Lung Cancer Essay (Case Study Sample)

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Lung cancer develops from mutation of epithelial cells lining the bronchi, bronchioles and the alveoli. Carcinogens attack the cell DNA triggering mutation of epithelial cells. Mutation of the cells triggers oncogenes, reduce tumor-suppressing factors or delete short arm chromosome 3(Braun & Anderson, 2012). This damage eventually generates cellular changes and abnormal cell growth resulting in a malignant cell. During cell division, the DNA changes move to daughter cells where they undergo further changes resulting in unstable cells and eventually a carcinoma (smeltzer, Bare, Hinkle, & Cheever, 2010). Exposure of lung epithelial cells to uranium triggered the process of carcinogenesis that occurs in three stages: initiation, promotion and progression (Penning, 2011).
Initiation is the first stage of carcinogenesis that involves the exposure of normal epithelial cells to carcinogens. The carcinogens interact with the cell DNA disrupting the genetic programming of the relevant cell (Weinberg, 2013). Various possible results may occur. The cell may; remain in non-dividing state, become non-responsive to tumor suppressing factors, undergo programmed cell death or undergo abnormal cell division. If the cell divides without the repair of DNA disruption, the change in genetic coding remains permanent (Penning, 2011).
At this stage, the initiated cells can remain latent for years or weeks or grow in an independent and clonal design. Cell division remains symmetrical through the action two processes mitosis and apoptosis inhibition (Penning, 2011). Mitosis causes an increase in the number of mutated cells while apoptosis inhibition prevents the death of mutated cells. Initiation is a fast and irreversible process, which transfers to daughter cells (Weinberg, 2013). The initiated cells then move to the second phase in the carcinogenesis model, promotion.
Promotion involves an accelerated rate of proliferation of the initiated cells resulting in the development of a neoplasm. This stage involves the action of tumor promoters, which induce cell proliferation without necessarily interacting with the cells’ DNA (Penning, 2011). This process therefore is reversible through the inhibition tumor promoting factors. On the other hand, tumor promoters can indirectly damage the cell through oxidation (Weinberg, 2013).
For effective results, the tumor promoting factors ought to be of high concentration and present in the target cells for sufficient time. The tumor promoters are effective only to initiate cells (Penning, 2011). The increasing neoplasm is vulnerable to further genetic modification predisposing the patient to genetic and epigenetic changes in cancer genes and the development of metastatic cancer (Weinberg, 2013).
Progression is the final stage in the carcinogenesis model. The phase involves genomic instability and amplification, alteration of chromosomal structure and number and disrupted gene expression (Penning, 2011). There is non-stimulated cell proliferation. In addition, irreversible morphological and biochemical changes to the cells cause rapid cell growth and metastasis of the neoplasm. Angiogenesis that occurs during epigenetic modification facilitates malignancy, which occurs in this phase (Penning, 2011).
Cachexia in cancer patients is a due to altered metabolism of fats, carbohydrates, protein and anorexia that restricts dietary intake (Seyfried, Cancer as a Metabolic Disease, 2012). The process is complex and involves the action of two factors: host factors like interleukins (IL-1 & IL-6), interferon gamma, leukemia inhibitory factors, tumor necrosis factors and tumor products that cause catabolism of body tissues.
Interleukins (IL-1), tumor necrosis factor (TNF) suppress lipoprotein lipase and promote the intracellular breakdown of lipids. Interleukins (IL-1) trigger anorexia that reduce caloric intake (Allegra, 2015). Interferon gamma and tumor necrosis factor cause an increase in the rate of glycerol and free fatty acid turnover (Seyfried, Cancer as a Metabolic Disease, 2012).
Reduced caloric intake due to anorexia leads to hypoglycemia. Demand for source of energy by the brain cells leads to increased breakdown of glycerol and fatty acids in the liver to generate ketone bodies, an alternative source of energy to the brain (Allegra, 2015). Increased rate of lipolysis and reduced rate of lipogenesis lead to loss of adipose tissue with resultant cachexia(Seyfried, Cancer as a Metabolic Disease, 2012).
Interleukin (IL-6 and IL-8), proteolysis inducing factor (PIF) and tumor necrosis factors triggers an acute phase response (APR) (Seyfried, Cancer as a Metabolic Disease, 2012). During this phase, the function of the liver shifts from the synthesis of albumin to the production of C-reactive protein, serum amyloid-A protein and beta two macroglobulin. At the same time, proteolysis inducing factor and tumor necrosis factor trigger the proteolytic pathway (Seyfried, Cancer as a Metabolic Disease, 2012). The rate of intracellular protein breakdown increases while that of protein synthesis decreases. The expression of uncoupling protein 3 in skeletal muscle cells also increases, increasing their metabolic demands (Allegra, 2015). These mechanisms eventually result in significant loss of muscle mass.
Nevertheless, the resting energy expenditure (REE) in patients with lung cancer increases (Allegra, 2015). This is due to the effects of uncoupling protein 3 on mitochondrial RNA (mRNA). Increased production of systemic inflammatory mediators and acute proteins further increase the resting energy expenditure (Seyfried, Cancer as a Metabolic Disease, 2012).
Moreover, the high rate of cell division during carcinogenesis increases the basal metabolic rate and thus demand for glucose (Allegra, 2015). However, the dietary source of glucose in these patients is impaired due to anorexia. Besides, the neoplasm predominantly consumes glucose generated through gluconeogenesis and oxidative phosphorylation (Allegra, 2015). There are diminished energy reserves for the patient causing loss of strength and general body weakness (Allegra, 2015).
Small cell lung cancer causes paraneoplastic neurologic disorders, which manifest with impaired cerebral function (Seyfried, Cancer as a Metabolic Disease, 2012). Paraneoplastic cerebellar and autonomic degeneration is the most common disorder and causes abnormal muscle function (Seyfried, Cancer as a Metabolic Disease, 2012). Cancerous cells express intracellular onconeural antigens that trigger the body’s im...