Evidence for a causal involvement of HPV in the pathogenesis of OPSCC comes from epidemiologic and molecular studies. The earliest suggestion of a possible link between HPV and squamous cell carcinomas of the oral cavity (OSCC) was made by Syrjanen et al (1983) where the group observed that some of these tumours have morphological and immunohistochemical features indicative of HPV infection. 59 Subsequent studies have supported the predilection of the virus for oropharyngeal cancers. In two case series (1996 and 1997), 50% and 60% of tonsillar carcinomas were HPV positive, respectively, in comparison to 6% and 10% of tumours at other oral sites.60,61 Additionally, Gillison et al (2000) and Stransky et al (2011) confirmed that the only HNC subsite with a demonstrated carcinogenic role for HPV was the oropharynx.21,62 …show more content…
Nasman et al (2009) analysed the increased incidence of tonsillar cancer in the Stockholm area between 1970 and 2007. They showed that the percentages of tonsillar cancers that were HPV-positive was 23%, 29%, 57% and 79% during the 1970s, 1980s, 1990s and 2000–2007, respectively.63 Similarly, in the UK, Scache et al (2011) demonstrated an increase in the prevalence of HPV positivity in OPSCC 14% in the period 1998 to 2009 to 57% in the period between 1998 and 2009.64 In the United States, Chaturvedi et al (2011) confirmed the temporal increase in the proportion of OPSCC that were HPV positive from 20% in 1988 to more than 70% in 200465,66.
The last 25 years has seen an exponential growth in the literature surrounding this field, and there is now a strong and consistent molecular evidence base for a causal role of HPV in OPSCC. Indeed, in 2009 HPV was authoritatively recognised as a causal agent in the development of
In addition, the immune system of most women will usually suppress or eliminate HPVs. This is very important because only an ongoing persistent infection has the potential to lead to cervical cancer (HPV). Eleven thousand cases of this kind of cancer were confirmed in 2007 in the United States; the amount undiagnosed is still unclear but believed to be in the tens of thousands. But to give some perspective of the problem you need to understand its effects on a global level. On the world wide scale cervical cancer strikes nearly half a million women each year, claiming more than a quarter of a million lives. “High risk” HPV types 16 and 18 are implicated in Seventy percent of cervical cancers and are hence selected for vaccine targets (The HPV).
HPV is the single biggest cause of cervical cancer and oropharyngeal cancers, according to the CDC. Between 2008 and 2012, almost 39,000 U.S. citizens were diagnosed with HPV-related cancer every year. Fifty-nine percent of them women and 41 percent men, researchers report. But while Pap smears and HPV tests have reduced rates of cervical cancer in woman, rates of oral cancer are growing in men.
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
Among the 12, 200 new cases of cervical cancer ninety-percent of them are caused or attributed to HPV.
Human Papilloma Virus (HPV) is currently thought to be the most common sexually transmitted infection (STI) in the United States with roughly 79 million Americans currently affected (CDC,2015). There are over 120 identified types of HPV (CDC, pink book); most of which infect the cutaneous epithelium and cause common skin warts. Approximately 40 types of HPV infect the mucosal epithelium and are categorized according to their epidemiological association with cervical cancer: low risk type is associated with non-oncogenic types and cause benign or low-grad cervical cell abnormalities, genital warts and laryngeal papillomas. High Risk Types can cause low-grade cervical cell abnormalities, high grade cervical cell abnormalities or anogenital cancers less common than cervical cancer, such as cancer of the vulva, vagina, penis and anus. The purpose of this paper is to explore and discuss differences in the vaginal microbiome and metabolome of women who have been classified as HPV positive vs women who have been classified as HPV negative. These differences are based upon a preliminary analysis which showed pathway enrichment of lipids, sphingolipids and estrogen when comparing women that were HPV positive with women that were HPV negative. This paper is exploratory in nature; as these topics hold great value for the rest of my dissertation, I briefly explored the following topics of interest in order to gain further insight: HPV, the vaginal microbiome, the life-cycle of HPV, HPV
Human Papilloma Virus (HPV) is one of the most common sexually transmitted infections in the United States. HPV belong to a family of viruses that cause cell changes in the epithelia resulting in benign skin lesions called warts and verrucae. Type 6 and 11 cause warts and are included under the low risk HPVs,Types 16,18,31,33,45 cause cervical cancer and are included under high risk HPVs(CDC,2014). The virus affects the skin and mucous membrane especially of the reproductive organs. Cervical Cancer and other Ano-genital cancers are seen in women with persistent genital HPV infection. HPV that affects the
Bladder cancer is one of the most common types of cancer with an incidence rate of about 2.4 times greater in males than females, but with a far worse prognosis in females 1. With multiple risk factors including most importantly smoking1 we will discuss the controversial role played by HPV , a virus proved to be the primary suspect in cervical carcinoma and multiple other carcinomas in the skin and mucous membranes such as head and neck carcinomas 2.
