The Differences Between Tumours and Kidneys (Essay Sample)

BIOLOGY:
The differences between tumours and kidneys
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The differences between tumours and kidneys
A tumour is formed when normal cells change and grow uncontrollably, the mass of tissues that can be classic signs of inflammation and can be benign or malignant (cancerous) while a Kidney is a pair of bean – shaped organs that are in the back part of the abdominal cavity of a human being. These organs form and excrete urine, regulate fluid and electrolyte balance and act as endocrine glands. The attempt to give a description of what a tumour is is hopeless simply because there are several tumours with different origin and characteristics and there are several concurrent causes of tumour development.
Tumours have no specific structure, due to its many forms but mostly they occur in cells. Kidneys, on the other hand, have a definite structure. As illustrated by Jean Hamburger et al., It comprises of renal veins and capillaries that play a part in blood supply to the organ and nephrons that filter blood to generate a filtrate composed of water and soluble (glomerular filtration). Which then passes through a tubule that progressively modifies the filtrate, mainly by reabsorbing desirable solutes and water. The complicated structure of the renal vascular system is crucial for the proper functioning of the kidney.
Tumour growth is a simple exponential process terminated by the exhaustion of the nutritional support provided by the host. In most cases tumour growth is smoothly curvilinear on a semi – log plot throughout observed growth. This shows that the specific growth rate of tumours is usually not constant even for a short time, but can decrease steadily. Tumour formation is a very complex process and it involves many types of changes in the normal cell. Tumour evolution involves straight rounds of mutation and ordinary variety. For tumours to grow without limits, the tumour cells must be able to motivate the progress of the blood vessels to bring the nutrients and oxygen. They usually grow by various mechanisms e.g. the host vascular network expands by growing of endothelial sprouts or angiogenesis. Its growth is dependent upon new blood vessel formation; all solid tumours, irrespective of their tissue of origin, the specific oncogenes or tumour suppressor genes expressed.
Tumour angiogenesis takes place when there is staffing of new blood vessels synchronised by the manufacture of angiogenic stimulators including members of the fibroblast growth factor and vascular endothelial growth factor families. It enhances entry of tumour cells into the circulation by providing an increased density of immature, highly permeable blood vessels that have minute cellar covering and less intercellular junctional complexes than normal mature vessels. In Kidneys, quiescent endothelial cells have long half – lives and are protected by autocrine signals such as vascular endothelial growth factor (VEGF), angiopoietin and notch. These cells are surrounded by pericytes, which secrete paracrine signals such as VEGF and angiopoietins to maintain endothelial cell homoeostasis. When these cells are exposed to angiogenic stimuli pericytes, detach from the vessel walls via the antagonistic role of angiopoietin permitting these cells to develop. Among several angiogenic factors, VEGF is thought to play an artificial role in the maintenance of peritubular capillaries.
In Tumours, Hypoxia results from an imbalance between the cellular oxygen consumption rate and the oxygen supply to the cells. It typically occurs in an extensive series of hard tumours due to abnormal vasculature; it affects many natural procedures at molecular, cellular and tissue levels. Adaptive responses to oxygen deficiency shape signal transduction, cell metabolism, proliferation, etc. and thereby contributing to tumour invasion and metastasis. Usually, the presence of tumour hypoxia is largely associated with poor prognosis and therapy resistance. In kidneys, hypoxia occurs when there is a loss of peritubular capillaries preventing the redifferentiation of regenerating tubules; this is turn decreases VEGF expression in these tubules and maintains the hypoxic state through impaired angiogenesis forming a vicious cycle between de – differentiated tubules with decreased VEGF expression resulting in capillary rarefaction (Luoto et al. Genome Integrity 2013).
Parada et al., state that in tumours, the outcome of typical medical radiation management is determined by the 5 R's of radiobiology: Redistribution acknowledges the fact that cells exhibit differential radiation sensitivity. Repopulation of lumps may be one of the most widespread grounds of the malfunction of usually fractionated routes of radiation therapy. In reoxygenation, Oxygen has been known as one of the strongest modifiers of radiation sensitivity and hypoxic cells have been frequently shown to be 2–3 times more defiant to radiation. Repair of DNA Damage enhances repair of sublethal damage between radiation fractions is exploited in radiation therapy because critical normal tissues and tumours often differ in their ability to repair radiation damage. And in the case of kidneys, Repair of DNA Damage If unrepaired, t...