Magic™ Mouse Anti-HPV16 E7 Monoclonal Antibody, clone E2DD

The World Health Organization has called for the elimination of cervical cancer using techniques for the early detection of premalignant tumors, and one promising strategy is the use of serum profiling antibodies to the HPV16 and HPV18 early oncoproteins, E6 and E7, as biomarkers for the early detection of invasive cervical cancer (ICC). HPV-induced cancers are dependent on the expression of oncogenes E6 and E7, and their combined action is required for the development and maintenance of the transformed phenotype. The E6 protein binds to the E3 ubiquitin ligase E6-related proteins and the tumor suppressor protein p53 and is involved in the control of cell growth processes and apoptosis. The presence of E7 in human cells prevents phosphorylation of retinoblastoma proteins, leading to uncontrolled cell proliferation. Removal of E6 and E7 expression in tumors or tumor-derived cell lines results in growth arrest and rapid death of tumor cells due to apoptosis or senescence, which makes E6 and E7 ideal potential targets for therapeutic intervention in HPV-induced cancers.

E6 and E7 are key factors in maintaining the malignant phenotype of HPV-positive cancer cells. They are the only genes that are consistently retained and expressed in HPV-positive cancer cells and have transformative potential in a variety of experimental settings. In xenograft models and transgenic mice, the growth of HPV-positive cancer cells is also dependent on sustained E6/E7 expression. In contrast, inhibition of E6/E7 expression rapidly induced senescence in HPV-positive cancer cells. E7 is a relatively small protein with no enzymatic activity that manipulates host cells by forming complexes with cellular proteins. E7 binds to pRb, leading to degradation and functional inactivation of pRb.

Figure 1. Induction of Senescence in HPV-Positive Cancer Cells upon Inhibition of E6/E7
(Source: Hoppe-Seyler K, et al. 2018)

In principle, treatment for E6/E7 should provide a highly specific regimen for HPV-positive preneoplastic and neoplastic lesions, while also protecting uninfected healthy tissue and avoiding side effects. However, fewer immunotherapies are currently used in this category, which may be related to the fact that oncogenic HPV can induce multiple immune evasion mechanisms, including impairment of antigen processing and presentation mechanisms and disruption of cytokine signaling.

Anti-Human papillomavirus 16 E7 Monoclonal Antibody