6 and E7 gene sequences were obtained from 12 samples of Indonesian isolates, which were compared with HPV16R (prototype) and 6 standard isolates in the category of European (E), Asian (As), Asian-American (AA), African-1 (Af-1), African-2 (Af-2), and North American (NA) branch from Genbank. Bioedit v.7.0.0 was used to analyze the composition and substitution of single amino acids. Phylogenetic analysis of E6 and E7 genes and proteins was performed using Clustal X (1.81) and NJPLOT softwares. Effects of single amino acid substitutions on protein function of E6 and E7 were analysed by SNAP.Results: Java variants and isolate ui66* belonged to European branch, while the others belonged to Asian and African branches. Twelve changes of amino acids were found in E6 and one in E7 proteins. SNAP analysis showed two non neutral mutations, i.e. R10I and C63G in E6 proteins. R10I mutations were found in Af-2 genotype (AF472509) and Indonesian isolates (Af2*), while C63G mutation was found only in Af2*.Conclusion: E6 proteins of HPV16 variants were more variable than E7. SNAP analysis showed that only E6 protein of African-2 branch had functional differences compared to HPV16R.
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Nguyen, Christine L., and Karl Münger. "Human Papillomavirus E7 Protein Deregulates Mitosis via an Association with Nuclear Mitotic Apparatus Protein 1." Journal of Virology 83, no. 4 (December 3, 2008): 1700–1707. http://dx.doi.org/10.1128/jvi.01971-08.

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ABSTRACT We previously observed that high-risk human papillomavirus type 16 (HPV16) E7 expression leads to the delocalization of dynein from mitotic spindles (C. L. Nguyen, M. E. McLaughlin-Drubin, and K. Munger, Cancer Res. 68:8715-8722, 2008). Here, we show that HPV16 E7 associates with nuclear mitotic apparatus protein 1 (NuMA) and that NuMA binding and the ability to induce dynein delocalization map to similar carboxyl-terminal sequences of E7. Additionally, we show that the delocalization of dynein from mitotic spindles by HPV16 E7 and the interaction between HPV16 E7 and NuMA correlate with the induction of defects in chromosome alignment during prometaphase even in cells with normal centrosome numbers. Furthermore, low-risk HPV6b and HPV11 E7s also associate with NuMA and also induce a similar mitotic defect. It is possible that the disruption of mitotic events by HPV E7, via targeting of the NuMA/dynein complex and potentially other NuMA-containing complexes, contributes to viral maintenance and propagation potentially through abrogating the differentiation program of the infected epithelium. Furthermore, in concert with activities specific to high-risk HPV E6 and E7, such as the inactivation of the p53 and pRB tumor suppressors, respectively, the disruption of the NuMA/dynein network may result in mitotic errors that would make an infected cell more prone to the accumulation of aneuploidy even in the absence of supernumerary centrosomes.
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Santin, Alessandro D., Stefania Bellone, Michela Palmieri, Alessandro Zanolini, Antonella Ravaggi, Eric R. Siegel, Juan J. Roman, Sergio Pecorelli, and Martin J. Cannon. "Human Papillomavirus Type 16 and 18 E7-Pulsed Dendritic Cell Vaccination of Stage IB or IIA Cervical Cancer Patients: a Phase I Escalating-Dose Trial." Journal of Virology 82, no. 4 (December 5, 2007): 1968–79. http://dx.doi.org/10.1128/jvi.02343-07.

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ABSTRACT The safety and immunogenicity of the human papillomavirus type 16 (HPV16) or HPV18 (HPV16/18) E7 antigen-pulsed mature dendritic cell (DC) vaccination were evaluated for patients with stage IB or IIA cervical cancer. Escalating doses of autologous DC (5, 10, and 15 × 106 cells for injection) were pulsed with recombinant HPV16/18 E7 antigens and keyhole limpet hemocyanin (KLH; an immunological tracer molecule) and delivered in five subcutaneous injections at 21-day intervals to 10 cervical cancer patients with no evidence of disease after they underwent radical surgery. Safety, toxicity, delayed-type hypersensitivity (DTH) reaction, and induction of serological and cellular immunity against HPV16/18 E7 and KLH were monitored. DC vaccination was well tolerated, and no significant toxicities were recorded. All patients developed CD4+ T-cell and antibody responses to DC vaccination, as detected by enzyme-linked immunosorbent spot (ELISpot) and enzyme-linked immunosorbent assays (ELISA), respectively, and 8 out of 10 patients demonstrated levels of E7-specific CD8+ T-cell counts, detected by ELISpot during or immediately after immunization, that were increased compared to prevaccination baseline levels. The vaccine dose did not predict the magnitude of the antibody or T-cell response or the time to detection of HPV16/18 E7-specific immunity. DTH responses to intradermal injections of HPV E7 antigen and KLH were detected for all patients after vaccination. We conclude that HPV E7-loaded DC vaccination is safe and immunogenic for stage IB or IIA cervical cancer patients. Phase II E7-pulsed DC-based vaccination trials with cervical cancer patients harboring a limited tumor burden, or who are at significant risk of tumor recurrence, are warranted.
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Nguyen, Christine L., Catherine Eichwald, Max L. Nibert, and Karl Münger. "Human Papillomavirus Type 16 E7 Oncoprotein Associates with the Centrosomal Component γ-Tubulin." Journal of Virology 81, no. 24 (October 3, 2007): 13533–43. http://dx.doi.org/10.1128/jvi.01669-07.

