Powerful genotoxic reagents such as Mitoxantrone, Docetaxel, Hydrogen Peroxide, Bleomycin and radiation have been recently investigated in PSC27(Normal Human Prostate Stromal Cell Lines) cell lines and prostate cancer cell lines such as PC-3, LNCaP, DU145, BPH1 and M12 cells. These chemotherapy reagents are ultimately DNA-damaging mechanisms that break hydrogen bonds and DNA strands in DNA. There are great implications associated with the employment of chemotherapy agents. Patients who have prostate cancer are often subjected to one or five of those core treatments. But recent studies have shown that 90% of patients with metastatic carcinomas experience some type of resistance, because these chemotherapy agents essentially induce the overexpression of the WNT16B protein in PSC27 cells that are located in surrounding tumor areas. Once this expression has occurred significantly, it reduces the overall competency of chemotherapy agents and results in its ineffectiveness. This is a huge problem for the patient and those who make these chemotherapy agents. To test for the expression of the WNT16B protein, an RT-PCR (Reverse-Transcription Polymerase Chain Reaction) analysis will be conducted for LNCaP and PC-3 cells treated with Mitozantrone, Docetaxel and Hydrogen peroxide before and after treatment process.
Introduction
Current research has profoundly indicated that there are negative implications associated with the employment of chemotherapy agents among prostate cancer patients. The recently publish article from 2012, titled “Treatment Induced damage to the tumor microenvironment promotes prostate cancer resistance through WNT16B,” showed a clear analysis of how genotoxic reagents such as Mitoxantrone, Bleomycin, Docetax...
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...xicity of chemotherapy agents inducing the expression of the WNT16 gene it can also render other negative consequences. The chemotherapy drug Mitoxantrone can engender debilitating health implications such as heart failure and progress one’s chances of acquiring acute leukemia. The drug Docetaxel can promote cardiotoxicity or heart damage. The drug Bleomycin promotes pulmonary toxicity. These are some of the few negative consequences in which these drugs can render, in which prostate cancer patients use. There is a long laundry list of side-effects, and high death rates and resistance associated with the use of the chemotherapy agents.
Works Cited
Sun, Y., Campis, J., Higano, C., & Beer, T. (2012). “Treatment-induced Damage to the
Tumor Microenvironment Promotes Prostate Cancer Therapy Resistance Through WNT16B." Nature Medicine. 18(9), 1–23.PDF
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The concept of tumor heterogeneity being related to the course of the disease and clinical outcome in cancer patients draws additional attention in the era of personalized medicine (1). Current cancer treatment strategies are based on the site of origin of the primary tumor. However, it was shown that tumors developed from distinct cell types differ in their prognosis and response to cytotoxic therapies (2...
Pharmaceuticals have examined and found to ”work by changing the biological functions of the target cells in the body through chemical agents“ (Doweiko, 2015, p. 16). ”Many people in the past have thought that drugs that
In 1896 the scientist Beatson reported that the removal of the ovaries resulted in the reduction of breast cancer tumours (Russo and Irma 1998). Breast cancer is a malignant, metastasizing cancer of the mammary gland. It is the leading cause of death in woman between the ages of 35 - 45. Breast cancer can also occur in males, although less frequent, around 400 men die each year from breast cancer in the united states. (Martini, F., 2004). Studies on rats have shown considerable evidence that rat oestrogens are mammary carcinogens. Oestrogens have shown to stimulate the hormone prolactin. Through studies involving the use of antioestrogens, for example, tamoxifen, "Tamoxifen alone or in combination with the retina all trans-N-(4 hydroxyphenyl)-retinamide (4-HPR) reduces the incidence of NMU-induced mammary tumours in Sprague-Dawley rats." (Jane M. Ussher Ph.D. 1996). This suggests that Oestrogens and Prolactin's can have the effect of the development of breast cancer since the pathogenesis of spontaneous breast cancer in humans is similar to that of chemical-induced rodent mammary cancer. (Jane M. Ussher
Chemotherapy drugs are more dangerous than other drugs because of their narrow therapeutic index. What is therapeutic index you ask? It is the ratio between a toxic dose and a therapeutic dose of a drug so any medication error with chemotherapy drugs could be a fatal one. Chemotherapy drugs can be very toxic even at the prescribed therapeutic level recommended by the physician. The findings in this article shows that the patient themselves are the first line of defense in spotting errors in medications they receive because they obs...
