Pathogenesis of Cervical Cancer

Cancer, medically called ‘tumorigenesis’ (Thaker, Lutgendorf, & Sood, 2007, p.430) occurs when cells in the body orient themselves for malignant growth. Such cells show ‘self-sufficiency in growth signals’, are ‘insensitive to anti-growth signals’ and have ‘limitless replicative potential’ (Thaker, Lutgendorf, & Sood, 2007, p.430). Once a particular set of cells become malignant, the malignancy can spread to other set of cells in different organs due to ‘crosstalk’ between the affected cells and their surrounding ‘tissues’ and ‘micro-environments’(Thaker, Lutgendorf, & Sood, 2007, p.430).

Almost all cervical carcinomas are caused by Human papillomavirus (HPV). Cervical cancer can be a life-threating disease. However, over recent years the occurrence of cervical cancer has declined as well as the chance of dying from it. A huge contributing factor to this decline is the importance of a regular pap smear. A pap smear can find cervical pre-cancer before it turns into cancer. Recently, a vaccine for HPV, has been on the market, which provides close to a 100% protection against pre-cancer and general warts. HPV and cervical cancer are two disease that are closely related. However, each disease effects not only similar populations, but also different populations, as well as having its own signs and symptoms, detection procedures,

Angiogenesis must be present for this occur, allowing cancer to spread to the blood, "thus the higher the density of new blood vessels within some tumors, the higher is the risk of metastasis of that tumor" (Mandal, 2014). Tumors have been documented to grow and spread without a direct blood supply and due to this physicians' are trying to discover ways to block tumor angiogenesis by investigating natural and synthetic inhibitors called "antiangiogenic agents" (National Cancer Institute, 2011). The goal is to slow the growth of cancer or prevent the disease entirely. According to the National Cancer Institute, "when vascular endothelial growth factor (VEGF) and other endothelial growth factors bind to their receptors on endothelial cells, signals within these cells are initiated that promote the growth and survival of new blood vessels" (2011, p. 1).

Cervical cancer is the leading cause of cancerous death, in women, since 1950. Approximately 200,000 cervical cancer patients die each year in developing countries. Strains like HPV 16 and 18 cause about 70% of cervical cancer in women– one of the top causes of death in the world (WebMD, 2010, p.1). In the Unites States, about 10,000 women acquire the disease and 3,700 die annually Human Papilloma Virus (HPV) is directly associated as a cause of cervical cancer. This virus affects the skin and genital area and, in some cases, it can also infect the throat and mouth. Since the HPV is passed from one person to another through skin-to-skin or sexual contact, sexually active people are more prone to this virus. Merck

Did you know there is more of a link between cervical cancer and HPV than smoking and lung cancer? Cervical cancer is currently the fourth most common cancer in women and the second leading cause of death from cancer in women. Along with those statistics, human papillomavirus is the most common sexually transmitted viral disease amongst men and women worldwide. The prevalence of women having a strain of HPV that ultimately leads to or increases the chance of cervical cancer is highly relatable. What is pathophysiology, signs, symptoms, prevention, and treatments of this ailment? You might ask will be covered in the next few pages of this paper.

Human Papillomavirus (HPV) is a double -stranded deoxyribonucleic acid (DNA) virus that only infects humans with an attraction to both cutaneous and mucosal surfaces such as the cervix, anus, tonsil, and oropharynx (Clark, 2013). HPV is a type of oncogenic virus that goes into the cells and can cause several diseases. Over the years, research has surfaced connecting genital HPV to several types of cancer. There are over a hundred strains of HPV but the most high risk strains, 16 and 18, have been shown to cause vulvar, vaginal, anal, and the most concerning, cervical cancer (Chan, Ng, & Wong, 2012). Genital HPV

such examples include IL1, IL6, IL10, PGE2, TGF-β, VGEF, MCSF, MIF & GM-CSF (Saskia J. A. M. Santegoets, 2016). VEGF exerts a variety of effects on vascular endothelial cells which promotes the formation and growth of new blood vessels. VEGF induces calcium transients, which causes stimulation of endothelial cells, which leads them to migrate and divide. Tumour cells are also capable of ‘shedding’ alarm proteins, such as MHC-1 complex, which as a result can have a dampening effect on NKG2D mediated activation of T cells/NK cells (Saskia J. A. M. Santegoets, 2016). As chemokines, matrix metalloproteases (MMP’s), DNA, RNA and exosomes are all highly soluble, they can not only operate within the tumour microenvironment (TME), but can enter the circulation, and subsequently effect distant mediators, such as bone marrow or lymph nodes, which can in turn suppress immune response.

