Essay On Prevalence Of Human Papillomavirus, Associated Oropharyngeal Cancer

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

From 1998 to 2003, the incidence rates for HPV-associated cancers of the tonsils and tongue increased 3.0% per year, while non-HPV cancers of the mouth and throat decreased during this time (Ramqvist and Dalianis, 2010).

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

Human Papilloma Virus (HPV) accounts for the third most prevalent cancer in females worldwide,15 as it is the most common sexually transmitted infection (STI).2 There are more than 100 subtypes of HPV; 16 of those subtypes are known to be high-risk.15 HPV is a crucial precursor to cervical cancer in 99.8% of those affected,2 with subtypes 16 and 18 being the most common types.15

Hpv is a virus that produces epithelial tumours in both the skin and mucous membranes2, however these tumours have different probabilities of forming cancers according to the subtype of the virus causing the infection for example tumours due to Hpv 16, 31, and 70 have a high probability of forming tumours where as Hpv 84 has a much lower risk of turning the tumour malignant3.

a. The rise in oral cancer cases is being described as a pandemic in young adults

The human papilloma virus (HPV) is the most common sexually transmitted disease, with a worldwide point prevalence of 11.7%., in the United States over 79 million people are already infected with HPV, and over 14 million new HPV infections occur each year CITE 1,2,5. HPV affecting both men and women, has an estimated lifetime prevalence of 80-90%, it is likely that most sexually active people will become infected with HPV before the age of 45 CITE 1, 3. Although over 100 HPV genotypes have been identified, only 40 infect the genital area. These 40 are further subdivided into high risk oncogenic genotypes, and low risk the genotypes responsible for genital warts and recurrent papillomatosis CITE 8,3. HPV is associated with virtually all cervical cancers, and over 90% of anal cancers CITE 1. The cost of preventing and treating HPV and its associated diseases is estimated at eight billion dollars annually

In the United States, cervical cancer is known as one of the most common cancers amongst females and it is estimated that 1/3 of the females diagnosed will die (Parkin, Bray, Ferlay, & Pisani, 2005). HPV 16 is the most common detected virus in cervical cancer patients, but there are 14 HPV types that are considered high-risk (Parkin, Bray, Ferlay, & Pisani, 2005). HPV is related to cervical cancer as the virus changes the cells of the cervix and causes cervical dysplasia, which untreated, leads to cancer (Dizon & Krychman, 2010). Examining the problem from a global perspective, Biological Study on Cervical Cancer (IBSCC) study group, concluded that “HPV DNA was detected in 93% of the tumors and … HPV 16 was present in 50% of the specimens…” (Bosch, Manos, Muñoz, Sherman, Jansen, Peto & Shan, 1995). This group collected samples of 1000 patients whom were diagnosed with stage 3 cervical cancer from 32 hospitals in 22 countries (Bosch, Manos, Muñoz, Sherman, Jansen, Peto & Shan, 1995). As, represented earlier with current statistics, it’s evident that more people are diagnosed each year with cervical cancer that have HPV present

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

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

Oropharyngeal (oral) cancer can be associated to the exposure of HPV strain type 16 which is high risk. This strain type is believed to be caused by the changes in sexual practices. Though oral cancer due to HPV is very rare, it’s still cause cell changes in the oral cavity. HPV has been detected of approximately 26% of all squamous-cell carcinomas of the head and neck (D 'Souza et al., 2007). HPV positive oral or throat cancer are starting to become more prevalent among adolescents and adults. About 3% of men and few percent of women have HPV 16 found in their saliva (Human HPV and Throat/oral cancer, n.d). Individuals who have more than 3 or 6 sexual partners and perform various sexual practices are usually at an increased risk of contracting the virus.

Human papillomavirus (HPV) is a common sexually transmitted infection. HPV family of viruses comprises many oncogenic and non-oncogenic types that cause anal, penile, and oropharyngeal cancers and anogenital warts in men respectively. Men who have sex with men (MSM) are at particularly high risk for HPV infection and HPV-related disease (Markowitz et al., 2014). In one study, oncogenic HPV types 16 and/or 18 were detected in 37% of MSM between ages 16 and 30 years (Glick et al., 2014). Anal cancer rates are more than 17 times higher among MSM compared to their heterosexual counterpart (Daling et al., 2004, Joseph et al., 2008; Machalek et al., 2012). Anal cancer rates are even higher among HIV-positive MSM (Silverberg et al., 2012). Moreover, recent data revealed a rapid increase in HPV associated oropharyngeal cancers rates among men in the United States (Charturvedi et al., 2011). Aside from cancer, HPV associated anogenital warts negatively affect quality of life and are expensive to treat (Woodhall et al., 2011). Close to 7% of gay and bisexual men report history of genital warts. (Dinh et al., 2008)

Of the more than 100 known strains of HPV, fifteen types have been found to be the most carcinogenic and contribute to 95% of all cervical cancers. HPV-16 accounts for at least 50% of all cervical cancer while HPV-18—the second most carcinogenic—accounts for at least 10%. At the same time, HPV-16 alone accounts for more than 80% of all vulvar and vaginal cancer (p. 250). But cervical, vulvar, and vaginal cancers represent only a portion of the carcinogenic effects of HPV. Nearly a decade after the studies that linked HPV to genital cancers, Cleveland et al. (2011) completed a meta-analysis study of The Cochrane Library and the National Guideline Clearinghouse between January 2005 and May 2011, finding that “HPV-16 alone is associated with 85 to 95 percent of oropharyngeal cancers” (p. 917). Furthermore, the meta-analytical study of more than one million women on five continents by Bruni et al. found that between 14.0 and 24.0% of women studied were infected with a form of potentially cancer-causing HPV (p. 1790). Prior to Bruni et al.’s study, it had been presumed that only 10% of the world’s women were infected with HPV (de Sanjose et al., 2007), the true rates being 40% to 140% greater than expected. In other words, once a direct cause-effect relationship between HPV and cancer was found, the need to prevent HPV infection became an exigent, global issue for both men and women’s health.

The mucosal lining of the oropharynx and oral cavity are becoming areas of concern in diagnosing cancer of the head and neck. The oropharyngeal squamous cell carcinoma (OPSCC) is one histological types of carcinoma that is rising in incidence on the base of the tongue and in the tonsil area in the back of the throat [17][18][19]. Following infection of the tonsillar crypts, HPV integrates its genome into the host genome, expressing the E6 and E7 proteins responsible for the oncogenesis of this virus [17]. The demographic of individuals diagnosed with oropharyngeal squamous cell carcinoma are not clinically defined by smoking history or excessive drinking, these individuals are generally white males

HPV detection may be performed by means of a variety of methods, including p16 as a surrogate immunohistochemical marker, in situ hybridization and/or polymerase chain reaction detection of viral DNA or RNA [4,46–48]. Chandan et al found glucose transporter-1 immunostaining to be a useful adjunct in differentiating BrCC from cystic metastasis of H&N SCC [49]. Pai et al reported that p16INK4A immunohistochemical staining was helpful in distinguishing BrCC from cystic metastasis H&N SCC originating from the oropharynx [50]. Based on our proposed algorithm,