Thought to be an oncogene, a gene that has potential in transforming normal cells into tumor cells, p53 was regarded as the most prominent tumor suppressor gene [1]. P53 is a gene which signals apoptosis (programmed cell death) if a cell cannot be repaired due to an extensive amount of damage. As stated in the textbook, p53 regulation occurs by an E3 ubiquitin-protein ligase known as MDM2 [1]. "Controlling the controller" is a statement that describes the molecular interaction where the presence of MDM2 targets the p53 for proteosome via degradation. With three main checkpoints in cell cycle, the literature states p53 functioning from G1 into S phase in a chaotic cell [2]. The normal state of cells is to keep p53 levels low in order to prevent uncontrolled apoptosis and random cell cycle arrest from occurring. In a further note, although p53 promotes apoptosis and cell cycle arrest, cancer may result from p53 unable to recognize the problematic site. In turn, a mutation in p53 may result engaging in new activities. These activities include cellular transformation, tumor metastasis,...
During the winter of my sophomore year of high school my aunt, whom I am very close with, was diagnosed with stage three ovarian and cervical cancer. She underwent various surgeries and chemotherapy treatments, spent weeks in the hospital, and many more weeks battling the effects of the chemotherapy from home.
The article begins by stating that the tumor suppressor p53 has great importance in the prevention of cancer growth and expansion. Although cancer is the most spoken about topic and p53’s significance against it, p53 also has a hand in ischemia, neurodegeneration, and ageing. While this tumor suppressor seems to be very busy it also regulates the repair of DNA and death of the cell, just to name a few. The activity of p53 can be seen when binding to the DNA at target sequences for transcription. It was pointed out that the doings of p53 are not designated to the nucleus such as other transcription factors as determined over time. Further mentioned in the introduction is a statement that lists this as the most studied mechanism while also related to the material covered in class is apoptosis. P53 inducts apoptosis in the by intrinsic mitochondria-mediated pathway, also transcriptionally through pro-apoptotic parts of the pathway, and in a transcription–independent way which has been recently been looked further into. As if the roles above were not plentiful enough cytoplasmic p53 is also thought to influence autophagy, movement of vesicles, signal transduction, cell metabolism and possibly stem cell expansion, but all are truly determined. Towards the end of the introductory section the authors state that there are still many mechanisms of cytoplasmic p53’s activation leading to apoptosis that are uncertain as well as some p53 missense mutants that lead to oncogenesis. The authors express that the article mainly will speak about the proper or improper activities performed by p53 on the mechanism in the cytoplasm while also looking for areas where beneficial treatments may be used.
Newbold, R. F. (2002). The significance of telomerase activation and cellular immortalization in human cancer. Mutagenesis, 17(6), 539-550.
Cancer is a genetic disease because it can be traced to alteration within specific genes, but in most cases, it is not an inherited disease. The genetic alterations that lead to most cancers arise in the deoxyribonucleic acid (DNA) of a somatic cell during the lifetime of affected individual. Because of these genetic changes, cancer cells proliferate uncontrollably, producing malignant tumour that invade surrounding healthy tissue. As long as the growth of tumour remains localized, the disease can usually be treated and cured by surgical removal of tumour. But malignant tumours tend to metastases, that is, to spawn cells that break away from the parent mass, enter the lymphatic or vascular circulation, and spread to distant sites in the body where they establish lethal secondary tumours (metastases) that are no longer amenable to surgical removal. Despite, various exogenous and endogenous factors are known to affect the normal pattern of cell growth, by which cell becomes a cancerous. Species specificity and identity of biological organisms maintain by the unchanged genomic structure throughout their life period. The ratio of cell growth and cell death is strictly balanced through developmental and homeostatic processes in multi-cellular organisms (Bolsover et al, 1997).
Cancer has been seen in humans as one the most potentially fatal disease for thousands of years and only in the recent couple of hundred years have we discovered that most information necessary to bring us to today’s understanding and knowledge (Kenny 2007, Weinberg 1996) was achieved by extensive research of cells, DNA, and epidemiology studies. As we know, currently cancer is acknowledged as having over a hundred different diseases, and is known to be the result of mutations of the genes and almost similar DNA which are responsible for the amount of cell division and production (Kenny 2007). Restraint of cell growth modulators can be a direct lead and result of certain tumours being developed and subsequently allow these tumours to acquire the ability to attack and occupy the bloodstream and essentially be able to travel via the bloodstream to other parts and organs in human bodies which is known as metastasis (Loeb et Al 2003). Once this has occurred , the cancer is then categorized as malicious and becomes a dangerous and serious threat to the carrier (Weinberg 1996). In this essay I will describe and explain the process of this and how our genes mutate and lead to metastasis of cancer cells.
While chemotherapy is beneficial at curing or helping a disease such as cancer, it can has a negative effect on a person’s body too.
Cancer develops when cells in a part of the body begin to grow out of
These oncogenes cause cancer because they do not allow the cells to self-destruct or become epistatic. There have been several research projects which have been testing epistatis. Transfecting DNA To perform the experiments for this research, the researchers had to grow certain pieces of DNA.... ... middle of paper ...
25 April 2014. Muller, F. Toxicological Sciences. 2014. The 'Standard' of the 'Standard'. 24 April 2014. National Cancer Institute.