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ABSTRACT Expression of a high-risk human papillomavirus (HPV) E7 oncoprotein is sufficient to induce aberrant centrosome duplication in primary human cells. The resulting centrosome-associated mitotic abnormalities have been linked to the development of aneuploidy. HPV type 16 (HPV16) E7 induces supernumerary centrosomes through a mechanism that is at least in part independent of the inactivation of the retinoblastoma tumor suppressor pRb and is dependent on cyclin-dependent kinase 2 activity. Here, we show that HPV16 E7 can concentrate around mitotic spindle poles and that a small pool of HPV16 E7 is associated with centrosome fractions isolated by sucrose density gradient centrifugation. The targeting of HPV16 E7 to the centrosome, however, was not sufficient for centrosome overduplication. Nonetheless, we found that HPV16 E7 can associate with the centrosomal regulator γ-tubulin and that the recruitment of γ-tubulin to the centrosome is altered in HPV16 E7-expressing cells. Since the association of HPV16 E7 with γ-tubulin is independent of pRb, p107, and p130, our results suggest that the association with γ-tubulin contributes to the pRb/p107/p130-independent ability of HPV16 E7 to subvert centrosome homeostasis.
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Zhou, Fang, JieZhong Chen, and Kong-Nan Zhao. "Human papillomavirus 16-encoded E7 protein inhibits IFN-γ-mediated MHC class I antigen presentation and CTL-induced lysis by blocking IRF-1 expression in mouse keratinocytes." Journal of General Virology 94, no. 11 (November 1, 2013): 2504–14. http://dx.doi.org/10.1099/vir.0.054486-0.

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Human papillomavirus 16 (HPV16) infection causes 50 % or more of cervical cancers in women. The HPV16 E7 oncogene is continuously expressed in infected epithelium with its oncogenicity linked to cervical cancer. The E7 protein is an ideal target in control of HPV infection through T-cell-mediated immunity. Using HPV16 E7-transgenic mouse keratinocytes (KCs–E7) to investigate T-cell-mediated immune responses, we have shown previously that HPV16-encoded E7 protein inhibits IFN-γ-mediated enhancement of MHC class I antigen processing and T-cell-induced target cell lysis. In this study, we found that HPV16 E7 suppresses IFN-γ-induced phosphorylation of STAT1(Tyr701), leading to the blockade of interferon regulatory factor-1 (IRF-1) and transporter associated antigen processing subunit 1 (TAP-1) expression in KCs–E7. The results of a 51Cr release assay demonstrated that IFN-γ-treated KCs–E7 escaped from CTL recognition because HPV16 E7 downregulated MHC class I antigen presentation on KCs. Restoration of IRF-1 expression in KCs–E7 overcame the inhibitory effect of E7 protein on IFN-γ-mediated CTL lysis and MHC class I antigen presentation on KCs. Our results suggest that HPV16 E7 interferes with the IFN-γ-mediated JAK1/JAK2/STAT1/IRF-1 signal transduction pathway and reduces the efficiency of peptide loading and MHC class I antigen presentation on KCs–E7. These results may reveal a new mechanism whereby HPV16 escapes from immune surveillance in vivo.
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Hayashi, Shigenori, Takashi Iwata, Ryotaro Imagawa, Masaki Sugawara, Guanliang Chen, Satoko Tanimoto, Yo Sugawara, et al. "Transcription Factor Homeobox D9 Drives the Malignant Phenotype of HPV18-Positive Cervical Cancer Cells via Binding to the Viral Early Promoter." Cancers 13, no. 18 (September 15, 2021): 4613. http://dx.doi.org/10.3390/cancers13184613.

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Persistent infections with two types of human papillomaviruses (HPV), HPV16 and HPV18, are the most common cause of cervical cancer (CC). Two viral early genes, E6 and E7, are associated with tumor development, and expressions of E6 and E7 are primarily regulated by a single viral promoter: P97 in HPV16 and P105 in HPV18. We previously demonstrated that the homeobox D9 (HOXD9) transcription factor is responsible for the malignancy of HPV16-positive CC cell lines via binding to the P97 promoter. Here, we investigated whether HOXD9 is also involved in the regulation of the P105 promoter using two HPV18-positive CC cell lines, SKG-I and HeLa. Following the HOXD9 knockdown, cell viability was significantly reduced, and E6 expression was suppressed and was accompanied by increased protein levels of P53, while mRNA levels of TP53 did not change. E7 expression was also downregulated and, while mRNA levels of RB1 and E2F were unchanged, mRNA levels of E2F-target genes, MCM2 and PCNA, were decreased, which indicates that the HOXD9 knockdown downregulates E7 expression, thus leading to an inactivation of E2F and the cell-cycle arrest. Chromatin immunoprecipitation and promoter reporter assays confirmed that HOXD9 is directly associated with the P105 promoter. Collectively, our results reveal that HOXD9 drives the HPV18 early promoter activity to promote proliferation and immortalization of the CC cells.
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Huh, KyungWon, Xiaobo Zhou, Hiroyuki Hayakawa, Je-Yoel Cho, Towia A. Libermann, Jianping Jin, J. Wade Harper, and Karl Munger. "Human Papillomavirus Type 16 E7 Oncoprotein Associates with the Cullin 2 Ubiquitin Ligase Complex, Which Contributes to Degradation of the Retinoblastoma Tumor Suppressor." Journal of Virology 81, no. 18 (July 3, 2007): 9737–47. http://dx.doi.org/10.1128/jvi.00881-07.

