Gene And Protein As A Therapeutic Agent For Cancer

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

It has broad variety of anti-tumor activity and forms the backbone of combination chemotherapy regimes presently

Besides inducing apoptosis and controlling the cell cycle, p53 has been demonstrated to be a central component and key regulator of the metabolic stress machinery. The metabolic balance between glycolysis and oxidative phosphorylation is heavily coordinated by p53 activity, which is activated by

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

Cancer is a disease caused by an uncontrolled division of abnormal cells. The DNA sequence in cells can be changed as a result of copying errors during replication. If these changes whatever their cause are left uncorrected, both growing and non-growing somatic cells might gain many mutations that they could no longer function. The relevance of DNA damage and repair to the generation of cancer was obvious when it was recognized that everything that causes cancer also cause a change in the DNA sequence. Tumor suppressor genes are protective genes and normally they limit cell growth by monitoring the speed of cell division, repair mismatched DNA and control when a cell dies. When a tumor suppressor gene is mutated cells grow

There are twelve major types of cancer that affect most Americans and they can be related by the mutation of genes. Cancer is not just one disease, but a massive group with over 100 diseases by unrestrained and vicarious growth of the cells in the body and have the ability of the cells to propagate. One out of every four Americans will die from cancer. It is the second leading cause of death in this country, surpassed only by heart disease. Five to ten percent of cancer are genetic and hereditary. 1.2 million new cases are found in every year the United States, “Men have a one in two lifetime risk of developing cancer, and for women the risk is one in three” (Freivogel 201).

Cancer known in medicine as a malignant neoplasm is one of the biggest killers worldwide. In 2007, cancer caused roughly 13% (7.9 million) of the planet’s deaths (Jemal, 2011). This will more greatly affect an aging society such as ours in years to come, and yet it is already the foremost cause of death in the developed world. The main reason cancer causes so many fatalities the body’s inability to mount an effective response to the failure of DNA replication within the body. This results in a mass

Drug discovery is expensive and challenging. One such challenge is identifying clinically active cancer targets out of a huge number of biomolecules that are known to have a role in cancer initiation and progression. Below I have outlined the key information that should be gathered about a novel drug target, the experiments that are required to validate such a target, and discussed what needs to be considered when deciding whether a target has been validated.

In America today finding a cure for cancer is a huge priority with clinical trails being a big part in these goal there are some newly developed drugs and technology that are making a huge impact in the cancer world.

Cancer is a leading cause of death and devastating experiences for patients’ family members and close friends. The disease undermines the emotional wellbeing of the survivors during and after treatment. It often affects the physical appearance and exposes the family members to financial constraints thereby leading to depression, reduced productivity at workplaces and many other social problems. However, the controversies over the causes of cancer continue to impact the awareness campaigns and the general population attitude towards treatment options. According to Thun, Linet, Cerhan, Haiman, and Schottenfeld (2017), many people believe that gene composition is the leading risk factor for cancer. In contrast, etiological studies have confirmed

Hu, Jing, Hui Jing, and Hening Lin. “Sirtuin Inhibitors as Anticancer Agents.” Future medicinal chemistry 6.8 (2014): 945–966. PMC. Web. 9 Apr. 2017.

The functions of telomeres includes protection of chromosomes from degradation and end to end fusions, maintains the stability of chromosomes, acts as a mitotic clock to understand the replicative history of a cell.Telomerase is a ribonucleoprotein DNA polymerase that helps in maintaining the telomeres by adding TTAGGG repeats at the ends of chromosomes (Greider and Blackburn,1989). Telomerase consists of two main subunits: telomerase RNA (hTR) and catalytic component human telomerase reverse transcriptase (hTERT). The enzymatic activity is usually absent in somatic cells but remains active in germ line cells,embryonic stem cells and tumor cells. Almost 80 to 90% of human cancers are characterized by the presence of telomerase activity.Studies on glioma shown that more than 50% of tumors have telomerase activity and its detection rate increases with the grades of malignancy (Tchirkov et al 2003). Therefore knockdown of hTERT expression may help in the development of novel therapeutic strategies. In the present study we evaluate the effect of siRNA to downregulate hTERT in LN18 cells and also investigated the effect on apoptosis and cell

TP53, also called tumor protein 53 is a tumor suppressor gene that encodes p53 and acts as a control center for the cell to act on when stressed (Brachova). Human p53 is a nuclear phsophoprotein of molecular weight 53kDa located on chromosome 17 containing 11 exons and 10 introns (Ling). One of its primary roles is as a transcription factor and in its active state is a homotetramer comprised of four 393 amino acid residues (Joerger , The tumor suppressor p53). Another main role p53 plays is as a tumor suppressor and once activated, protects against cancer by “functioning as a sequence-specific transcription factor, through protein-protein interactions, activating cell cycle arrest, apoptosis, and DNA damage repair (Brachova).”

This review will provide a brief investigation of current cancer therapies and the lack of effectiveness that these treatments provide while treating the disease. The aim of this review is to discuss the urgent need to develop new and effective cancer therapy options that can bridge the gap between the various types of cancer and effective cancer targeting.

It may be possible to correct an abnormality in a tumor suppressor gene such as P53 by inserting a copy of the wild-type gene; in fact, insertion of the wild-type P53 gene into P53-deficient tumor cells has been shown to result in the death of tumor cells (3). This has significant implications, since P53 alterations are the most common genetic abnormalities in human cancers. The over expression of an oncogene such as K-RAS can be blocked at the genetic level by integration of an antisense gene whose transcript binds specifically to the oncogene RNA, disabling its capacity to produce protein. Experiments in vitro and in vivo have demonstrated that when an antisense K-RAS vector is integrated into lung cancer cells that over express K-RAS their tumorigenicity is decreased (4).