Essay On Crvical Cancer

HPV, human papillomavirus is a communal infection that is common among adults. It is one of the main sources of sexual transmitted infection. Over 75% of women that are sexually active are most likely to be infected at least once in their life. This virus is known to be a worldwide disease. According to the World Health Organization, the risk of acquiring HPV infection is highest soon after a sexual encounter. Most of these infections are self-limiting and harmless. The virus is harmless because a number of people don’t realize they are infected, because the virus is often subclinical. Persistent infections with oncongenic HPV types can cause cervical cancer in women. Even though, both male and female can be affected by the

The advent of new human papilloma virus (HPV) vaccines with the potential to prevent the majority of cases of invasive cervical cancer presents a remarkable public health achievement (Markowitz et al., 2007). This is because cervical cancer is the commonest female cancer worldwide and it has been associated with HPV infection (Franceschi et al., 2009). In just 2015, there will be 12,900 new cases of cervical cancer in the United States with 4,100 estimated deaths (Siegel, Miller, & Jemel, 2015).

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

Cervical cancer is the second foremost occurring cancer in women after breast cancer. Cervical cancer is a sexually transmitted disease caused by the human papillomavirus, or HPV. Infection by HPV typically occurs in the early years of sexual activity according to the World Health Organization (WHO), but it can take up to a full twenty years for it to develop into a full-blown malignant tumor. Scientists believe that for all intents and purposes all cervical cancer cases are caused by infection with a few types of cancer. Great strides have been made in recent years in the development of a vaccine to treat the cervical cancer. Scientists have cultivated a prophylactic vaccine that would protect against the human papillomavirus. HPV's

Currently, cervical cancer remains one of the most preventable causes of cancer deaths. According to the Centers for Disease Control and Prevention, in 2014 12,578 women were diagnosed with cervical cancer and 4,115 died of cervical cancer (CDC, 2014). HPV, or the Human Papilloma Virus has been found to be the cause of cervical cancer in women. The Papanicolau test, or Pap test has been around for decades and it is the test where cervical cytology is examined for any change in the cells of the cervix that may lead to cancer. Early detection of cervical dysplasia or cervical cancer has prevented cervical cancer deaths. Currently, high-risk HPV

Research proves that certain cervical cancers can be prevented by simply getting vaccinated against the Human Papillomavirus (Shafer, Cates, Diehl, & Hartmann, 2011). This virus is responsible for 99% of the cervical cancers (Smith, 2008). The Human Papillomavirus (HPV) is the most sexually transmitted disease in the world (Nath &Thappa, 2009). Four main strains of HPV exists, 6,11,16 and 18 (Smith, 2008). HPV strains 16 and 18 are the causative factors for 70% of the cervical cancers (Smith, 2008). HPV strains 6 and 11 cause about 90% of genital warts (Smith, 2008). Without serious side effects the Human Papillomavirus (HPV) Vaccine is 100% effective in preventing the two HPV strains that cause the largest percentages of cervical cancer

With more than 500,000 new cases being detected each year, cervical cancer is one of the leading causes of cancer affecting women worldwide.1, 2 A very high burden of cervical cancer mortality is found in developing countries, where nearly 9 out of 10 cases result in cervical cancer-related mortality among women.3, 4 These healthcare disparities can be largely explained by the lack of access to effective cervical cancer screening programs in low-resource settings, such as Sub-Saharan Africa (SSA), that allow for early detection and treatment.5 African women have an extremely high incidence of cervical cancer, with approximately 420,000 new cases, half of which die per year.6 Kenya has the second highest incidence of invasive cervical cancer (ICC) in Africa.6,7 The

Cervical cancer is one of the commonest causes of death worldwide. (Chabra 2016). This is the third most common cancer (9%) in women and seventh (4%) among all cancer deaths. (Chabra 2016). Cervical carcinoma is mostly preventable as screening is available for early diagnosis and there is existence of highly efficacious treatment regimens for early stage disease. (Marcus, Crane, 1998). That’s why death from cervical carcinoma is categorized as “avoidable mortality”, even though, it is killing many women every year worldwide. Though, the incidence, and mortality of cervical cancer is decreasing by 40% in the developed country since early 1970, the developing countries are not following this decreasing trend and about 88% of the cervical cancer cases are occurring in the developing countries. (Quinn, Babb, Jones, Allen, 2011); (Chabra 2016). To maintain this decreasing trend in developed country and prevent the new onset of this cancer in the developing country, attention and emphasis should be given on screening procedures for early diagnosis of any cervical pathology.