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ABSTRACT Human papillomavirus type 16 (HPV16) and other high-risk HPVs are etiologically linked to the development of cervical carcinomas and contribute to a number of other tumors of the anogenital tract, as well as oral cancers. The high-risk HPV E6 and E7 oncoproteins are consistently expressed in cervical cancer cells and are necessary for the induction and maintenance of the transformed phenotype. An important aspect of HPV16 E7's oncogenic activities is destabilization of the retinoblastoma tumor suppressor (pRB) through a ubiquitin/proteasome-dependent mechanism, although the exact molecular mechanism is unknown. Here, we report that HPV16 E7 is associated with an enzymatically active cullin 2 ubiquitin ligase complex and that the HPV16 E7/pRB complex contains cullin 2. Depletion of cullin 2 by RNA interference causes increased steady-state levels and stability of pRB in HPV16 E7-expressing cells, and ectopic expression of HPV16 E7 and the cullin 2 complex leads to pRB ubiquitination in vivo. Hence, we propose that the HPV16 E7-associated cullin 2 ubiquitin ligase complex contributes to aberrant degradation of the pRB tumor suppressor in HPV16 E7-expressing cells.
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Dissertations / Theses on the topic "HPV16 E7"

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Ruiz, Elena. "DNA fusion vaccines against HPV16 E7 antigen-associated cancers." Thesis, University of Southampton, 2011. https://eprints.soton.ac.uk/374745/.

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To date, the success of cancer vaccines in human clinical trials has been limited. One of the reasons for this is the immunological tolerance to tumour antigens found in cancer patients. A novel DNA fusion vaccine design which links a pathogen-derived domain (DOM) of fragment C from tetanus toxin to a peptide epitope from a tumour antigen has been developed in our laboratory. The microbial sequence is able to activate a non-tolerised pool of helper T cells, providing T-cell help for immune induction against the linked tumour-specific sequence. The main aim of this project was to produce a therapeutic DNA vaccine against human papillomavirus (HPV)-associated cancers. A number of DNA fusion vaccines against the E7 antigen from HPV16 were constructed, including pDOM.E749-57, which encodes a well described H-2Db-binding epitope from E7 fused to the DOM sequence. CD8+ T-cell responses to the vaccines were demonstrated using flow cytometry and functional assays. Importantly, these responses were stronger than those induced by a published synthetic long peptide strategy. In vivo tumour challenge experiments showed that DNA vaccines had a protective and therapeutic effect. The vaccines were then tested in transgenic mice which develop spontaneous E7-expressing tumours in a setting of tolerance. DNA vaccine-mediated E7-specific CD8 + T-cell responses were successfully induced in these mice, together with a reduction in the mass of spontaneous tumours. This is the first demonstration of pDOM-epitope DNA vaccine-mediated therapy for spontaneous tumours and bodes well for translation into the clinic. One limiting factor for DNA vaccination in humans may be the delivery system. Electroporation (EP) is one approach which may overcome this. Therefore, a secondary aim of this project was to investigate the impact of EP on immune responses to DNA vaccination in more detail. EP proved essential for generating T-cell and antibody responses to the pDOM.E7 49-57 vaccine in sub-optimal conditions. This information will be crucial for the planning of therapeutic vaccination protocols in patients.
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Eberhard, Jeremy. "Studies on the Nucleocytoplasmic Transport of the E7 Oncoprotein of High-Risk HPV Type 16." Thesis, Boston College, 2013. http://hdl.handle.net/2345/3293.

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Thesis advisor: Junona Moroianu
Human papillomaviruses (HPVs) have been estimated to be the most common sexually transmitted infection in the United States. In addition to condyloma accuminata, infection of the squamous basal epithelium by high-risk HPVs, notably type 16 (HPV16), has been shown to be the primary etiological agent in the majority of cervical carcinomas. The E7 major transforming protein of HPV16, along with E6, has been linked to tumorigenesis and malignancy. While the E7 protein itself possesses no enzymatic activity, its ability to bind a number of nuclear and cytoplasmic targets subverts a variety of cellular regulatory complexes and facilitates viral replication. Previous studies in the Moroianu Lab have shown the HPV16 E7 oncoprotein to translocate across the nuclear pore complex (NPC) in a facilitated manner dependent on a non-canonical, c-terminal, nuclear localization signal (cNLS) for import, and a consensus leucine-rich nuclear export sequence (NES) for export (28). While the leucine-rich NES has been characterized, a full examination of the cNLS has yet to be performed. Here we present evidence that the karyopherin independent nuclear import mediated by the cNLS of 16E7 is dependent on its c-terminal Zn binding domain. Furthermore, we demonstrate that nuclear import is mediated by the direct interaction of a small patch of hydrophobic residues, 65LRLCV69, with the FG domain of the central FG-nucleoporin Nup62. In addition, we examined a potential regulatory mechanism of 16E7 nucleocytoplasmic translocation. Previous work has shown that a serine conserved in the high-risk HPVs at position 71 is phosphorylated by an unknown kinase. Here we present evidence that while phosphorylation of S71 is not required for either 16E7 nuclear localization or nuclear export in HeLa cells, mimicking phosphorylation of the S71 residue results in a statistically significant shift in the distribution of localization phenotypes of the resultant cell population toward a larger percentage exhibiting more nuclear localization. These data suggest that nucleocytoplasmic transport of 16E7 is, at least in part, a regulated process
Thesis (PhD) — Boston College, 2013
Submitted to: Boston College. Graduate School of Arts and Sciences
Discipline: Biology
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Nicol, Clare. "Selection and characterisation of RNA aptamers to the human papillomavirus 16 (HPV16) E7 oncoprotein." Thesis, University of Leeds, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.535664.

