Essay On Hlc Transcriptomes

HeLa cells have had a positive influence on medicine in many ways including with giving us knowledge about the human papillomavirus (HPV) DNA and HPV18-positive. HeLa cells have been linked to changes in microRNA expression. Since HPV18 has been associated with very aggressive adenocarcinomas, this finding may explain why Dr. Gey was surprised by the prolific growth of HeLa cells in culture. Routine Papanicolaou smear screening may not detect rapidly progressive cervical carcinomas; the new HPV vaccine holds the promise of preventing these tumors. (Hutchins).

The HPV virus has gone unseen by many until the recent controversy over the vaccine. However, this virus is thought to be one of the world’s most wide spread STD’s. “According to the Centers for Disease Control and Prevention (CDC), about 6.2 million women and men are newly infected every year” with HPV. HPV has over 100 strains, with more than thirty that are sexually transmitted. Some of these strains are known to cause cervix, vulva, vagina, anus, or penis cancers and others can cause genital warts. “Studies have found the vaccine to be almost 100% effective in preventing diseases caused by the four HPV types covered by the vaccine—including precancers of the cervix, vulva and vagina, and genital warts” (“HPV Questions and

HPV is the number one sexually transmitted infection (STI) in the United States, and anyone who is sexually active is at risk of contracting the virus. HPV is transmitted through intimate skin-to-skin contact with someone who has the virus, and it is so common that most all sexually active men and women encounter a strain without ever knowing they’re infected (CDC). There are many strains of the HPV virus, some of which don’t cause cervical cancer. To help understand and classify the types of HPV, the terms low-risk and high-risk HPV are used. Some

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

Cervical cancer is formed in the tissues of the cervix, an organ that connects the uterus and the vagina. Virtually all cervical cancers are caused by Human papillomavirus (HPV) infections (Schiffman et. al., 2007). HPV is the most common sexually transmitted infection in the United States. According to the CDC, 75% of sexually active people aged 15-49 have the infection at some point in their lives. (CDC). Because HPV infection is usually asymptomatic, infected people do not know exactly when they get the infection. In most cases, the body is able to fight off the virus before any symptom. However, health problems such as genital warts and cancer may

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

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

Human papillomaviruses (HPVs) are a group of more than 200 related viruses. More than 40 HPV types can be easily spread through direct sexual contact, from the skin and mucous membranes of infected people to the skin and mucous membranes of their partners. They can be spread by vaginal, anal, and oral sex. Other HPV types are responsible for non-genital warts, which are not sexually transmitted. High-risk HPV types cause approximately 5 percent of all cancers worldwide. In the United States, high-risk HPV types cause approximately 3 percent of all cancer cases among women and 2 percent of all cancer cases among men. High-risk HPVs cause several types of cancer: cervical cancer, vaginal cancer, vulvar cancer, anal cancer, penile

HPV works like all other viruses, the virus inserts its DNA into the cell and the cell begins to produce the protein that the virus encodes. HPV attacks epithelial cells, epithelial cells are what make up the outside layer of skin on the body, including the cervix. In types 16 and 18 the creation of HPV proteins interferes with the cell’s ability to prevent excessive growth. The cell grows uncontrollably and does not die. This excessive growth is manifested as a precancerous

Human Papilloma Virus (HPV) is a communicable, sexually transmitted disease with high prevalence rates in the general population (CDC, HPV, 2015). Although many people who contract this disease will never develop clinical symptoms, HPV may cause cancer many years later (CDC HPV, 2015). For example, one in every 142 women will develop cervical cancer due to HPV in her lifetime (CDC HPV, 2015). HPV vaccines have been developed and administered in recent years for the prevention of HPV and cervical cancer, but it must be given prior to HPV exposure (CDC HPV, 2015). The HPV vaccine is greater than 90% effective in eradication of the HPV strains that cause cancer (CDC, HPV, 2015). HPV has unique public health implications since it is rare that vaccines can prevent future cancers.

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

Treatment consists of surgery in early stages and chemotherapy and radiotherapy in advanced stages of the disease. An effective HPV vaccine against the two most common cancer-causing strains of HPV has recently been licensed in the U.S. These two HPV strains together are

The early viral genes E6 and E7 can influence both replication and transcription of the virus, and also interacts with host regulatory proteins [2]. Upon infection of the host, the viral genome ring is disrupted leading to its ability to incorporate its genome into that of the host's [2]. Once the viral early proteins interact with the host’s regulatory proteins, the host cells will lose function of regulating tumor suppression, ultimately stimulating the proliferation of the HPV infected cells [2][7]. Papillomaviruses tend to replicate within cells through the lysogenic pathway, and incorporate its viral genome into the host’s genome [7]. Stated earlier, early detection of this particular virus is challenging because the

Methods: We analyzed primary cervical carcinomas, peri-tumor biopsies and lymph nodes in 20 women with invasive cancer (FIGO stage I-II) who underwent radical pelvic surgery and lymphonodectomy. HPV DNA was searched by broad spectrum PCR in 142 DNA samples extracted from paraffin embedded tissues. Viral genotypes were identified by direct sequencing analysis.

In response to this serious health issue, more than 20 years of incremental research culminated in the development of HPV vaccines that elicit strong immunogenic reactions without the risk of causing infection. A review of the literature has revealed that persistent infection with an oncogenic strain of HPV is the known cause of cervical cancer and of the 40 HPV types that affect the genital area, at least 15 types are known to be oncogenic or cancer causative (Armstrong, 2010). Based on clinical trials, HPV vaccination is effective against the occurrence of precancerous lesions and according to Armstrong (2010), studies of the quadrivalent HPV vaccine revealed a 98% protection against high-grade precancerous lesions, whereas for bivalent HPV vaccine 93% efficacy has been demonstrated in females to HPV 16 and 18 who completed the 3-dose vaccine series prior to engaging in any type of sexual actitivities. Cook & et al (2010), acknowledges that there is no research available on long term efficiency of vaccines and also not everyone who initiates the vaccine series completes all 3 doses or completes all doses in the recommended 6-month time frame; this noncompliance and