Regression of Established Human Papillomavirus Type 16 (HPV-16) Immortalized Tumors In Vivo by Vaccinia Viruses Expressing Different Forms of HPV-16 E7 Correlates with Enhanced CD8<sup>+</sup>T-Cell Responses That Home to the Tumor Site

Lamikanra, Abigail; Pan, Zhen-Kun; Isaacs, Stuart N.; Wu, T. C.; Paterson, Yvonne

doi:10.1128/jvi.75.20.9654-9664.2001

Cited by 87 publications

(67 citation statements)

References 44 publications

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“…Studies have suggested that cytotoxic T lymphocytes may mediate tumor regression in animal models and protect against persistant viruses (33)(34)(35). The E6 and E7 proteins are intracellular and represent genuine tumor-specific antigens that could act as targets for destruction of tumor cells without damage of healthy host cells, thus providing a clear opportunity for cervical cancer immunotherapy.…”

Section: Discussionmentioning

confidence: 99%

Cellular immunity induced by a novel HPV18 DNA vaccine encoding an E6/E7 fusion consensus protein in mice and rhesus macaques

Yan

Harris

Khan³

et al. 2008

Vaccine

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Human papilloma-virus (HPV) infection is the major cause of cervical cancer. HPV 18 is the most prevalence high-risk HPV after type 16 that accounts for the largest number of cervical cancer cases worldwide. Currently, although prophylactic vaccines have been developed, there is still an urgent need to develop therapeutic HPV vaccines for targeting tumors post infection. In this study, we utilize a novel multi-phase strategy for HPV 18 antigen development with the goal of increasing anti-HPV18 cellular immunity. Our data show that this construct can induce strong cellular immune responses against HPV 18 E6 and E7 antigens in a murine model. Moreover, when applied to Rhesus monkeys, this construct is also able to elicit cellular immunity. These data suggest such DNA immunogens are candidates for further study in the eventual context of immunotherapy for HPV-associated cancers.

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Section: Discussionmentioning

confidence: 99%

Cellular immunity induced by a novel HPV18 DNA vaccine encoding an E6/E7 fusion consensus protein in mice and rhesus macaques

Yan

Harris

Khan³

et al. 2008

Vaccine

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“…DOI: 10.3109/10717544.2013.801534 feasible option in therapeutic HPV vaccines (Lin et al, 2010). The Viruses include adenovirus (Gomez-Gutierrez et al, 2007), adeno-associated virus (Jin et al, 2005), vaccinia virus (Lamikanra et al, 2001) and alphaviruses (Cassetti et al, 2004). The tumor cells may express different levels of antigenic peptides loaded by class I MHC molecule.…”

Section: Discussionmentioning

confidence: 99%

A non-pathogenic live vector as an efficient delivery system in vaccine design for the prevention of HPV16 E7-overexpressing cancers

et al. 2013

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The attenuated or non-pathogenic live vectors have been evolved specifically to deliver DNA into cells as efficient delivery tools in gene therapy. Recently, a non-pathogenic protozoan, Leishmania tarentolae (L.tar) has attracted a great attention. In current study, we used Leishmania expression system (LEXSY) for stable expression of HPV16 E7 linked to different mini-chaperones [N-/C-terminal of gp96] and compared their immunogenicity and protective effects in C57BL/6 mice against TC-1 challenge. TC-1 murine model is primary C57BL/6 mice lung epithelial cells co-transformed with HPV16 E6, HPV16 E7 and ras oncogenes. Our results showed that subcutaneous administration of mice with both the recombinant L.tar-E7-NT

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“…33 TC-1 cells were maintained in RPMI (Invitrogen) supplemented with 2 mM l-glutamine; 100 U/ml penicillin; 100 µg/ml streptomycin; 10% FBS and geneticin (1 mg/ml) (Invitrogen) in a 5% CO 2 atmosphere at 37˚C.…”

Section: Methodsmentioning

confidence: 99%

Direct vaccination with tumor cells killed with ICP4-deficient HSVd120 elicits effective antitumor immunity

Benencia

Courrèges²,

Conejo-Garcia³

et al. 2006

Cancer Biology & Therapy

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We tested whether tumor cells were killed by replication-incompetent recombinant herpes simplex virus (HSV) d120 lacking immediate early gene ICP4 and whether HSVd120-killed tumor cells could be used directly for tumor vaccination. Vaccine efficacy was tested in TC-1, a murine adenocarcinoma transformed with HPV16 E6 and E7, and ID8-Vegf, a murine epithelial ovarian cancer model. HSVd120 killed tumor cells by apoptosis. Tumor cells infected by HSVd120 were engulfed more avidly by immature DCs and induced DC maturation more efficiently than tumor cells killed by ultraviolet B (UVB) radiation. HSVd120 infection induced stronger upregulation of GRP94 than UVB in cells undergoing apoptosis. Immunization of mice with HSVd120-killed cells elicited stronger antitumor T cell response, including tumor reactive interferon-gamma secreting and cytotoxic T cells, and resulted in significantly stronger delay in tumor growth than immunization with UVB-killed tumor cells. Thus, the use of replication-incompetent HSV strains lacking ICP4 offers possible advantages in the preparation of whole tumor cell antigen for direct tumor vaccination.

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Regression of Established Human Papillomavirus Type 16 (HPV-16) Immortalized Tumors In Vivo by Vaccinia Viruses Expressing Different Forms of HPV-16 E7 Correlates with Enhanced CD8⁺T-Cell Responses That Home to the Tumor Site

Cited by 87 publications

References 44 publications

Cellular immunity induced by a novel HPV18 DNA vaccine encoding an E6/E7 fusion consensus protein in mice and rhesus macaques

Cellular immunity induced by a novel HPV18 DNA vaccine encoding an E6/E7 fusion consensus protein in mice and rhesus macaques

A non-pathogenic live vector as an efficient delivery system in vaccine design for the prevention of HPV16 E7-overexpressing cancers

Direct vaccination with tumor cells killed with ICP4-deficient HSVd120 elicits effective antitumor immunity

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Regression of Established Human Papillomavirus Type 16 (HPV-16) Immortalized Tumors In Vivo by Vaccinia Viruses Expressing Different Forms of HPV-16 E7 Correlates with Enhanced CD8+T-Cell Responses That Home to the Tumor Site

Cited by 87 publications

References 44 publications

Cellular immunity induced by a novel HPV18 DNA vaccine encoding an E6/E7 fusion consensus protein in mice and rhesus macaques

Cellular immunity induced by a novel HPV18 DNA vaccine encoding an E6/E7 fusion consensus protein in mice and rhesus macaques

A non-pathogenic live vector as an efficient delivery system in vaccine design for the prevention of HPV16 E7-overexpressing cancers

Direct vaccination with tumor cells killed with ICP4-deficient HSVd120 elicits effective antitumor immunity

Contact Info

Product

Resources

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Regression of Established Human Papillomavirus Type 16 (HPV-16) Immortalized Tumors In Vivo by Vaccinia Viruses Expressing Different Forms of HPV-16 E7 Correlates with Enhanced CD8⁺T-Cell Responses That Home to the Tumor Site