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Soares, Alexandra Sabrina Antunes. "Purification of HPV16 E6/E7 DNA plasmid-based vaccine using a modified monolithic support." Master's thesis, Universidade da Beira Interior, 2013. http://hdl.handle.net/10400.6/1344.

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Human papillomavirus (HPV) is one of the most common sexually transmitted diseases in the world and has been associated with several human cancers, like cervical cancer. Thus, effective vaccination against Human papillomavirus represents an opportunity for the control of this cancer. The development of therapeutic Human papillomavirus vaccines is required to facilitate the control and eliminate on of a preexisting Human papillomavirus infection. In the last years, the expansion of efficient plasmid DNA purification processes has fostered therapeutics applications like gene therapy and DNA vaccination. Recently, the application of chromatographic operations based on affinity interactions between plasmid DNA or impurities with specific amino acids immobilized in stationary phases has demonstrated good results in the supercoiled plasmid DNA purification. Despite of selectivity achieved with these ligands, conventional matrices present limitations such as the low binding capacity and diffusivity for plasmid DNA samples. Owing to bottlenecks associated to conventional matrices, monolithic supports have emerged as interesting alternatives due to the versatility of their structural characteristics. The research work present in this thesis describes a new strategy that combines the selectivity of arginine as affinity ligand with the versatility of the epoxy-based monoliths to efficiently purify the supercoiled HPV-16 E6/E7 plasmid from other plasmid isoforms and Escherichia coli impurities present in clarified lysate. Additionally, breakthrough experiments were designed to compare the dynamic binding capacity of plasmid DNA to the conventional arginine-agarose matrix with the modified monolithic support. The dynamic binding capacity obtained for the arginine-epoxy monolith was significantly higher than the capacity achieved in the arginine conventional support. Quality control tests indicated that the plasmid sample resultant from the purification step presented a purity degree approximately 100% and an homogeneity higher than 97% of supercoiled isoform, with an extremely reduced level of impurities (RNA, proteins, genomic DNA and endotoxins). Overall, given that the plasmid DNA final product meets regulatory specifications, this combined support can be the key to obtain an adequate non-viral vaccine against a Human papillomavirus infection.
O Papiloma Vírus Humano é um vírus sexualmente transmissível que está relacionado com o desenvolvimento de vários cancros, como o cancro do colo do útero. Este tipo de cancro é a segunda maior causa de morte em mulheres, afetando mundialmente cerca de meio milhão de mulheres, das quais aproximadamente 274 mil morrem. A evidente associação que existe entre o Papiloma Vírus Humano e o cancro do colo do útero torna o Papiloma Vírus Humano um alvo interessante para o desenvolvimento de vacinas, no sentido de prevenir ou tratar o desenvolvimento do cancro. Atualmente, já são comercializadas duas vacinas preventivas, a Gardasil da Merck e a Cervarix da GlaxoSmithKline. Apesar de ambas mostrarem ser eficazes e seguras, possuem algumas limitações como elevado custo, não protegem contra todos os tipos de Papiloma Vírus Humano e trata-se de vacinas exclusivamente preventivas. Assim o desenvolvimento de vacinas terapêuticas pode ser uma estratégia promissora para colmatar estas falhas. A utilização do DNA plasmídico (pDNA) como uma vacina não viral tem-se tornado numa potencial estratégia terapêutica para prevenir ou tratar determinadas doenças de forma menos invasiva e segura comparando com os vetores virais. O mecanismo de actuação desta vacina baseia-se na expressão de proteínas antigénicas que desencadeiam uma resposta imunológica, evitando a progressão da doença . A preparação destas vacinas de DNA plasmídico requer o desenvolvimento de processos de produção e purificação que permitam obter grandes quantidades de plasmídeo na sua forma biologicamente ativa (isoforma superenrolada (sc)), cumprindo os requisitos das agências reguladoras no que diz respeito ao grau de pureza. Da ocorrência natural de complexos proteínas-DNA em sistemas biológicos sugeriu o desenvolvimento de uma estratégia de cromatografia de afinidade, utilizando matrizes convencionais de agarose com determinados aminoácidos imobilizados que reconhecem especificamente a isoforma superenrolada do DNA plasmídico. No entanto, as matrizes convencionais apresentam algumas limitações quando comparadas com os suportes monolíticos que possuem excelentes propriedades de transferência de massa e elevada capacidade de ligação para moléculas de grandes dimensões como o DNA plasmídico. Desta forma, o trabalho apresentado nesta tese consistiu na modificação de um monolito de epoxy por imobilização de aminoácidos de arginina, conjugando assim a selectividade deste ligando com a versatilidade do monolito de epoxy, tendo como finalidade purificar a isoforma sc do pDNA HPV-16 E6/E7. Numa fase inicial, foram realizados vários ensaios com amostras de DNA plasmídico pre-purificadas com o kit comercial, no sentido de avaliar e confirmar a presença dos ligandos de arginina, comparando o comportamento cromatográfico do monolito modificado com o mesmo suporte não modificado. Os resultados comprovaram que o monolito modificado reconhece especialmente o DNA plasmídico, permitindo a separação das isoformas superenrolada e circular aberta através de um gradiente por passos de NaCl. O mesmo não aconteceu com o monolito de epoxy não modificado, pois não ocorreu qualquer tipo de interacção do plasmídeo com o suporte. Posteriormente foi realizado um estudo de capacidade de ligação dinâmica para completar a caracterização do monolito com ligandos de arginina e comparar com a coluna convencional de arginina-argarose. Os resultados comprovaram que, para as mesmas condições de caudal e concentração de pDNA HPV-16 E6/E7, o monolito possui uma capacidade de ligação significativamente superior em comparação com a coluna convencional. Uma vez conseguida a separação das isoformas e a caracterização do monolito modificado com a arginina, a segunda fase do trabalho consistiu na purificação da isoforma sc do pDNA HPV-16 E6/E7 a partir de um lisado complexo de Escherichia coli. Os testes de controlo de qualidade revelaram que a amostra de sc de pDNA HPV-16 E6/E7, resultante da purificação com o monolito de epoxy modificado, apresentava um grau de pureza de aproximadamente 100% e uma homogeneidade superior a 97%. Para além disso, constituintes do hospedeiro como RNA e proteínas não foram detectados na amostra purificada e a quantidade de DNA genómico e endotoxinas estavam a baixo dos valores referenciados pelas agências reguladoras como a Food and Drug Delivery. Em suma, a combinação de ligandos de aminoácidos com suportes monolíticos pode ser uma solução promissora para obtenção de uma vacina não-viral baseada na isoforma sc do pDNA HPV-16 E6/E7, com o grau de pureza requerido para futuras aplicações terapêuticas contra a infecção por Papiloma Vírus Humano.
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D'ANNA-BEAUGIE, ROSSELLA. "Etude des effets de l'onco-proteine virale hpv16-e7 sur les cellules endotheliales humaines." Paris 6, 2001. http://www.theses.fr/2001PA066257.

