Prostate Carcinogenesis Essay

MacLean et al. (2015) addresses the efficacy for the GnRH antagonist TAK-385, based on a three-part, placebo-controlled study. The study examined (n=176) healthy UK males, with the age range of 19 to 75 years old. The first part included the dose of TAK-385 20-mg tablets or a placebo. The 14-day part two included the daily dose of TAK-385 20-mg tablets or a placebo. The 28-day part three included the daily dose of TAK-385 20- or 80-mg or a placebo. In part 1, luteinizing hormone (LH) levels decreased, as well as serum testosterone levels. In part 2, with doses of at least 40 mg/d, LH and follicle-stimulating hormone (FSH) levels decreased and after multiple doses the mean testosterone levels dropped below the threshold for medical castration. In part 3, serum testosterone levels dropped most rapidly and medical castration was achieved. Doses greater than 80 mg/d of TAK-385 reduced the serum testosterone levels below castration levels. Conclusively, GnRH is a valid option for testosterone suppression and ultimately serves as an effective prostate cancer hormone therapy treatment.

Your kidneys are two bean-shaped organs, each about the size of your fist. They're located behind your abdominal organs, one on each side of your spine. Like other major organs in the body, the kidneys can sometimes develop cancer. Your kidneys are part of the urinary system, which removes waste and excess fluid and electrolytes from your blood, controls the production of red blood cells, and regulates your blood pressure. Inside each kidney are more than a million small filtering units called nephrons. As blood circulates through your kidneys, the nephrons filter out waste products as well as unneeded minerals and water. This liquid waste — urine — flows through two narrow tubes (ureters) into your bladder, where it's

Within the Brugge Lab, we have investigated the role of various metabolic pathways in cancer including the role of antioxidants within the tumor cell. Although antioxidants were previously believed to scavenge harmful reactive oxygen species (ROS) and provide a protective benefit against cancer, clinical trials have demonstrated that supplementation with antioxidants actually increased prostate cancer incidence among healthy patients. I joined a postdoctoral fellow in the lab to determine whether depletion of glutathione, the major antioxidant within the cell, would put the cell in a sensitive state that made it vulnerable to inhibition of other major pathways. Through our screening effects, we discovered that triple negative breast cancer cells become exquisitely sensitive to treatment with inhibitors of deubiquitinating enzymes through an induction of a proteotoxic stress response. I look forward to sharing these findings with the scientific community as second author on the manuscript currently in preparation.

Cystoscopy dated 10/15/2014 showed a mild prostatic hyperplasia. The bladder had a mild to moderate trabeculations.

Another factor that contributes to the development of breast cancer is actually the hormone estrogen. This seems unusual because estrogen is a hormone that is essential to the bodies of women in various ways. Estrogen is necessary for normal growth and development of breasts and reproductive organs, as well as for the maintenance of a healthy heart and bones. However, lifetime estrogen exposure may increase a woman’s risk of developing breast cancer. It does not actually produce the mutation in the DNA, nevertheless Estrogen stimulates the proliferation of breast cells that already contain a mutation. These mutated cells will continue to reproduce and have an increased chance of becoming cancerous.

Chemicals are also suspected to cause breast cancer. Xenoestrogens are chemicals with estrogen-like effects, they are found in pesticides and other common industrial products. Other estrogen-like chemicals that have a stronger association with breast cancer include dieldrin and beta-hexachloraocyclohexane. Although these chemicals are very weak estrogens, one study showed that exposure to single weak-estrogen compounds isn’t a big risk but a combination of two or more chemicals result in extremely high estrogenic

Most people think of anti-bacterial chemicals as their protector from dangerous pathogens, but in reality the chemicals can bring some side effects. A study conducted in South Korea stated that triclosan, a chemical anti-bacterial agent, can disrupt the hormonal system. Triclosan is able to mimic estrogen hormone (feminization hormone) thus will alter the normal production of other hormones, such as testosterone. Changes in the level of production will cause an imbalance in the endocrine system and the imbalance will support the growth of abnormal cells. In women, abnormal cell growth is strongly associated with breast cancer cells. This conclusion has been demonstrated in a series of experiments on two groups of laboratory mice.

Various speculations of how cancer is produced have been looked into through numerous years and

Originally, anabolic steroids were created as a gerontological drug that could be used for older patients who were mainly bedridden to keep up their lean body mass, being that they had a lack of appetite, and did not exercise (Dobbins, B. 1996). The developments of anabolic steroids were used to enhance the anabolic effect without having the androgenic aspect; masculinization, due to the fact that it led to other unwanted effects. The unwanted effects are prostate hypertrophy and male pattern baldness. During the research project, a powerful oral steroid called Dianabol was given to a few patients. However, over time, many of those patients reported that this steroid caused negative side effects, such as liver damage (Dobbins, B. 1996). There are significant dangers that have to be considered before using anabolic

Prostate cancer is the one of the most lethal disease in the United Sates. The pattern of disease recurrence being the major cause of morbidity and mortality. In spite of recent advances in our understanding of the molecular mechanisms responsible for the development of prostate cancer, the survival rate of men with this disease has remained relatively unchanged in over the decades. Since the Nobel prize winning discovery by Dr. Huggins and Dr. Hodges (Huggins C., 1941) androgen deprivation therapy is being used by over a half of a century as a primary treatment for advanced prostate cancer. Even though androgen deprivation therapy remains a palliative treatment which lasts around 2-3 years on average, and turn to hormone-refractory (androgen-independent) prostate cancer with castrate level of testosterone. However, studies from the Sawyers group and others found that castration-resistant prostate cancers (CRPCs) remains on androgen receptor (AR) signaling which is reactivated despite low serum androgen levels and targeting the androgen receptor (AR)-signaling pathway remains a keystone of treatment.

Such findings, all of which relate to hormone-based life events, suggest that breast cancer is somehow affected by prolonged exposure to female sex hormones, such as estrogen. Women with a history of breast cancer in the family are also at greater risk. About five percent of all breast cancers have been attributed to a mutated, or structurally altered, gene known as BRCA1. Mutations in a second gene, BRCA2, contribute significantly to the development of breast cancer in Jewish women. Alcohol, high levels of fat in the diet, and not exercising regularly have also been linked to increased risk for breast cancer (Garber).

Current research is focusing on the role of ‘neuropeptides’ and ‘neurotransmitters’ in the occurrence of cancer. Researchers have observed that cancerous cells require nutrients and the diffusion of oxygen to proliferate malignantly. In this aspect, stress-related hormones act as inhibitors or stimulants to cancerous growth depending upon the type of hormone and the type of cancer. It has been established that ‘-agnostic

The impact of certain estrogenic xenobiotics on the reproductive system development and health of animals has been clearly documented. Findings, such as ours demonstrate thathumans are also exposed at risk. As data accumulate regarding to infertility, genital tract malformations and increasing cancer rates in estrogen target tissues (especially the breast),

Estrogen treatment: Estrogen-related drugs are sometimes used in hormonal therapy of men with prostate cancer. This treatment may cause a slight increase in breast cancer risk. However, this risk is small compared with the benefits of this treatment in slowing the growth of prostate cancer. Men taking high doses of

In 2002 a study conducted found that parabens mimicked the hormone estrogen by binding to estrogen receptors on cells. The study also discovered that parabens increase the expression of genes usually regulated by estradiol, the genes that cause human breast cancer cells to grow and