Cancer is also known as malignancy, is an abnormal growth of the cell, and there are more than 100 types of cancer, which include breast cancer, lung cancer, lymphoma, prostate cancer, and colon cancer. Cancer has increasingly become one of the deadliest diseases in the world, and it has claimed many lives over the last two decades. However, cancer has been in existence in the world for a long time. Cancer can manifest itself in anybody regardless of race, color, and socio-economic background. People have developed lung cancer despite not being cigarette smokers, and this is the devastation that the disease can cause and has caused the human population (Mermel, 2014). Typically, the condition is treated through surgery, radiation, and chemotherapy, but they are do not guarantee full treatment.
Tumour Suppressor Genes
Tumor suppressor gene, or anticogene, is a gene that can regulate a cell during cell replication and division. If the cell grows uncontrollably, the result could be the formation of cancer in the human body. The loss of these genes functions may prove to be more significant in the development of many different human diseases compared to the gene’s ability to activate oncogenes (Mermel, 2014). When this gene becomes this way, it is described as a mutation, and this leads to the uncontrollable growth of cells, which transforms into a tumor.
The examples of tumor suppressor genes include BRCA1, BRCA2, p53, or TP53, the oncogenes that are in question are described as genes which in certain circumstances, transform into tumor cells (Lawrence, 2013). The mutations that occur in the tumor suppressor genes are referred to as germline mutations. These mutations appear in BRCA1 or BRCA2, and they increase the risk of human beings developing certain types of cancers.
Role of Tumor Suppressor Cells
The TSC genes have a repressive effect or a dampening effect on the regulation of the cell cycle or promotion of apoptosis at times; it can be used to execute both functions. The functions of the TSC fall into several tasks and categories. The first functions are the repression of genes that are vital for the continuing of the cell cycle. If these genes are not expressed, the cell cycle will not continue, and this will hinder cell division. This inhibition of cell division leads to cell mutation, and it could eventually lead to the cells growing uncontrollably, and this is where the cancer forms (Lawrence, 2013).
The second function is DNA repair, and the DNA proteins are typically classified as tumor suppressors as well; mutations in their genes increase the risk of cancer, for instance, variations in MEN 11, BRCA, and HNPCC. To add to this, an increased mutation rate from a decrease in the number of DNA repair cells leads to an increase in the inactivation of other tumor suppressors and activation of oncogenes (Cibulksis, 2013). The third function is regarding cell adhesion, some of the proteins involved in cell adhesion prevent tumor cells from dispersing, and they block the loss of contact inhibition and inhibit metastasis.
Another function is concerning coupling the cell cycle, combining the cell cycle to DNA damage is essential. As long as there is damaged DNA in the cell, it is incapable of dividing, and it ought not to divide. If the damage can be repaired, the cell cycle can continue. If the damage cannot be repaired, the cell should be able to initiate apoptosis, which is referred to as programmed death of cells, which can remove the threat it poses to the organism as a whole (Vogelstein, 2013). If this cannot happen, then it could lead to mutations that could lead to the development of cancer in the body.
Types of Cancer Linked to Tumor Suppressor Genes
The germline mutations that take place in the human body are specific to BRCA1 and BRCA2 genes. When these mutations take place, they increase a woman’s risk of developing hereditary breast or ovarian cancers. The oncogenes are notorious for turning healthy cells into cancerous cells in the woman, the mutations in the discussion are not inherited from anyone, and they are as a result of the tumor suppressor genes failing to function appropriately (Vogelstein, 2013). In men, the germline mutations increase a man’s risk of developing hereditary prostate cancer or breast cancers. Breast cancers are not only subject to women, and men are also susceptible to this kind of exposure.
In men and women, there is also a risk of developing pancreatic cancer and melanoma, and there are two common oncogenes, which are HER2 and RAS. HER2 is a specialized protein that is responsible for the control of cancer growth and the spread of cancer (Alexandrov, 2013). This oncogene is found in some cancer cells, such as ovarian and breast cancer cells.
There are specific examples of tumor-suppressor proteins, and the first that was discovered was the retinoblastoma protein, which is present in the human retinoblastoma. There has been recent evidence that has been able to implicate pRb as a tumor-survival factor. This protein is capable of blocking gene cell proliferation, which can regulate the death of cells and also a division of cells (Cibulksis, 2013). There other TSG that stand out, such as the p53 tumor suppressor protein, which is encoded by the TP53 gene. P53’s primary functions are apoptosis and DNA repair in the cells; furthermore, they also regulate cell-cycle and transcription.