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L'infection par le papilloma virus humain est associee au cancer du col uterin, la premiere cause de deces par cancer chez les femmes. L'oncoproteine e7 codee par le hpv-16 et responsable de la transformation des keratinocytes infectes, est exprimee a toutes les etapes, de la simple infection jusqu'au developpement du cancer. Dans la premiere partie du travail, nous demontrons que l'oncoproteine e7 exprimee par les cellules cancereuses du col uterin est relachee dans le milieu extracellulaire ou elle induit, in vitro, la surproduction par les apc de la cytokine immunosuppressive ifn- et inhibe la reponse immunitaire des cellules t. De plus, le e7 declenche la production, par les macrophages et les cellules dendritiques, des cytokines tnf-, il-1 et il-6, a effet angiogenique. La deuxieme partie du travail porte sur les effets de e7 sur les cellules endotheliales humaines issues de la microvascularisation du col uterin (crmven) et d'autres organes, afin d'en comparer les reponses. L'endothelium vasculaire joue un role central dans la dissemination des metastases. Nous demontrons que le e7 penetre dans les cellules endotheliales et se localise au niveau peri-nucleaire. De plus, l'incubation des cellules endotheliales avec e7 induit : 1) le remodelage du cytosquelette d'actine ; 2) l'expression des molecules d'adherence icam-1, vcam-1 et e-selectine, facteurs cle de la dissemination tumorale ; 3) la production des interleukines il-6 et il-8, facteurs de croissance des cellules tumorales et puissants facteurs angiogeniques. Les taux d'il-6 et d'il-8 apres l'incubation avec e7 sont significativement plus eleves dans les crmven que dans les cellules endotheliales d'autres organes, indice d'un effet organo-specifique de l'oncoproteine vis-a-vis de l'endothelium. Ainsi, nos resultats suggerent que le e7, presente dans le microenvironnement, pourrait jouer un role dans la progression tumorale, vu ses effets immunosuppressifs et l'activation selective des cellules endotheliales.
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Ko, Kevin. "Investigation of the Interactions Between the DREAM Complex and HPV16." VCU Scholars Compass, 2019. https://scholarscompass.vcu.edu/etd/5786.

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According to the American Cancer Society, it has been estimated that in 2019 alone, there will be approximately 53,000 new cases of oropharyngeal cancers. Oropharyngeal cancers are the largest subset of head and neck squamous cell carcinomas (HNSCCs), which are the sixth most common cancer across worldwide populations. They, along with other HNSCCs, fall under a category of cancers known as Human papillomavirus (HPV)-associated cancers, and it has been found that upwards of 70% of these cancers can be attributed to high-risk HPV infections. Specifically, the high-risk HPV gene, E7, plays a key role in relieving cell cycle repression by disrupting the DREAM complex via competitive binding with p130, driving the cell cycle and cell proliferation. In order to combat this interaction, a LIN52-S20C mutation was developed, in hopes of reducing E7 binding of p130 and stabilizing the DREAM complex. We utilized human cervical cell lines, immortalized keratinocytes, and mouse fibroblasts, all of which contained the HPV16 genome, as models to observe the effects of the LIN52-S20C mutation on HPV-mediated hijacking of the cell cycle. Not only were we able to replicate the increased proliferation and upregulated DREAM gene expression in infected cells, but we were also able to observe some reversal of these effects in many of our cell models through the expression of the LIN52-S20C variant. The findings of these studies have been promising and provide a basis for future works, and we hope that the effects of the LIN52-S20C mutation can be translated into studies in in vivo models.
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Morale, Mirian Galliote. "Desenvolvimento de vacina terapêutica contra HPV16." Universidade de São Paulo, 2010. http://www.teses.usp.br/teses/disponiveis/46/46131/tde-26042010-160643/.

