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Cervical Cancer

Cervical cancer is the second most prevalent cancer seen in women worldwide, with about 500,000 cases and more than 270,000 deaths estimated annually. Sub-Saharan Africa, South America and Southeast Asia have the highest prevalence of HPV with 25, 15 and 8% of women infected, respectively. The central etiologic factor for the cervical cancer development is persistent infection with high-risk oncogenic HPV types. Other recognized risk factors for cervical cancer are related to the sexual acquisition of HPV as well as immune dysfunction, exposure to mutagens and hormonal factors. Studies in twins show that genetic background typically plays a small role in the development of cervical cancer. The most notable risks are early age of sexual activity, multiple sexual partners, exposure to other sexually transmitted diseases, oral contraceptive use, cigarette smoking, human immunodeficiency virus infection and immunosuppressive drug therapy.

Perhaps due to the relative rarity of locally advanced or metastatic cervical cancer in the developed world, there have been only a few published reports of profiling of cervical tumors to search for actionable driver mutations. The most common finding has been of abnormalities in the phosphatidylinositide 3-kinases (PI3K) pathway, as reported by Wright et al, who used the OncoMap platform to examine 80 cervical tumors for 1250 mutations in 139 genes. They identified PIK3CA mutations in 31% of cases, with shorter survival times observed in those patients with a mutation. However, targeting this pathway therapeutically has proven difficult. Wright et al also identified KRAS mutations in 17.5% of the adenocarcinomas but none of the squamous cell carcinomas, suggesting that these tumor subtypes will need different kinds of targeted therapies. Recently, Ojesina et al published the findings of deep sequencing of 115 cervical cancers to search for somatic mutations. They identified several novel somatic mutations in the squamous cell carcinomas profiled, including E322K substitutions in the MAPK1 gene (8%); inactivating mutations in the HLA-B gene (9%); and mutations in EP300 (16%), FBXW7 (15%), ERBB2 (6%), and TP53 (5%). Somatic mutations in ELF3 (13%) and CBFB (8%) were found in 24 adenocarcinomas.

The high prevalence of HPV-associated lesions and malignancies worldwide means that there is a pressing need to develop therapeutic vaccines against cervical cancer. Choosing adequate molecular targets is important for successful therapy. Several strategies of HPV therapeutic vaccines have been evaluated to reverse the effect of immunosuppression in the tumor microenvironment, including inhibition of HPV oncoproteins, activation of the host specific immune response against HPV antigens by costimulatory molecule expression, and administration of Th1 cytokines to activate the T-cell-mediated immune response. However, HPVs have developed different strategies to escape immune control and to establish persistent infection and remain restricted to the affected epithelium. To combat HPV's immune system escape mechanisms, innovative therapies have been developed to activate the immune response to control HPV infection and prevent or treat cervical cancer. Most therapeutic vaccines that have been tested in preclinical and clinical trials are focused on interacting with antigen-presenting cells (APCs) to stimulate cytokine production and T-cell activation. Therapeutic vaccines have also been developed to generate antigen-specific CD4+ and CD8+ T-cells. HPV E6 and E7 oncoproteins are excellent candidates for HPV therapeutic vaccination strategies, although immunization against them would circumvent some common cancer–vaccine-associated problems such as immune tolerance. On the other hand, HPV E1 and E2 proteins have been reported in humans and in animal models to induce a T-cell response in patients with persistent cervical neoplasia.

Creative Biogene, as a leading biotechnology company, can offer various cervical cancer pathway-related products including stable cell lines, viral particles, and clones for your pathogenesis study and therapeutic vaccines discovery projects.

References:
  1. Ibeanu O A. Molecular pathogenesis of cervical cancer. Cancer biology & therapy, 2011, 11(3): 295-306.
  2. Peralta-Zaragoza O, et al. Targeted treatments for cervical cancer: a review. OncoTargets and therapy, 2012, 5: 315.
  3. Small Jr W, et al. Cervical cancer: a global health crisis. Cancer, 2017, 123(13): 2404-2412.

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