Type of paper:Â | Essay |
Categories:Â | Medicine Cancer |
Pages: | 5 |
Wordcount: | 1273 words |
Three States of Carcinogenesis
Because of the exposure to the ionizing radiation, Kevin's DNA was damaged. Therefore, carcinogenesis occurred after radiotherapy and it developed in three stages including initiation, promotion, and progression. These staged often extend over a long period. The initiation stage encompassed a transformation in the genetic makeup of the cell(Clere, Faure, Carmen & Andriantsitohaina, 2011). It might have happened randomly or during the interaction between carcinogen and DNA resulting in damage. Though it was very hard for the initial stage to develop into cancer because the cell still contains numerous mechanisms that can repair damaged DNA. Consequently, in Kevin's case, the repair did not occur during the initiation stage. The damage to the DNA was also in the gene area which controls cell growth, development and proliferation, restoration of the DNA and the immune system functionality which made his cell more prone to attract cancer.
In the promotion stage, there was a stimulation of the mutated cell to develop and split in a short period which results in a populace of cells (Clere, Faure, Carmen & Andriantsitohaina, 2011). Here, Kelvin then experienced a benevolent tumor which made him start becoming weak because his hormones are affected due to the strong radiation. However, during this stage, the effects are not severe, and it could have been reversed if Kevin would have stopped working at the uranium mine upon discovery of the development.
The third stage is the progression phase which is hard to comprehend as there are further growth and development of the tumor cells. The tumor cells tend to supersede normal cells. Here, the genetic composition of the tumor becomes more fragile making it prone to different mutations (Remacle, Kravchenko-Balasha, Levitzki & Levine, 2010). Kevin will thus experience mutations in his genes which control growth and the operation of the cell, for example, the tumor suppressor genes, the oncogenes and the mismatch of the genes. These transformations lead to tumor development until transformation occurs when the developing tumor becomes wicked and perhaps metastatic.
Metabolic Changes seen with Cancer
Based on metabolic changes seen with cancer, Kevin experienced muscle wasting and weight loss though he has been active and fit since he has been eating a balanced diet. The metabolic changes will result in malnutrition which is a very common problem for individuals who have cancer(Ward & Thompson, 2012). In this case, Kevin might have experienced weight loss because of reduced food intake and anorexia due to development of cancer over the years. The cancer development also interfered with carbohydrates, protein, and fats metabolism that lead to a reduction of body energy and amino acid in his body. Complete comprehension of the pathophysiology of these alterations will offer to nourish better Kevin's situation which will improve his life quality.
The connection between malnutrition and cancer is well known, and the signs of a fatal ailment which are often implicated in the expansion of malnutrition is anorexia which causes a reduced food intake and weight loss. Because of lack of exogenous nutrients, Kevin's body will use endogenous fuel which has been preserved to maintain the current requirements of his body and tumor for energy and protein. In his condition, the existence of malignant development is enough to decrease nutrient intake. His weak body and weight loss are also a result of the impacts of the tumor on the intermediary metabolism of his body. Research also shows that tumor reduces nutrients that have been preserved because it consumes substances that are designed for normal tissue metabolism.
Compounding the impacts of the tumor on the availability of nutrients to his body are the nutritional reduction impacts designed to treat modalities issued singly or successively. Concerning the location of the tumor where in this case Kevin has lung cancer, surgical treatment can reduce ingestion and absorption of nutrients through the gastrointestinal tract (Ward & Thompson, 2012). The degree of weight loss and experienced by Kevin must also be investigated to understand the main cause which will assist in administering the required radiation therapy. If radiation therapy is applied, it might decrease nausea, vomiting, and diarrhea and other symptoms associated with loss of appetite which results in weight loss.
Markedly, the lung cancer itself and the kind of therapy designed to eliminate it usually produce different symptoms that result in weight loss and nutritional exhaustion. It usually affects the weight of every individual with cancer regardless of the location of cancer (Ward & Thompson, 2012). It can also result in substantial loss of adipose tissue and skeletal muscles. In simple words, the development of cancer in Kevin's body resulted in interference of the cellular metabolism pathways which mainly occurs in cancer cells and not in the regular tissue cells. The metabolic changes in the cancer cells were diverse, and it encompasses aerobic glycolysis and an increase in the creation of biosynthetic intermediates required for growth and development and proliferation of the cells inside his body.
Effects of Onconeural Antigens
In some instances, cancer patients might experience muscle weakness because of the production of onconeural antigens. Onconeural antigens are antigen located on the surface of a cancer cell which looks like nerve cells antigens (Zhang, Zhou, Wu, Ni, Zhu & Jin, 2013). The antibodies created by immune cells against onconeural antigens usually results in paraneoplastic syndromes. The onconeural antigens are related to paraneoplastic neurologic disorders (PNDs) which are said to be autoimmune deterioration of the neurons that form in different patients who have systemic cancer. There are different kinds of genes encoding of the neuronal proteins that have not been discovered but have been cloned by the use of antiserum from patients with paraneoplastic neurologic disorders.
Determining such onconeural antigens needs a re-categorization of the ailments into various groups including conditions with neuromuscular junction proteins, the protein related with nerve terminals and the neuronal RNA binding proteins. This examination takes into consideration the basic neurobiology and tumor immunology provided by the features of the onconeural antigens(Zhang, Zhou, Wu, Ni, Zhu & Jin, 2013). There is also an immune privilege of onconeural antigen where two factors are being considered while formulating the immune privilege and they include physical and molecular. Examples of a physical component include the blood-brain barrier which is formed partly by microvascular during the systemic circulation. However, some of these antigens tend to lack the blood-brain barrier.
In Kevin's case, the process will take in the form of tumor immunity in PND. In this case, the immune privilege of onconeural antigens will not function because the antigens will have been expressed in the tumor of Kevin. There will be an anticipated increase in some tumors which will draw immune reactions to these antigens. The small cell lung tumor will be linked to low antibodies, and thus Kevin will have increased number of restricted stage tumors. Therefore, ectopic expression of the onconeural antigen will be one of the main factors that affect his immunogenicity. Besides, the tumor cells can also recapitulate different elements of immune privilege for given onconeural antigens.
References
Clere, N., Faure, S., Carmen Martinez, M., & Andriantsitohaina, R. (2011). Anticancer properties of flavonoids: roles in various stages of carcinogenesis. Cardiovascular & Hematological Agents in Medicinal Chemistry (Formerly Current Medicinal Chemistry-Cardiovascular & Hematological Agents), 9(2), 62-77.
Remacle, F., Kravchenko-Balasha, N., Levitzki, A., & Levine, R. D. (2010). Information-theoretic analysis of phenotype changes in early stages of carcinogenesis. Proceedings of the National Academy of Sciences, 107(22), 10324-10329.
Ward, P. S., & Thompson, C. B. (2012). Metabolic reprogramming: a cancer hallmark even warburg did not anticipate. Cancer cell, 21(3), 297-308.
Zhang, H., Zhou, C., Wu, L., Ni, F., Zhu, J., & Jin, T. (2013). Are onconeural antibodies a clinical phenomenology in paraneoplastic limbic encephalitis?. Mediators of inflammation, 2013.
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