Week 9 PCL: Aidan's Mole
Hey all.
Aidan's Mole is almost diagnosed.
But, any questions regarding cancer, causes, effects, diagnosis, prognosis, and any other '-oses', feel free to post.
I'll post my research for this week.
Have fun, and enjoy your thursday night.
With love,
Tim
Once again, due to a lack of enthusiasm from Monash staff, the PCL for this week was not available online at time of publishing. I reserve the right to add it later! xx
Aidan's Mole is almost diagnosed.
But, any questions regarding cancer, causes, effects, diagnosis, prognosis, and any other '-oses', feel free to post.
I'll post my research for this week.
Have fun, and enjoy your thursday night.
With love,
Tim
Once again, due to a lack of enthusiasm from Monash staff, the PCL for this week was not available online at time of publishing. I reserve the right to add it later! xx
posted by timfazio at
9:50 pm
1 Comments:
Cancer Basics
What is a tumour?
A tumour is an abnormal growth. It can be either malignant or benign, that is ‘bad’ or ‘good’ respectively, and is now generally referred to respectively as ‘cancerous’ or ‘non-cancerous’. It is caused by abnormal proliferation of cells, and occasionally abnormal differentiation (cancer).
What is cancer?
Cancer is a growth of tissue which appears different to its surroundings. It results from both excessive proliferation, and lack of differentiation. The cells commonly have enlarged nuclei, and can both invade neighbouring tissues and vessels. Through the lymph system and through blood vessels, it can spread to other parts of the body, termed metastasis.
What kinds of genes are damaged in tumours?
Both tumour suppressor genes and genes which activate oncogenes are damaged in tumours. Proto-oncogenes, which are normally partially responsible for the proliferation of cells are, through a genetic mutation, changed to oncogenes. This enhances cell growth.
The tumour suppressor genes, normally responsible in part for DNA repair, cell apoptosis and repressing genes responsible for the continuation of the cell cycle, are also affected, and hence the body’s natural defence mechanism against the oncogenes is also destroyed.
It is in this manner that, generally, more than one gene mutation is required to cause cancer.
The way in which these mutations manifest is often through the manipulation of growth hormone receptors, namely tyrosine-kinase. Instead of reacting to the growth hormone intake from the body and the self regulation of that hormone by the body, the receptors instead are able to bind, and with ATP, phosphorylate, causing a permanent ‘on’ state. The cells hence grow excessively.
It is believed that approximately 90% of all genetic mutations causing cancer are somatic, that is they are acquired throughout the life of the patient, rather than inherited.
What significance does this have on risk factors for melanoma?
The main risk factor for melanoma is exposure to excessive amounts of UV radiation, normally through sun light. The UV radiation aids in mutation of these genes, and is therefore a primary cause of cancer. Less exposure to the sun would mean less chance of mutation. This would result in less chance for cancer.
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timfazio, at 9:54 pm
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