HALLMARKS OF CANCER
The hallmarks of cancer are characteristics that distinguish the traits of normal cells from cancer cells in relation to how cancer develops. Thera are several hallmarks of cancer; however, there are six main hallmarks that aid in the progression of cancer: self-sufficiency in growth signals, insensitivity to antigrowth signals, evading apoptosis, limitless replicative potential, sustained angiogenesis, and tissue invasion and metastasis.
Self-sufficiency in growth Signals
Growth factors are substances in the body that control the multiplication of cells. Normal cells are dependent on mitotic growth signals from growth factors in order to divide. Without these signals, the cells will not divide. In cancer cells, growth signals are not required for their growth. Cancer cells are able to synthesize and secrete some of their own growth factors which reduces their dependency for the growth signals that normal cells use. Cancer cells can also change or alter the growth receptor so that more of these factors are present on the surface of the cancer cell. When this happens the cancer cell can become hyper responsive, which can result the receptor to be permanently on
Insensitivity to Antigrowth Signals
In normal cell tissues, there are many antiproliferative signals that maintain homeostasis within the cell throughout growth inhibitors and immobilized inhibitors. Normal cells have antigrowth signals that block proliferation by forcing cells out of the active proliferative cycle or induced to permanently stop their proliferation potential. Cancer cells evade these antiproliferative signals if they want to succeed. Cancer cells that have defects within the Retinoblastoma which permits constant cell division.
Evading Apoptosis
The ability for tumor cell populations to grow in number is based on their rate of attrition. One of the main processes in attrition is programed cell death or apoptosis. Apoptosis uses a protein, p53, to drive it function. The p53 protein induces apoptosis by increasing the production of the pro-apoptotic protein Bax, which stimulates the mitochondria to release cytochrome c causing cell death. Cancer cells can evade this apoptosis process because they are missing the p53 protein or they can inhibit the activity of the p53 protein by increase inhibitors of p53 or stopping its activators.
Limitless Replicative Potential
Normal cells have a timer that keeps track of the number of times they divide and grow by using telomeres. Telomeres are regions within DNA that keep ends of chromosomes from fusing or degrading with other chromosomes. Without telomeres, DNA would be loss and the chromosomes would get smaller and smaller. Most tumor cells seem to be immortalized, which suggests that they have limitless replicative potential, which is important for malignant growth. Cancer cells have to maintain all of their telomeres and do so by increasing the production of telomerase.
Sustained Angiogenesis
Angiogenesis is a process of developing new blood vessels. In adults, angiogenesis is switched on during processes such as healing or menstruation. In cancer cells, angiogenesis is always switched on, which is ultimately the factor that feeds their growth. VEGF or vascular endothelial growth factors are what regulate angiogenic growth, in which it either signals or blocks angiogenesis. Cancer cells activate angiogenesis by changing the balance of angiogenesis induces and inhibitors in the surrounding cell environment. Oncogenes such as Ras are increased during VEGF productions and cancer cells stop producing angiogenesis inhibitors. Thrombospondin is an angiogenesis inhibitor that is produced by the p53 gene; however, since most cancer cells have a loss in p53 production, this inhibitor cannot be made, this allowing the tumors to be feed with blood vessels and grow.
Tissue Invasion and Metastasis
Once a tumor is growing, it will eventually spread and more from its original place in the body. The ability of a cancer to metastasize enables the cancer cells to find new areas in the body where nutrients are everywhere, allowing the cancer to spread. Cancer cells lack the protein E-cadherin’s which exerts growth signals for contact inhibition that keeps cells that touch each other from growing. A dis-functioning E-cadherin protein allows invasive and metastatic phenotypes.