The Impact Of Traditional Chemotherapeutic Agents On Patients

One of them is Gleevec (Imatinib mesylate), a tyrosine kinase inhibitor, was called a “magical bullet”. This was the first targeted therapy drug used to treat cancer. It was invented in the late 1990’s, to treat “chronic myeloid leukemia and gastrointestinal stromal growth”. Imatinib is tyrosine kinase inhibitors. Tyrosine kinase is a protein that cells use to signal to each other to grow (Iqbal and Iqbal, 2014, p.1). It works by preventing a tyrosine kinase enzyme and therefore inhibits growth factor-induced receptor phosphorylation and blocks the PDGF/PDGFR and P13-k/Akt pathway (Kheradmand, et.al.2016, p.83). According to Richardson (2010, p.679), the drug Velcade was also known as “Bortezomib” is useful in the treatment of multiple myelomas. The main goal of this drug is to lower the tumor growth significantly. The American cancer society (2013, para.20) studies show Bortezomib is a “proteasome inhibitor”. It works by blocking or slowing down the action of proteosome is to break down protein in both healthy and cancerous cells. When proteosome activity is blocked, proteins in the cells accumulate. This accumulation may cause cells to stop growing and multiplying, and cause them to die and Sutent (Sunitinib) is a drug used to treat metastatic renal cell carcinoma. It is currently approved as a second-line treatment of MRCC. Sunitinib inhibits the vascular endothelial growth factor receptor and stops the growth of tumors (Kolesar, et.al. 2008, pp.123 131). It is considered as a multi- targeted kinase inhibitor because it is a type of VEGF inhibitor, an angiogenesis inhibitor, and it blocks an enzyme called tyrosine kinase. By doing all of this, it slows cancer growth and keeps tumors from making their own blood vessels to help them grow and spread (American

Imatinib is a Abl/c-kit/PDGFR inhibitor. Abl is a proto-oncogene related with chronic myelogenous leukemia. c-kit is a protein on the surface of various types of cells. PDGFR is a cell surface tyrosine kinase receptor for members of the platelet-derived growth factor family.

Some of traditional drugs may be effective in patients whose cancers have a specific molecular target, and not for other patients. To solve this problem of patient-specificity, pharmaceutical research have seen the expansion of individually tailored cancer treatment, which is an application of targeted therapy, and this is where biopharmaceuticals are. As an increasing part of the population is diagnosed with cancer and as these patients live longer, increasing care will be given to patients who have received these drugs. Moreover, in the case of cancer therapy, those drugs and especially with mABs are a promise of less side effects : recombinant DNA technology makes it possible to genetically engineer an antibody to reduce the risk of host immune response.

A team from the Brazilian university says the experimental drug binds with tumor cells and causes the loss of key molecules.

While the steps to bring a new drug to market may seem extensive and costly, they are a necessity. Clinical drug trials provide options for people with diseases while also allowing doctors to improve the way they diagnose and treat these diseases. The process is long, but the benefits that new drugs have to offer, is

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.

Opdivo was approved previously to treat advanced melanoma among people who don 't respond to other medicines. ( 'FDA Expands Approved

To first identify novel drug targets, I would thoroughly search the literature, look at online cancer resources and discuss potential targets with scientific experts at the Beatson and externally. Below I have outlined the key information that should be gathered.

Abl is known to mutate its kinase domain so that Gleevec cannot effectively inhibit it and cellular proliferation (Lovera et al., 2015). A western blot will be run to determine the extent this mutation will affect our experiment at the beginning and 4 months into our experiment. Some tumors from all three cell lines will have their cells lysed and run through the gel, which will test for both Abl and Abl-Gleevec compound, as well as a major substrate for Arg-Abl, ArgBP2.

In 2016 the FDA gave breakthrough status and approval, which will allow hundreds of patients to be treated

In February 2013, an anti-HER2 antibody trastuzumab was approved by the FDA following the positive outcome of the Phase III EMILIA trial.

The Inter-Individual response to pharmacotherapy can range from no response to adverse drug reactions that can be life threatening.

BRAF is a gene target that affect downstream protein synthesis. BRAF inhibitors will target the melanoma cancer cells. If BRAF is inhibit this will have a impact on the cancer cell, it will stop the cell during cell cycle, and prevent from carrying out different function or produce protein. These inhibitors are target process that affect abnormal pathways. This can also prevent the tumor cell from growing. One of the most common BRAF inhibitors is called Vemurafenib.

Other formulations of TKIs include erlotinib (Tarceva), canertinib, vatalanib, dasatinib, and sorafenib to name a few. This manuscript will be discussing Imatinib Mesylate in further detail and reviewing many of the pharmacological and antitumor and anticancer properties of the drug in more detail. The use and increased acceptance towards targeted cancer therapies is not without its imperfections. As with any medication or therapy, not every individual is the same and the overall response rates may change from person to person and from population to population. As more research is done, the introduction of new inhibitors as well as the improvement of current inhibitors will help to increase the overall response rate in patients as well as help to increase the ability for patients to receive even more selective and specific care for their disease.

Phase I trials can involve toxicity and only provide a minimal chance of direct benefit to the child – 6.8% for single novel agent and 20.1% for novel agent/known anti-cancer drug combination4