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O câncer cervical é o segundo câncer mais comum entre mulheres no mundo. A maioria dos casos (83%) ocorre em países em desenvolvimento, onde são encontrados em estágios relativamente avançados e, conseqüentemente, a sobrevida média é de cerca de 49% após cinco anos. Portanto, uma vacina eficaz contra as infecções pelo HPV pode levar ao controle do câncer do colo do útero. Apesar de prevenir, a vacina profilática não é acessível em função do alto custo, além de não eliminar o vírus em mulheres já infectadas pelo HPV. Assim, propusemos o desenvolvimento de uma vacina terapêutica eficaz utilizando duas abordagens: VLPs (virus-like particles) quiméricas, que poderiam apresentar propriedades profiláticas e terapêuticas, obtidas da fusão das proteína L1 e E7; proteínas quiméricas obtidas a partir da fusão de epítopos das proteínas E6 e E7 do HPV16, com e sem ubiquitina. Após subclonagens, com a obtenção dos vetores pPICHOLI-L1ΔCE71-50 e pPICHOLI-L1ΔCE743-77, partiu-se para a indução da expressão das VLPs quiméricas em Pichia pastoris, das quais não foram detectadas expressão protéica. Realizaram-se inúmeras modificações no protocolo de indução. Mesmo após essas alterações não foi detectada nenhuma expressão das fusões L1ΔCE71-50 ou L1ΔCE743-77. Como alternativa de uma vacina terapêutica, nos propusemos a expressar em E. coli proteínas sintéticas originadas da fusão entre epítopos das proteínas E6 e E7 do HPV16, com ou sem Ubiquitina, visando aumentar a apresentação de peptídeos via MHC de classe I de modo a estimular a eliminação de células infectadas com HPV16, evitando e regredindo o desenvolvimento dessas células cancerosas. Com a proteína E6E7 solúvel e purificada, realizou-se um ensaio de imunização. Nesse experimento, 20% dos animais imunizados com a proteína E6E7 não apresentaram desenvolvimento de tumor após a inoculação de células TC1. Assim isso nos leva a crer que com o aumento da concentração de proteína e utilização de adjuvantes seria possível aumentar o número de animais resistentes ao desenvolvimento do tumor. Em um segundo experimento de imunização, comparamos as proteínas E6E7 e E6E7Ub, em duas concentrações, 15 e 40 µg, e também com ou sem o adjuvante whole cell pertussis (WCP). Independentemente da concentração e presença ou ausência de WCP, os grupos imunizados com E6E7Ub apresentaram proteção contra o tumor entre 80% e 100% dos camundongos, enquanto os grupos imunizados com E6E7 apresentaram proteção entre 0% e 25%. Esses resultados são promissores, ainda que preliminares, indicando um potencial de uso da proteína E6E7Ub como imunógeno para vacina terapêutica contra o câncer cervical induzido por HPV16
Cervical cancer is the second most common cancer among women worldwide. Most cases (83%) occur in developing countries, where they are found in relatively advanced stages and, consequently, the median survival is about 49% after five years. Therefore, an effective vaccine against HPV infections can lead to control of cancer of the cervix. Although preventable, the prophylactic HPV vaccine is not accessible to all due to their high cost and in addition the vaccine does not eliminate the HPV in infected women. We have therefore proposed the development of effective therapeutic vaccines using two approaches: chimeric VLPs (virus-like particles), endowed with prophylactic and therapeutic properties, obtained from the fusion protein L1 and E7; chimeric proteins derived from the fusion of epitopes of proteins E6 and E7 of HPV16 with and without ubiquitin. After subcloning, we obtained the vectors pPICHOLI-L1ΔCE71-50 and L1 pPICHOLI- L1ΔCE743-77. After transformation of yeast Pichia pastoris with these constructions, the cells were induced, but it was not possible to detect any recombinant protein expression. As an alternative, we proposed the expression of synthetic proteins in E. coli derived from the fusion between epitopes of E6 and E7 proteins of HPV16 with or without Ubiquitin, in order to enhance the presentation of peptides through MHC class I to stimulate the elimination of HPV16-infected cells, preventing and regressing the development of cancer cells. Soluble E6E7 protein was purified and, 20% of the animals immunized with this protein did not develop tumor after inoculation of TC1 cells. In a second immunization experiment we compared the proteins E6E7 and E6E7Ub, in two concentrations, 15 and 40µg, with or without the adjuvant whole cell pertussis (WCP). Regardless of concentration and presence or absence of WCP, all the groups immunized with E6E7Ub showed protection against tumor between 80% and 100%, while the groups immunized with E6E7 showed protection from 0% to 25%. These results are promising and although preliminary, indicate the potential of E6E7Ub protein as an immunogen, for a therapeutic vaccine against cervical cancer induced by HPV16
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MARZANO, VALERIA. "Indagine di proteomica su linee cellulari polmonari umane stabilmente infettate con gli oncogeni E6 ed E7 di HPV16." Doctoral thesis, Università degli Studi di Roma "Tor Vergata", 2008. http://hdl.handle.net/2108/435.