Human Papillomavirus (HPV) is a sexually transmitted virus that spreads from person to person by direct contact of infected tissue. According to the CDC, nearly all men and women will contract HPV at some point in their life (Centers for Disease Control and Prevention [CDC], 2013). HPV can cause cervical, vaginal and vulvar cancers in females. HPV can also cause anal, throat, and neck cancer in both males and females. HPV is also known to cause genital warts in both males and females. According to the National Cancer Institute (2013), “approximately 12,340 new cases of cervical cancer will be diagnosed in the US, and 4,030 US women will die

Human Papilloma Virus (HPV) is the causative operator of cervical disease, which is a standout amongst the most unmistakable tumors in ladies. HPV is a sexually transmitted malady that can influence both men and ladies. The immunizer discovery systems uncovered that the greater part of the ladies (those that are sexually dynamic) worldwide and roughly 70% of the sexually dynamic ladies of US populace have been presented to the papilloma infection sooner or later in time. The African area is having the most astounding rate of commonness with an expected number of 379153 cases amid the year 2000.

Cervical cancer is a typically slow-growing type of gynecologic carcinogenesis caused predominantly by persistent infection with the human papillomavirus (HPV), most commonly the high-risk genotypes HPV-16 and HPV-18.3 Cervical cancer typically originates in the transformation zone of the cervix, where there is a junction of ectocervix and endocervix. The most common type of cervical carcinoma is squamous cell carcinoma and makes up 70-80% of cervical cancers. This type of cervical cancer occurs in the squamous cells of the ectocervix. The second most common type is an adenocarcinoma, occurring in glandular cells of the endocervix, and makes up 10-15% of cervical cancers. Cervical cancers can also be a mixture of dysplastic squamous cells and glandular cells; this type of carcinoma is termed adenosquamous carcinoma and makes up 1-2% of cervical cancers. The final type of cervical cancer is associated with HPV-6 rather than HPV-16 or HPV-18. It is termed verrucous squamous carcinoma and is very rare.5, 6

There are many different stages of cervical cancer. The first stage is Carcinoma in Situ (stage 0). In this stage abnormal cells are found in the lining of the cervix, and if not treated, it may spread into surrounding healthy tissue. Stage 1 is found in the cervix only, and divided into two different stages, 1A and 1B. 1A is also divided into 2 stages as well, 1A1 and 1A2, these are based on the size of the tumor. In stage 1 there is a small amount of cancerous cells from the cervix, but they are only able to be seen under a microscope. In stage 1A1 the cancer is no more than 3 millimeters deep and 7 millimeters wide. In stage 1A2 the cancer is between 3-5 millimeters deep and not more than 7 millimeters wide. Stage 1B is also divided into 2 stages, 1B1 and 1B2, also depending of the size of the tumor.

Cancer is one of the leading causes of death worldwide as it can develop in almost any organ or tissue. Significant advances in understanding the cellular basis of cancer and the underlying biological mechanisms of tumour has been vastly improved in the recent years (Jiang et al. 1994). Cancer is a genetic disease which requires a series of mutation during mitosis to develop, its characteristics can be associated with their ability to grow and divide abnormal cells uncontrollable while in the mean time invade and cause nearby blood vessels to serve its need. Even though many people are affected by cancer today, the abilities which cancer cells have make it hard to find a single effective treatment for cancer. The focus of research now lies

Although the human papillomavirus (HPV) has been implicated in 90% of cervical cancer cases, HPV infection is transient and usually doesn’t lead to cancer, indicating that oncogenic

Cervical cancer affects about 200 women in New Zealand per year and almost 70 women die every year because of it. This commonly happens to women whom are in their 30’s and often with no symptoms (Southern Cross, 2015). This problem is caused by a type of human papilloma virus or HPV which is commonly transmitted thru sexual contact and an estimated count of 80% on sexually active women are affected in their lives. About 40 types of Human Papilloma Virus are linked with

In cervical cancer, there is an abnormal proliferation of cells in the lower part of the uterus –cervix – that connects it to the vagina. It usually begins in the cells that line the cervix. The normal cervix of a woman looks smooth, shiny and pink. When abnormal cells first develop into pre-cancerous cells, changes in the shape, size as well as number of cells occurs in the surface of the cervix. These changes may or may not turn into cancer slowly overtime.