Human papilloma virus (HPV) is a name derived from group of viruses that affect the human skin and other moist areas found in the human body, such as the cervix, anus, mouth and throat. There are more than 100 species of HPV, of which only thirty of them affect the genital area. Genital HPV is very contagious and are spread during sexual intercourse and skin to skin of the genital areas. Some HPV can be physically detected, when there are visible genital warts seen around the site. HPV that do not exhibit clinical symptoms are known as sub-clinical HPV, which connotes that they are not visible, neither do they have recognizable symptoms (Women 's health specialist, November, 2009). Most of the time, Sub - clinical HPV is discovered when there is an abnormal results from pap smear. On the other hand, research also shows that men do encounter sub-clinical HPV, but the test does not work for them. Therefore, men may have it without knowing.
Human papillomavirus (HPV) is one of the most common sexually transmitted viral infections in the United States. There are nearly 1 out of 4 women who have been diagnosed with HPV (CDC, 2015). The Centers for Disease Control and Prevention (CDC) reported that at least 80% of women acquire a genital HPV infection by the age of 50 (CDC, 2015). HPV is an important topic that needs to be discussed because it has been estimated that 6.2 million cases of HPV has been reported (CDC, 2015). HPV is one third of all new sexual transmitted infections (CDC, 2015).
Human Papilloma Virus (HPV) is one of the most common sexually transmitted infections in the United States. HPV belong to a family of viruses that cause cell changes in the epithelia resulting in benign skin lesions called warts and verrucae. Type 6 and 11 cause warts and are included under the low risk HPVs,Types 16,18,31,33,45 cause cervical cancer and are included under high risk HPVs(CDC,2014). The virus affects the skin and mucous membrane especially of the reproductive organs. Cervical Cancer and other Ano-genital cancers are seen in women with persistent genital HPV infection. HPV that affects the skin can be transmitted by skin to skin contact with an affected person and Genital HPV is spread through Kissing and Oral
Human Papillomavirus (HPV) is a DNA virus that infects the keratinocytes of human skin and mucous membrane. It is the most common sexually transmitted infection in the world. An estimate of 79 million people in the United States are currently infected with HPV(1). With over 100 types of the virus, at least 40 types can infect the genitalia, mouth and throat. Particularly, HPV-16 and HPV-18 cause approximately 70% of cervical cancers. Transmission occurs through sexual intercourse, but can also occur through non-penetrative sexual activities.
As mentioned earlier, HPV is a non-enveloped, icosahedral capsid, double-stranded circular DNA virus (Morshed, 2014). Infection of HPV occurs in the cervix, glans of the penis, penile shaft, scrotom and anal verge by interactions with putative “host cell surface receptors such as heparin sulfate proteoglycans and alpha-6 integrins” Schafer, 2015; Letian, 2010). Most studies suggest that HPV16 enters the cell via clathrin-mediated endocytosis (Day, 2003, Bousarghin, 2003, Smith, 2007, Hindmarsh, 2007), however, notably, a few contradictory studies suggest that HPV16 is clathrin and caveolaen independent (Spoden, 2008). Once the virus has entered the cell, it then un-coats and delivers its genome (8 genes) to the host cell nucleus to be expressed. These eight genes are named for when they are expressed during the virus’s occupation of its host: early (E) and late (L). The proteins E1, E2, E4 and E5 play an important role in genome replication (Beutner, 1997; Gnanamony, 2007) while E6 and E7 are oncogenes and are capable of causing cancerous growth of host cell (Gnanamony, 2007; Sikorski, 1998). E6 is thought to complex with p53 which is a cellular tumor repressor (Werness, 1990); when E6 complexes with P53, it is thought to promote the degradation of p53 via the ubiquitin pathway (Schffner et al., 1990). This degradation of p53 contributes to the oncogenic potential of high-risk HPVs (Stewart, 2005, Thomas, 1999). Crook showed that E6 can bind with p53
Although the worldwide incidence of Head and Neck Squamous cell carcinoma (HNSCC) has been steadily declining over the past 20 years, it is still the sixth most common cancer by incidence with about 50% of mortality. Traditionally, the most notable risk factors for HNSCC are alcohol consumption and various forms of tobacco use, the combination of the two having a significantly synergistic effect on carcinogenesis. More recently, human papillomavirus (HPV)-associated oropharyngeal cancers are increasing and becoming a significant problem, especially in the young population. The reasons are unclear although it has been postulated that an increased practice of oral sex may be a factor.
It is estimated that 79 million Americans are currently infected with a strand of Human Papillomavirus (HPV), and that 14 million Americans become infected annually (CDC HPV Questions and Answers, 2016). Human Papillomavirus can cause penile cancer in men, cancer of the vulva, vagina or cervix in females, and esophageal, oropharyngeal, and anal cancers in both men and women (CDC HPV Questions and Answers, 2016). Consequently, 27 million Americans annually are diagnosed with cancer from HPV (CD11.7C What Is HPV, 2016). The morbidity and mortality rates for cervical cancer caused by HPV in the United States are 8.1 and 2.4 per 100,000 respectively; worldwide, the cervical cancer mortality rate is