DNA repair genes
DNA repair genes are vital for the maintenance of the integrity of the genome; the dysregulation of DNA repair genes can be associated with significant health effects. These health effects include increased prevalence of congenital disabilities, and it also enhances the risk of cancer in human beings. The DNA repair genes can fix mistakes when the DNA is copied; most of these genes functions as tumor suppressor genes; for instance, BRCA1, BRCA2, and p53 are all regarded as DNA repair genes (Vogelstein, 2013). These genes function in a diverse set of pathways that involve recognition and removal of DNA lesions, protection from errors of incorporation made during cell replication and DNA repair, and also tolerance to DNA damage.
There are additional genes that indirectly affect DNA repair, and they do this by regulating the cell cycle. This regulation is made to provide an opportunity for repair or to direct the cell to apoptosis (Lawrence, 2013). Distinct pathways of repair minimize toxic and mutagenic consequences. The cellular DNA is subjected to continual attack, and this is done by both reactive species inside cells and by environmental agents.
DNA repair is classified as a collection process by which a cell identifies and corrects damage to the DNA molecules that encode its genome. In human cells, environmental factors and normal metabolic activities can cause DNA damage. This results in as many as 1 million individual molecular lesions per cell per day. Many of these lesions are responsible for structural damage to the DNA molecule and can be able to alter or eliminate the cell’s ability to transcribe the gene that affects the DNA encodes (Mermel, 2014). There are other lesions the induce potentially harmful mutations in the cell’s genome, which affects the survival of its daughter cells after mitosis.
Role of DNA repair genes
If an individual has an error in a DNA repair gene, it means that there are inevitable mistakes that need to be corrected. These mistakes often result in mutations, and these mutations lead to the uncontrollable growth of cells in a human being. In this case, they are caused by environmental factors or metabolic activities that can produce toxins within the human body. These mutations may eventually lead to cancer, and they may lead particularly to variations in the tumor suppressor genes or the oncogenes (Mermel, 2014). As a consequence of mitosis, the DNA repair process is always active as it responds to damage in the DNA structure.
When the normal repair process fails to take place, and when cellular apoptosis does not occur, there could be an occurrence of irreparable DNA damage. This may include double-strand breaks and DNA cross-linkages. This eventually leads to malignant tumors or cancer as per the two-hit hypothesis. The rate at which DNA is repaired is dependent on several factors, which include the age of the cell, the cell type, and the extracellular environment. Once a battery has been exposed to a large amount of DNA damage, or it can no longer effectively repair the cost incurred to its DNA damage, it can enter into three possible stages, which are apoptosis, irreversible dormancy, and uncontrolled cell division (Alexandrov, 2013).
The ability of a cell to repair its DNA is of extreme importance to the integrity of that DNA’s genome and, ultimately, to the standard functionality of that organism. Many genes responsible for DNA repair have been shown to influence life span, and they have turned out to be involved in DNA protection and restoration (Alexandrov, 2013). The cells can be damaged, either endogenously or exogenously.
Types of Cancer caused by DNA repair genes
Mutations in DNA repair genes may be acquired or inherited, and the lynch syndrome is one that can manifest from this type of genes. This is unlike the tumor suppressor genes, which are known to be more of hereditary than inherited. The risk of getting cancer due to mutation is very high in human beings, and once the genome is altered, it could lead to a range of diseases (Vogelstein, 2013). This occurs once the DNA cannot be repaired, and through this, there could lead to the uncontrollable growth of cells in the body (Cibulksis, 2013). The genetic and inherited cancers are not easy to debunk, and it is difficult to determine what type a person has unless the disease is detected early. To engage these types of cancer, it has to manifest itself in a person first. It becomes difficult to treat a person before cancer shows itself in the body.
Early screening and detection have led to lives being saved in the battle with cancer, but there is still a long way to go in dealing with this deadly disease. More research and studies continue to be done by experts to enable the reduction of cancer in the population. Several factors have contributed to people having the disease, and this includes the foods and the materials we use day by day.
Alexandrov, L. B., Nik-Zainal, S., Wedge, D. C., Aparicio, S. A., Behjati, S., Biankin, A. V., … & Boyault, S. (2013). Signatures of mutational processes in human cancer. Nature, 500(7463), 415.
Cibulskis, A. S., & Carter, S. L. (2013). Mutational heterogeneity in cancer and the search for new cancer genes. Nature, 499(7457), 214-218.
Lawrence, M. S., Stojanov, P., Mermel, C. H., Robinson, J. T., Garraway, L. A., Golub, T. R., … & Getz, G. (2014). Discovery and saturation analysis of cancer genes across 21 tumor types. Nature, 505(7484), 495.
Lawrence, M. S., Stojanov, P., Polak, P., Kryukov, G. V., Cibulskis, K., Sivachenko, A., … & Kiezun, A. (2013). Mutational heterogeneity in cancer and the search for new cancer-associated genes. Nature, 499(7457), 214.
Vogelstein, B., Papadopoulos, N., Velculescu, V. E., Zhou, S., Diaz, L. A., & Kinzler, K. W. (2013). Cancer genome landscapes. science, 339(6127), 1546-1558.
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