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Negli ultimi anni sono emerse evidenze che supportano un ruolo di HPV nella patogenesi del cancro al polmone ed è stata riscontrata la presenza e l’espressione, attraverso distinte linee di ricerca, degli oncogeni di HPV nei tumori polmonari supportando l’ipotesi che forme oncogeniche del virus possano agire come cofattori nel processo carcinogenico. Per chiarire il ruolo di HPV nello sviluppo del tumore del polmone abbiamo utilizzato la linea cellulare polmonare A549 come modello cellulare e, dopo infezione con costrutti esprimenti gli oncogeni E6, E7 ed E6/E7 di HPV16, con un approccio di tipo proteomico, abbiamo studiato i cambiamenti nel profilo di espressione proteica delle diverse linee cellulari infettate, rispetto alla controparte normale, associate alla presenza degli oncogeni. Dall’analisi dei replicati dei gels bidimensionali tra le cellule non infettate e infettate stabilmente con HPV16E6/E7, si sono trovate 17 proteine differenzialmente espresse di almeno 2 volte, la cui intensità media normalizzata fosse statisticamente significativa (p<0.05). L’identificazione delle proteine è stata effettuata con esperimenti di spettrometria di massa MALDI-TOF-MS e nLC-ESI-Q-TOF-MS/MS. Le possibili relazioni e associazioni funzionali tra le proteine espresse differenzialmente nelle linee infettate con gli oncogeni di HPV16 sono state valutate tramite il programma bioinformatico Ingenuity Pathway Analysis. Il risultato, derivante da tutte e tre le diverse condizioni di infezione, suggerisce un coinvolgimento funzionale di processi di inibizione dell’apoptosi e le proteine Annexin IV, Gp96, Hsp27 e Tumor protein-translationally controlled 1 identificate come regolatori principali della sopravvivenza cellulare e inibizione della morte cellulare programmata.
In recent years data have accumulated implicating the involvement of oncogenic HPVs in bronchial carcinogenesis and the presence and expression of oncogenic HPV transcripts in non-small cell lung cancers have been reported throughout distinct studies. Taken together these data seem to support the hypothesis that oncogenic HPVs could act as co-factor in lung carcinogenesis. To further understand the role of HPV in the development of lung cancer we employed the lung cell line A549 stably infected with HPV16E6, HPV16E7 and HPV16E6/E7 constructs to investigate by a proteomic approach the protein profile changes associated with the expression of these oncogenes. Replicated 2-DE gels from uninfected and stably HPV16E6/E7 infected A549 cells were compared for changes in protein profile. We identified 17 different polypeptides whose average normalized spot intensity was statistically significant (p<0.05) and differed by 2- fold. The protein identification was achieved by peptide mass fingerprinting by MALDI-TOF-MS and nLC-ESI-Q-TOF-MS/MS peptide ladder sequencing Relationships between differentially expressed proteins and the HPV-induced infection mechanism have been clustered by knowledge-base database functional association network analysis. The results, deriving from the networks obtained from all three different infection conditions, suggested the functional involvement of a cell death inhibition pathway with central nodes including Annexin IV, Gp96, Hsp27 and Tumor protein-translationally controlled 1 as major key proteins for cell viability and inhibition of apoptosis pathway.
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Kavati, Erica Akemi. "Interação de oncoproteínas virais E6 e E7 de HPV16/18 com alvos celulares potenciais para o desenvolvimento de estratégias terapêuticas." Universidade de São Paulo, 2012. http://www.teses.usp.br/teses/disponiveis/87/87131/tde-26112012-103224/.

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O potencial oncogênico do papilomavírus humano (HPV) baseia-se na capacidade das oncoproteínas virais E6 e E7 alterarem o ciclo celular, levando à imortalização e malignidade das células. O importante papel das oncoproteínas na progressão tumoral e na interação com inúmeros alvos celulares tem relevância em estudos para o desenvolvimento de vacinas e terapias contra os cânceres associados ao HPV. Este estudo investigou a localização intracelular das oncoproteínas E6 e E7 de HPV16/18 e seus possíveis alvos celulares. Demonstrou a presença de E6 nuclear, citoplasmática e intramitocondrial, tanto em células naturalmente transformadas por HPV, como em células transfectadas com o oncogene E6 viral. E7 foi detectada no núcleo e citoplasma, porém nunca ocorreu E7 intramitocondrial. Confirmou a hipótese da presença intramitocondrial da oncoproteína viral E6 de HPV16/18 de alto risco. Dado inédito cuja relevância está relacionada com a aplicação clínica, no desenvolvimento de imunobiológicos e fármacos capazes de neutralizar a ação deste importante alvo terapêutico.
The oncogenic potential of HPV is based on the capacity of viral oncoproteins E6 and E7 to change cellular cycle leading to immortality and malignancy. The important role of oncoproteins in tumor progression and its interaction with numerous cellular targets have relevance in studies to the development of vaccines and therapies against HPV associated cancers. This study investigated intracellular localization of E6 and E7 HPV16/18 oncoproteins and its possible cellular targets. It showed the presence of E6 in the cellular nucleus, cytoplasm, and intramitochondrial in naturally HPV transformed cell, as well as in cells transfected with E6 viral oncogene. E7 was detected inside nucleus and cytoplasm, but E7 intramitochondrial did not occur. This study confirmed the hypothesis of the intramitochondrial presence of E6 viral oncoprotein from high risk HPV. This is an original data whose relevance is directly related to clinical application in the development of immunobiologicals and drugs, which are able to neutralize the action of this important therapeutic target.
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Giannouli, Christina. "Evaluation pré-clinique de vaccins contre le cancer du col utérin basés sur la vaccination avec des protéines E7 de HPV16 recombinantes." Doctoral thesis, Universite Libre de Bruxelles, 2002. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/211393.

