Anticancer Drugs And Its Effects

According to the oral cancer foundation, “Chemotherapy is the use of chemicals to destroy cancer cells. Chemotherapy works by interfering with the cancer cell's ability to grow. It is one of the three main methods utilized to treat cancer.” With cancer being a potentially fatal disease it is important to diagnose it as soon as possible. the oncologist have to study the chemicals used so that they can determine what chemicals will treat the cancer or disease the best and what chemicals can be mixed together without any major side effects. The drugs can be divided into groups based on how they work, their chemical structure, and their relationship to other drugs.

I can draw from these results that as the chemotherapeutic drug concentration is increased the cell viability decreases. In HEPG2 the viability at the control was 100% but when the drug was added at concentration of 40µm the cell viability decreased to 2.62%. From these examples we can deduce that the chemotherapeutic drug added is successful in its use and that it is targeting the cancerous cells. The drug damages the genes present inside the cell line

In the past, most of the cancer drugs were developed to hinder the growth of tumors. The main strategy was so called “targeted therapies, which interfere with genetic signals that act like accelerators, causing tumors to grow.”1 However, because there are too many pathways and signals that can act as an accelerator of the cancer growth, a single drug was usually not enough to suppress the cancer.

Chemotherapy is a very term used to describe a wide variety of several different ways to treat cancer. "Chemotherapy is treating cancer with drugs. But this is different from most kinds of drug therapy. Drugs that kill cancer do affect the rest of the patient's cells. Doctors try to work with what makes the cancer cells different to find ways to kill the cells without harm to the rest

Tumour cells contain many mutated and misregulated genes, some of which the tumour requires for its survival, growth or metastasis. Overexpressed proteins have previously made good drug targets, for example Trastuzumab targets Her2 in breast cancer and Gleevec targets BCR-ABL in CML. When studying a potential novel drug target, I would search the literature and online databases such as Oncomine to determine whether the gene is known to be misregulated or mutated in human cancers. I would be particularly interested in studies on the effects of tumourigenesis when the potential target has been overexpressed or knocked-down/out,

Chemotherapy is another treatment used to kill cancer. Chemicals kill cancer in this treatment. Sometimes combining chemotherapy and radiation therapy make the treatment more

Cancer unlike other illnesses is very unique in the fact we have to accept a certain level of toxicity well above that of any other group of pharmacologic agents. It is the toxicity of these agents which is the single most important factor preventing their use in doses that could often be curative. Ultimately the utility of most chemotherapy drugs depends on their therapeutic-to-toxic ratio, comparing the good and bad effects (Alwood et al, 1997). Other variables include the severity, predictability and reversibility of side effects. Although we are learning a lot more about the predictive side effects of many individual cancer drugs, most cancer patients require multi-drug therapies. Cancer patients often have chemotherapy regimens consisting of three or four different compounds along with other supportive therapy.

Cancer can’t be cured, but it may be controlled for a time by chemotherapy. Its goal is to stop or slow down the growth of a tumor or shrink it at least partially or to decrease any pain, bleeding, abstractions or any symptoms of cancer. As a result patients may live better and longer.

Chemotherapy is done to either cure cancer or to prolong life. The chemotherapeutic agents used in this process, acts by targeting cancer cells. In this process, they also harm the normal cells in the patient’s body, leading to adverse health effects. Most of the conventional chemotherapeutic agents available today, do not have the expected specificity, and can end up harming normal cells to varying

Cancer is the most prevalent public health challenge worldwide, hence becoming the second leading cause of death in 2013 (cite!). The illness develops when abnormal body cells survive and new cells grow, which are to replace old and damaged ones (cite!). Healthcare professionals associate cancer prevalence with risk factors such as smoking and obesity (cite pg#87) and according to research studies, one in every three individuals will develop cancer (cite!). Such statistics correspond to the occurrence of cancer in the United States, with prostate cancer affecting 105.3 per 100,000 people nationwide (cite!). For the past decade, cancer drugs have increased from $10,000 in the 1990s to $100,000 by 2012; therefore, many patients may die because

There are two types of drug resistance: intrinsic and adaptive (acquired)69,70. In melanoma, the most notorious resistance revolves around mutant B-RAF and its feeder pathway, the ERK cascade, and BRAF inhibitors. Patients who respond well to vemurafenib and dabrafenib treatment at the initial stages would eventually suffer relapse in approximately 6-8 months after treatment and develop a more robust and aggressive recurrence.

According to the Office of National Statistics, in 2013, 29% of deaths in the UK were cancer related, making it the leading broad cause of death in the population. In the United States, 1 in 4 deaths are cancer related, and it is estimated that in a lifetime, there is 44% chance of contracting an invasive cancer if you are male, and a 38% chance if you are female  (Siegel et al. 2014). So, although our knowledge and education into different cancer mutagens such as UV radiation, chemical carcinogens and viruses  (Alberts et al. 2002), as well as cancer physiology and treatments may have improved, leading to a decrease in cancer related mortalities, there are still huge advances to be had in the field  (CRUK 2013).

As can be shown, studying the side effect of chemotherapy is still on going. However, the doctors quickly

WEfforts over the past decade to characterize the genetic alterations in human cancers have led to a better understanding of molecular drivers of this complex set of diseases. Although we in the cancer field hoped that this would lead to more effective drugs, historically, our ability to translate cancer research to clinical success has been remarkably low1. Sadly, clinical trials in oncology have the highest failure rate compared with other therapeutic areas. Given the high unmet need in oncology, it is understandable that barriers to clinical development may be lower than for other disease areas, and a larger number of drugs with suboptimal preclinical validation will enter oncology trials. However, this low success rate is not

Cancer cell have different metabolism compare to normal cell and the modification in the metabolism turn normal cell to cancer cell (Akhdar et al 2012, p.137). In the human body, anticancer drug need to pass several metabolism to change it into other form before it will distributed to the target site and will be excreted through bile or urine. There are two different phases of enzymatic system that anticancer drug will become metabolite, namely phase I and phase II (Gonzalez 2005, p. 71).