Human papillomavirus (HPV) infections cause cervical cancers, and some cancers of the vulva, vagina, penis, anus, and oropharynx. Two prophylactic HPV vaccines (Gardasil® and Cervarix®) can block new infections from a subset of the most prevalent HPV types, but have shown no therapeutic effect against pre-existing diseases. No effective therapeutics exists at present, and the mechanisms of HPV-associated disease progression and cancer are not well understood.

Human papillomavirus (HPV) is a double stranded DNA virus that has more than 40 different types that are transmitted through sexual contact. HPV is the most common sexually transmitted disease affecting more than 79 million people worldwide with more than 14 million new people being affected each year (CDC 2015). HPV is so common that more than half of all sexually active adults will be infected in their lifetime (AULT 2006). Most of the 40 types of HPV pose no health risk and are usually fended off by the body’s immune system but the four most common types of HPV, HPV16, 18, 11 and 6 are known to cause either cervical cancer (HPV16 and 18) or genital warts (HPV11 and 6). Different types of HPV

Cervical cancer is the fourth most common cancer in women, attributing to 266,000 deaths per year worldwide, a female gynecological cancer mortality rate second only to breast cancer. Although the human papillomavirus (HPV) has been implicated in 90% of cervical cancer cases, not all causes of cervical cancer are known, representing a critical barrier to progress in therapeutic development. Current therapies include a combination of hysterectomy and radiation or chemotherapy, all of which have significant side effects. New and improved treatments are therefore needed to minimize adverse effects and preserve fertility, especially for women of childbearing age.

Cervical cancer is the 4th most commonly diagnosed cancer among women worldwide and the 14th in the U.S. (Kessler, 2017). This year the cervical cancer prevalence was estimated to be 256,078 and incidence was 12,820 in the

It may be possible to correct an abnormality in a tumor suppressor gene such as P53 by inserting a copy of the wild-type gene; in fact, insertion of the wild-type P53 gene into P53-deficient tumor cells has been shown to result in the death of tumor cells (3). This has significant implications, since P53 alterations are the most common genetic abnormalities in human cancers. The over expression of an oncogene such as K-RAS can be blocked at the genetic level by integration of an antisense gene whose transcript binds specifically to the oncogene RNA, disabling its capacity to produce protein. Experiments in vitro and in vivo have demonstrated that when an antisense K-RAS vector is integrated into lung cancer cells that over express K-RAS their tumorigenicity is decreased (4).

According to the Centre for Health Protection of the Department of Health (2011), cervical cancer becomes the tenth commonest cancer in Hong Kong in 2008. Cervical cancer usually arises from sexual activity and human papillomavirus (HPV) (Bellentir, 2002). In this essay, Human papillomavirus would be further discussed. For example, the signal transport pathway of HPV 16 and HPV 18, which many scientists believe that they are closely related of causing cervical cancer, as well as the HPV vaccine and chemotherapy of cervical cancer, would be discussed.

Rational and Hypothesis: My hypothesis in this aim is that mutations in UPF1 inhibit NMD thereby stabilizing premature transcripts that are translated to produce truncated proteins which promote pancreatic ASC. Previous studies have demonstrated that a subset of transcripts inhibited upon UPF1 knockdown are stabilized and translated. My objectives in this aim are: a) To determine global occupancy of mutant UPF1 on RNA b) To analyze if the mutant UPF1 bound RNA fragments are translated c) To determine which of the targets are essential to promote tumorigenesis.