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Book chapters on the topic "HPV16 E7"

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Phelps, W. C., C. L. Yee, K. Münger, and P. M. Howley. "Functional and Sequence Similarities Between HPV16 E7 and Adenovirus E1A." In Transforming Proteins of DNA Tumor Viruses, 153–66. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-74578-2_19.

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Londoño, Patricia, Robert Tindle, Ian Frazer, Steve Chatfield, and Gordon Dougan. "Use of Double Aro Salmonella Mutants to Stably Express HPV16 E7 Protein Epitopes Carried by HBV Core Antigen." In Immunology of Human Papillomaviruses, 299–303. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4615-2449-6_46.

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Liu, Xiang, Yongwei Lai, Hailin Yao, Mengmeng Zhang, Hao Zhou, Tongcun Zhang, and Hongpeng He. "HPV18 E6 and E7 Influence the Expression of Cancer Related LncRNAs in HeLa Cells." In Lecture Notes in Electrical Engineering, 719–27. Singapore: Springer Singapore, 2017. http://dx.doi.org/10.1007/978-981-10-4801-2_74.

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Feltkamp, Mariet C. W., Michel P. M. Vierboom, Jan ter Schegget, Cornelis J. M. Melief, and W. Martin Kast. "Fine Characterization of the HPVI6 E7 49-57 Tumor Protective Cytotoxic T Cell Epitope “Rahynivtf”." In Immunology of Human Papillomaviruses, 275–81. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4615-2449-6_43.

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Conference papers on the topic "HPV16 E7"

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Jadaun, Alka, Sourabh Prakash, and Saurabh Gupta. "Identification of Novel Inhibitors Against HPV16/18-E7 for Cancer Therapy." In 2018 International Conference on Bioinformatics and Systems Biology (BSB). IEEE, 2018. http://dx.doi.org/10.1109/bsb.2018.8770694.

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Agarwal, Maria, Ashley Saint-Fleur, Jie Fu, Hyam Levitsky, and Cornelia L. Trimble. "Abstract 4048: HPV16 immunity induced by immune responses to mutations in E6 and E7 proteins." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-4048.

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Abboodi, Fadi F., Kim E. Creek, and Lucia A. Pirisi. "Abstract LB-329: Molecular mechanisms of loss of E7 expression in HPV16-transformed human keratinocytes." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-lb-329.

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McGhee, Eva, Mengtao Li, Yi-Ling Lin, Khadijah Lang, Meidrah Tyler, Judith Okoro, Mai Do, et al. "Abstract 3789: Genomic instability changes acquired by HPV16 E6/E7 targeting multipolar mitoses aneuploidy: Cellular sequelae." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-3789.

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McGhee, Eva, Mengtao Li, Yi-Ling Lin, Khadijah Lang, Meidrah Tyler, Judith Okoro, Mai Do, et al. "Abstract 3789: Genomic instability changes acquired by HPV16 E6/E7 targeting multipolar mitoses aneuploidy: Cellular sequelae." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-3789.

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Jian, Z. "29 E6-P53 AND E7-RB co-mediated higher carcinogenic ability of HPV16 than HPV58 in cervical cancer." In IGCS Annual 2019 Meeting Abstracts. BMJ Publishing Group Ltd, 2019. http://dx.doi.org/10.1136/ijgc-2019-igcs.29.

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McGhee, Eva, Mengtao Li, Yi-Ling Lin, Liliana Zarate, Naomi Long, Mai Do, Chinelo Ezechukwu, et al. "Abstract 3326: Upregulation of epigenetic changes acquired by HPV16 E6/E7 oncoproteins in mouse keratinocytes: Targeting ATM/PI3K." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-3326.

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Gosmann, Christina, Stephen R. Mattarollo, Antje Blumenthal, and Ian H. Frazer. "Abstract A47: Increased levels of IL-12, IL-23 and IL-18 in skin expressing HPV16 E7 protein." In Abstracts: AACR Special Conference on Tumor Immunology: Multidisciplinary Science Driving Basic and Clinical Advances; December 2-5, 2012; Miami, FL. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.tumimm2012-a47.

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Grunwitz, C., V. Jahndel, J. Braun, D. Schwarck-Kokarakis, F. Vascotto, J. Setzer, E. King, CH Ottensmeier, Ö. Türeci, and U. Sahin. "PO-516 E6/E7 RNA(LIP): a novel liposomal RNA vaccine for treatment of patients with HPV16-positive malignancies." In Abstracts of the 25th Biennial Congress of the European Association for Cancer Research, Amsterdam, The Netherlands, 30 June – 3 July 2018. BMJ Publishing Group Ltd, 2018. http://dx.doi.org/10.1136/esmoopen-2018-eacr25.531.

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Chung, Christine, Dimitrios Colevas, Douglas Adkins, Jong Chul Park, Cristina Rodriguez, Michael Gibson, Ammar Sukari, et al. "681 A phase 1 study of CUE-101, a novel HPV16 E7-pHLA-IL2-Fc fusion protein, as monotherapy and in combination with pembrolizumab in patients with recurrent/metastatic HPV16+ head and neck cancer." In SITC 37th Annual Meeting (SITC 2022) Abstracts. BMJ Publishing Group Ltd, 2022. http://dx.doi.org/10.1136/jitc-2022-sitc2022.0681.

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