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Cancer is the uncontrolled division of mutated cells. Cancer is considered a disease when mutated cells invade and suffocate cells that behave normally. The normal life cycle of a cell is regulated by many processes but three (apoptosis, mitosis, and contact inhibition) are important for understanding cancer because they control cell longevity, and cell division. Apoptosis (some call apoptosis "cell suicide") is the process that controls the death of cells or the time a cell has to live; mitosis controls cell division; and contact inhibition controls how a cell responds to cells around it. These three processes have been shown to be regulated by two genes: : proto-oncogenes, which direct synthesis of products needed for cell growth and development, and tumour suppressor genes which work to stop a cell from growing out of control. Proto oncogenes control cell growth and division; Tumor suppressor genes control apoptosis and go to work when cell growth goes out of control.
Cancer occurs when proto oncogenes mutate and become oncogenes which cause uncontrollable cell division. They also affect contact inhibition so the cell is not restricted by the cells around it - this results in uncontrolled cell growth. Mutated Tumour Suppressor Genes also cannot prevent oncogenes from growing uncontrollably. Tumor suppressor genes also control apoptosis and, if mutated, will prolong the life of the cell.
Lung cancer at the molecular level has been shown to be influenced by carcinogens that damage lung cell genes. Tobacco smoke contains over 50 carcinogens that have been shown to damage the genes that control and regulate lung cell division. When lung cells divide uncontrollably, small tumors can develop that can then metastasize: Metastasis is the ability of cancer cells to separate themselves from a tumor and spread to other parts of the body: cancer cells are usually transported through the blood supply from the site of the cancer to other parts of the body. A metastasized cancer, such as lung cancer, is known to spread to specific locations - Lung cancer usually metastasizes to bone, but this should not be considered a bone cancer.
More than 50% of lung cancers are caused by mutated
p53 genes but Myc, Ras and EGFRs are also important. Mutations in these 4 genes are described below to illustrate how lung cancer works at the molecular level. D
ifferent mutations can occur on the same gene and exposure to different carcinogens can lead to different mutations The type of mutation of the p53 gene can tell us which carcinogen is associated with lung cancer development. For example, the types of p53 mutations found in individuals exposed to cigarette smoke are different from those found in individuals exposed to other carcinogens such as radon or metals.
P 53 is a tumor suppressor gene produced by chromosome 17 at position 13. In a normal cell, the protein produced by this gene regulates cell division and uncontrolled cell growth. When the p53 attaches to DNA and other proteins within the cell, it can tell if they are damaged. If the DNA or protein is damaged it will initiate apoptosis, killing the DNA or protein and stop making damaged genes so that it does not spread. Maintaining regularity in the cell is the main job of p53.
When p53 becomes mutated in any manner (i.e. exposure to carcinogens or some type of radiation) it will no longer function properly within the cell. So if it doesn't function properly anymore it will not detect and kill mutated DNA\protein and this can lead to an outbreak in cellular division and uncontrolled tumor growth.
Another gene important for lung cancer EGFR (epidermal growth factor receptor), also known as ebr1 and Her1 . This gene is encoded to produce a protein, tyrosine kinase in the cell membrane of epithelial cells. EGFR in the right conditions causes the division of epithelial cells.
When EGFR becomes mutated it will lead to continual stimulation and high rates of division of these cells causing over expression of epithelial cells. These epithelial cells overcrowd the surrounding area causing the growth of a tumor.
Ras is a proto oncogene involved in the kinase signalling pathway. This pathway controls the transcription of genes and keeps them the same. To turn on the pathways, Ras has to bind to GTP, a molecule that causes the transcription to start. To stop the process of transcription, the GTP molecule must be broken up.
When Ras becomes mutated it can no longer break up and release the GTP molecule. When the pathway is activated, and it is stuck in the on position, it has no choice but to continually reproduce itself. This results in continuous cell production which is an important step in development of cancer.
Myc is a protein and a proto oncogenes which affects the transcription factor of the cell. The transcription factor is when a protein such as Myc binds to the DNA to begin transcription of the DNA. Myc also controls the expression of many genes within the cell.
Myc can be mutated by the rearrangement of genes or by amplification. Amplification takes place when the gene continually replicates; rearrangement of genes takes place when the nucleotide in the DNA strand is not put in the proper order. This leads to the development cancerous cells.
While these four genes are involved in the development of lung cancer, many other genes and processes have been shown to be involved in its development.
Symptoms of lung cancer include shortness of breath, infected spit, blood in spit, coughing and chest pain. These symptoms occur because tumors grow into the lumen restricting passage of air into the lungs. Tumors can also affect near by nerves resulting in paralysis of the section of the lung affecting inflation and deflation. It can also affect the alveoli and cause them to explode and decrease the surface area where gaseous exchange takes place. Symptoms usually appear when a tumor or tumors have grown large enough to put pressure on other structures and organs.
Increased understanding of the molecular changes in lung cancer can help us to fight this cancer. Several treatments have been developed to treat lung cancer including removal of cancerous tissue for cancers that have not spread. By removing a cancerous tissue that is growing uncontrollably the spread may be stopped or diminished. Radiation has also been used to target cancer cells and may be used at the same time as other treatments to improve the odds of destroying all cancer cells. Toxic chemicals, chemotherapy, are also to kill off fast growing cancer cells. Since cancer cells have lost the ability to regulate cellular processes in the same way as normal cells do, they are more sensitive than normal cells are to cellular poisons. Three types of drugs are also to target different components of the cellular process: Anti-metabolites interfere with the building blocks of DNA; Genotoxic drugs are used to damage cancer cell DNA, and this affects replication and cell division; and Spindal inhibitors prevent proper cell division, stopping cancer cells from dividing into two. Other drugs which do not fall into the above categories are also used in the treatment of lung cancer,.
Unfortunately, chemotherapy brings side effects. Since the drugs target rapidly dividing cells, they also affect normal cells which divide rapidly. These include hair cells and cells that line the gut, giving rise to nausea, vomiting and diarrhea. As we gain more and more understanding of the changes and genes we should be able to make treatments more specific and decrease side effects.
Since we are aware the tobacco smoke contains so many carcinogens and can that smoking can lead to cancer, we must increase awareness of the link between carcinogens and gene alterations.
The understanding of genes and their impact on the progression of tumor growth and development will help scientists to develop new drugs and treatments which can target the changes and mutations that are taking place in the genes, either stopping the changes from happening or changing the course of tumor development.