Essay on Bacteria are the Causative Agents of Malignancy in a Human

Stomach cancer, also known as gastric cancer, is a type of cancer that develops slowly over many years. Most frequently, stomach cancer starts in the lining of the stomach otherwise knows as the mucosa, and then develops into the other layers of the stomach. There are many ways in which stomach cancer spreads. In some cases it invades near by organs or it can also travel through the bloodstream to for cancer in other organs. There are many statistics and organizations of support for stomach cancer, as well as, symptoms, risk factors, screening and diagnosis’ and, treatments. Like all cancers, stomach cancer is a deathly disease and one of the major leading causes of cancer deaths in countries other than the U.S.

Even though H. pylori is a "neutralophile", it can survive in the very acidic environment in the human stomach due to a variety of acidic-adaptive mechanisms, such as the ability to utilize urease to break down urea

H. pylori thrives in the acidic environment of the stomach and the finding that this bacteria contributed to the condition was remarkable news and led to the standard practice of treating peptic ulcers with antibiotics. As a result, the rate of H. pylori-induced ulcers has dropped by more than 50 percent. (Ackerman, 2012)

Have you ever wondered how cancer forms? Well, cancer starts when a cell's DNA becomes

According to the National Cancer Institute, not all human papillomaviruses (HPV) cause cancer. There are two types of categories; the low risk and high risk human papillomaviruses. If one contracts a high risk HPVs, they have a chance of developing cancer. High risk HPVs can lead to cervical cancer, anal cancer, oropharyngeal cancer, vaginal cancers, vulvar cancers, and penile cancers (1). The National Cancer Institute states that HPVs account for causing 5% of cancers and Nathan Seppa proclaims “that the two cancer-causing virus subtypes... HPV-16 and HPV-18, account for more than half of cervical cancers” (1 and 2). This demonstrates the overall impact HPV has on causing cancer.

Many humans in the world suffer from cancer. This disease has caused many people to lose their life or even their loved one’s life. Researchers have done many studies to try and tackle this deadly infection, but everything they have tried has either caused cancer to progress or come

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

H. pylori relies heavily on the activation of the host inflammatory response in order to utilize host metabolites as well as various cytokines, and chemokines, namely IL-8. Given the knowledge on H. pylori genetic diversity, it is important to note the functionality of the cag pathogenicity island (cagPAI) encoded by H. pylori’s genome. This pathogenicity island along with the plasticity zone is a major contributor to the development of disease from pathogenic strains of the bacteria. The cag pathogenicity island also encodes for H. pylori’s Type IV secretory system used to transport virulence proteins. CagPAI activation of the inflammatory response in the stomach also results in the apoptosis of T cells. All these factors and more contribute to H. pylori’s persistence in the host and mechanisms for inducing disease. The following pages will detail how genetic diversity along with the utilization of the Type IV secretion system and vacA toxin cause such severe gastric carcinogenesis and ulcer formation, as well as the role horizontal gene transfer has on strain specific diversity and pathogenesis of

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.

pylori in a common infection, the host undergoes a period of rapid bacterial duplication and subsequent inflammation following colonization of the viscous mucus layer of the stomach. The penetration of the layer is assisted by the bacteria’s flagella and spiral morphology. The low oxygen level and neutral pH of the mucus act as a prime environment for the microaerophilic H. pylori. (Kusters, 2006) Preferably a lumenal pathogen, host cells are rarely invaded by the microbial. Associated with the inflammation is hypochlorhydria that can persist for months, during which the pathogen is released through fecal shedding in large amounts. After at least a few weeks, an immune response develops but it is not very effective in removing H. pylori. Eventually the inflammation subsides to a stable state and the infection becomes asymptomatic but may persist for decades. (Blaser,

The E6 and E7 proteins play and important rule in oncogenic property of human papillomavirus that can cause anogenital cancers as their high risk factor and warts as their low risk factor. E6 AND E7 proteins promote cell growth by inactivating the tumor suppressor proteins P53 and PRb (5).

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

Viral Oncology is the study of virus caused cancers. These cancers include Adult T-cell Leukemia, Kaposi’s Sarcoma, Cervical Carcinoma, Hepatocellular Carcinoma, and Burkitt’s Lymphoma. Viruses that can cause cancer are known as oncoviruses. Known oncoviruses are: Hepatitis B and C (HBV and HCV, respectively), Human T- Lymphotropic Virus (HTLV-I), Human papillomavirus (HPV), Kaposi’s Sarcoma- Associated Herpesvirus (HHV-8), and Epstein- Barr Virus (EBV).

The article published by News Rx in Health and Medicine Week in 2007, “Cancer; Cancer-fighting virus shows promise in early clinical trial”, the researcher uses a virus called “NV-1020”, a modified herpes simplex virus that replicates in cancer cells and kills them. It does not affect normal, healthy cells, just like the JX-594 virus, and the expectation is to fight cancer without affecting the rest of the body with side effects. A trial was conducted in patients with colorectal cancer metastatic to the liver, showing positive results. In one of the cases presented, a patient with cancer spread to the liver and lungs, was given the virus, and followed by chemotherapy. After six months, the liver masses had noticeably reduced in size, almost disappearing. After the treatment, the patient survived for another 12 months, a longer life expectancy compared to the usual prognosis of three to four months of life. The treatment seems to be tolerable and safe for the patients, and researchers are hoping to extend survival time. The latest findings show that the virus is effective in killing colorectal and liver