Oncogenes, also known as “cancer promoting genes”, are specific genes whose mutations can lead to the excessive proliferation of cells and lead to the development of cancer. These genes are divided into classes based on their “cancer-promoting” abilities (Alberts 2007). Proto-oncogenes are the first gene class. They cause a “gain-of function mutation” which can lead a cell to a proliferative cancer form (Alberts 2007). The resulting mutant, which is then “overactive or overexpressed” is the oncogenic form (Alberts 2007). The second class of these genes are ones that cause a “loss-of-function mutation”. These are tumor suppressor genes, which can also lead to cancer. Both of these gene classes have similarities in the ways in which they contribute to cancer proliferation, and are therefore considered to be “flip sides of the same coin” (Alberts 2007).
One of the recent developments in the research behind oncogenesis and its relationship to cancer is the theory of “oncogenic addiction”. This theory explains the phenomena of “a tumor cell seemingly exhibiting dependence on a single oncogenic pathway or protein for its sustained proliferation and/or survival” (Sharma & Settleman 2007). These findings suggest that there may be a way to “switch off the crucial pathway of dependence”, which in theory should negatively affect or inhibit the cancer, “while sparing normal cells that are not similarly addicted” (Sharma & Settleman 2007). This has been established with the ability to inactivate “counterparts of oncogenic proteins in normal tissues” and see that there is toleration without “obvious consequences” (Sharma & Settleman 2007). This is the concept of “addiction” in cancer, and the dependence on particular genes to activate prolifer...
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...need to be developed to begin this study, we can infer from past research the steps in which determination of these relationships could be done. After developing a line in which a proper analysis can be done, where the phosphorylation of Src can be analyzed, western blotting would be the first major step in this experiment (Pillay et al. 2009). The Western blot would be used here to determine the levels of Src-kinase and phosphorylated Src-kinase in the cancer cells (Pillay et al. 2009). The lysates from the cells would be immunoprecipitated and analyzed for these levels as well as the levels of EGFR in the cells (Pillay et al. 2009). After the samples are transferred to the proper membrane, a designed monoclonal antibody (mAb) would be used to probe for the phosphorylated Src-kinase. Similarly a mAb would be used for probing the attached EGFR (Pillay et al. 2009).
LJI308 is a potent and selective inhibitor of RSK. The p90 ribosomal S6 kinase (RSK) comprises a family of serine/threonine kinase which is expressed in various human cancers. RSK is the cytosolic substrate for the ERK (extracellular sianal-regulated kinase), involved in direct regulation of cell survival, proliferation, and cell polarity. Previous studies have demonstrated that RSK pathway is important for the growth and proliferation of cancer stem cells [1,2].
The process by which Gleevec acts to inhibits bcr-abl in CML patients is by helping to reverse uncontrolled cell growth where Gleevec acts on a molecular target by a method that is more specific to cancer cells. It was shown that there is a substantial in vivo inhibition of the enzymatic activity of BCR-ABL at the 400 mg dose. which decreases phosphorylation of CRKL (a substrate of BCR-ABL). Since Gleevec was designed as an inhibitor of a specific receptor linked with CML, Gleevec also inhibits the Platelet-derived growth factor receptor tyrosine kinase and the c-kit tyrosine kinase.
The cancer stem cell theory hypothesizes that tumors or cancers arise from mutations or epigenetic changes in normal stem cells. These mutated or genetically altered stem cells possess the properties of the normal stem cells such as the ability to self-renew, differentiate into any type of body cell, and resist apoptosis. Hence, the cancer stem cells (CSC) are named so. It is also suggested that because of the above-mentioned properties of the cancer stem cells, the current anti-cancer therapies are not entirely successful (Gil et al, 2008). Despite surgery and other therapies, even if very few of these cancer stem cells survive, they can continue to act as a source for more tumors, even though the therapies eliminate all visible signs of cancer.
Cancer starts when certain cells in the body are mutated or changed and begin to divide. Cancerous cells grow differently than normal cells, instead of progressing through the normal cell lifecycle, cancer cells continue to grow and create more abnormal cells. A specific trait of cancer cells is that they have the ability to infiltrate and grow into surrounding tissues, developing out of control and causing serious damage to the host (Vincent, 2008). Cells become cance...
Li, Y., Wicha, M. S., Schwartz, S. J., & Sun, D. (2011, February 4). Implications of Cancer Stem Cell Theory for Cancer Chemoprevention by Natural Dietary Compounds. Retrieved December 12, 2013, from http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3248810/
...the activation of MAP kinases (Block et al., 2003). MAPK pathway influence regulation and transformation processes of cell growth (Finkel and Holbrook, 2000). Studies of oxidative stress mechanisms have shown that MAP kinases may be associated with the pathogenesis of diseases related to oxidative stress (Thannickal and Fanburg, 2000).
The cell cycle is the process by which cells progress and divide. In normal cells, the cell cycle is controlled by a complex series of signaling pathways by which a cell grows, replicates it’s DNA and divides, these are called proto-oncogenes. A proto-oncogene is a normal gene that could become an oncogene due to mutations. This process has mechanisms to ensure that errors are corrected, if they are not, the cells commit suicide (apoptosis). This process is tightly regulated by the genes within a cell’s nucleus. In cancer, as a result of genetic mutations, this process malfunctions, resulting in uncontrolled cell proliferation. Mutations in proto-oncogene or in a tumour suppressor gene allow a cancerous cell to grow and divide without the normal control imposed by the cell cycle. A change in the DNA sequence of the proto-oncogene gives rise to an oncogene, which
Tumors are formed by the alteration of the body’s own cells. This can be caused by environmental factors such as radiation, like UV exposure, chemicals or viruses 1. These can disrupt genes that control growth and cause an increase in cell division and proliferation. Proto-oncogenes are those genes that control normal but essential cell processes that keep cell growth and death in check. Two important categories are apoptosis genes, which regulate cell death, and tumor suppressor genes, which decrease cell propagation 1 . If these genes were mutated to the point where they cannot produce a functioning protein, cell division would continue far past what it was supposed to and unhealthy cells would be allowed to live and continue to multiply. This is what creates a malignant tumor. Certain conditions in the body can also promote the growth of cancer cells. One of these is a deficiency of natural killer (NK) cells, which are able to kill cancer cells by creating a pore in the cell membrane with perforin and releasing granzymes into the cell. Low levels of perforin allow for tumor growth 1. Chronic inflammation can also ...
Healthy cells grow and divide in a way to keep your body functioning properly. But when a cell is damaged and becomes cancerous, cells continue to divide, even when new cells aren't...
16. Describe two evolutionary consequences if the process of crossing over in meiosis ceased to occur. If crossing over in meiosis ceased to occur there would be less genetic variations and no diversity among a species. This would essentially mean that a species would not be able to adapt to an issue that could arise in the future, meaning that its species could potentially become extinct due to climate change or other arising events.
The American Cancer Society publishes current advances made in cancer research on their website. Many of the exciting discoveries about how best to treat the disease focus on the genetic aspects associated with certain types of cancer. In addition, treatments aimed at genetic solutions to cancer may be more effective and may cause fewer adverse side effects than traditional cancer treatments (American Can...
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 ...
Blood and urine based biomarkers used in molecular pathology are only indicative of the average response of the cell population affected with little or no information of the range of response or variability form areas of tissue (Naddler and Langley 2001)