Analysis Of The Hallmarks Of Cancer

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).

This was launched by Novartis and Broad Institute3. According to Mark Fishman, President of the Novartis Institutes for Biomedical Research, “Probing cell lines with medicines targeted at specific pathways, as done for the Cancer Cell Line Encyclopedia, provides a powerful tool for design of cancer treatment.” Even though cancer cell lines are important model system, the scientific community questions the reliability of this system. During the first passages, the cell lines show chromosome abnormalities, molecular/ morphologic characteris... ... middle of paper ... ... J.-P., Varma, S., & Gottesman, M. M. (2013). The clinical relevance of cancer cell lines. Journal of the National Cancer Institute, 105(7), 452–8.

Cancer stem cells are a type of cancer cell that play an intimate role in determining the potential aggressive behavior of cancer. Cancer stem cells have taken the research world by storm, and although heavily debated, could potentially lead to the development of cancer therapies and impact the future of cancer treatment, or even a cure. In order to understand cancer stem cells, one must first understand stem cells in general. The idea of cancer stem cells was proposed over 100 years ago, but has recently become a major focus because of the similarities they share with normal stem cells. The idea of cancer stem cells generated research because sub-components of stem cells have been located in tumors of the breast, brain, and other organs.

To begin to answer this question it is useful to examine cancer cells and their interactions with the immune system in more detail. 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.

The most common cancer cells are present in rearrangements and chromosomal aberrations. The cancer cells will development from multistep process such as mutation and the cells selection for progressively increasing for proliferation, invasion, survival and metastasis process. The cancer cells origins from a single Primary tumor, arising in an identified organ and presumed to be derived by cell division that has undergone some heritable changes to outgrow its neighbors (Bruce. Alberts, 2002). The abnormal cells will proliferation then leads to increased growth the cells will derived tumor cells.

Cells will migrate towards the direction of chemical signals like epidermal growth factor, keratin growth factor, insulin like growth factor etc (van Golen et al., 2002). This will lead to the activation of different pathways, but the precise pathways for each molecule are not well understood. The inhibitor studies done by Kaladhar B Reddy et al provides new insights to a mechanism by which cancer cell progression can happen by the activation of MAPK in MDA MB 231 and MCF 7 cell lines. Their study proves that the prolonged MAPK (MEK) activation can regulate cell migration in human breast cancer cell lines when they stimulated them using TGF-α(Krueger et al., 2001).They also shows that the MAPK activation is critical for the cell migration in ER-negative cells and the duration of migration correlates with the duration of MAPK activation. Another study done by Thomas Pento et al also suggests that the KGF induced breast cancer cell motility depends on another MAPK protein ERK1/2(Zang et al., 2004).

One of the most promising approaches to emerge from the improved understanding of cancer at the molecular level is the possibility of using gene therapy to selectively target and destroy tumor cells, for example, the loss of tumor suppressor genes ... ... middle of paper ... ...rine Interleukin-4 Displays Potent Anti-tumor Activity In Vivo. Cell 57. P. 503-512. 8. Trojan, J.

Summary: Background and objective. Tumor heterogeneity is shown to be related to clinical outcome in cancer patients. The concept of a small subset of cancer stem cells being responsible for tumor relapse and metastasis comes out as a promising strategy for targeted cancer therapy. However, cancer stem cells are not easy to identify and isolate. The aim of this study was to determine the putative colon cancer stem cell subsets in human colon cancer cell lines HCT116 and HT29, which differ in their aggressiveness and differentiation capacity.

Cells are also stimulated to divide through the two proteins, cyclins and cyclin-dependent kinases. When these two join together, this stimulates cell division. These proteins act on the growth inhibitor proteins P53 and PRP, which are growth inhibitor proteins. Tumours may be malignant, spreading or benign, non-spreading. Malignant tumours are aggressive, invasive, and mobile.

After this classification the tumors are further divided depending on the different cell types. Most importantly carcinomas, which are characterized by specific cells that commonly found in the internal and external lining parts of the body, for instance, lung, breast, and colon cancer. Cancer formation cascade and cancer causes. Cancer is formed by a mutation in cells. Stem cells divide to produce more cells which are called progenitor cells.