This blog seemed to be lacking entries but I can't think of any constructive posts.

Anyways, both of us are kicking and alive and banedon probably have forgotten the existence of this blog. My mindset is more of the crapping mindset so ya.... I think not much will come from me too.

Something about tumour that you might want to know.

From the time that we detect tumour existence to the time where it will kill us only takes around 10 doublings (increasing its size by 10 times.) As not all the cells are dividing at the same time, the time taken to reach this tumour size depends on the mutation that is acquired by the cell. Thus, besides finding the cure for tumour, researchers are also finding ways to detect and excise tumours earlier so that it won't be too late.

You must be thinking why cancer is such a difficult illness to treat. Why does patients develop resistance to chemotherapy?

Tumour are also known to be heterozygous in its population. Cells that are makes up tumours have different properties. What is currently observed and proposed is tumour cells have the ability to acquire mutations as they divide because they are genetically unstable. This means checkpoints of the cell cycle is not their job properly and the cells have an enhanced mutation rate as compared to normal cells.

In the epithelial carcinoma, the normal epithelial becomes hyperproliferative when 5q chromosome FAP/APC. It will then develop into an early adenoma when there is hypomethylation where some oncogenic genes get turned on. An intermediate adenoma results when ras gene of 12p chromosome gets mutated. Late adenoma results when DCC from 18q chromosome and carcinoma when p53 gene from 17p chromosome gets mutated. There are several other mutations before tumour is able to the metastasize to other sites.

So what are the normal cell cycle guardians that keeps us from getting mutations?

Under normal circumstances, the cells have cell cycle checkpoints that are responsible for (obviously) checking whether the cell cycle is functioning properly. When there are mutations, signals will be send from the damaged DNA to activate p53 via phosphorylation. The activation of p53 will remove the MDM2 protein that is responsible for inhibiting its activity through blocking its basal transcription apparatus (aka machinery)and targeting ubiquitin-mediated degradation. Thus p53 will be able to activate transcription of various genes, in particular p21. The production of the p21 protein will in turn inhibit the activity of G1/S-Cdk and S-Cdk. The inhibition of G1/S-Cdk and S-Cdk will stop the cell cycle from proceeding, stopping the whole process. In 50% of the cancers, p53 has been shown to be mutated.

There is a disease known as Li-fraumeni Syndrome. This syndrome is an autosomal dominant mutation (which means the chance of a guy or a girl getting this disease when one of the gene is mutated.) The phenotype of this syndrome is the acquisition of multiple primary tumours when the patient is young and as the patients exhibiting this phenotype gets younger down the generation. This phenomenon is known as anticipation. The cause of this syndrome is the mutation of p53 and normally patients is heterozygous for p53 gene (one of the allele is normal while the other is mutated) You might be thinking why would the patient be exhibiting the cancer phenotype since it has a normal copy? The reason behind is a loss of heterozygosity of p53 gene where the mutated p53 gene will have influence on the normal p53 gene and change normal gene to the mutated one. I do not know how this happen because it is not known/ I haven't found out yet. Will tell you guys as soon as I find it out.

Facts on biuret test:

If you have forgotten what you learn in secondary school or not in contact with biology at all, this test is to test for presence of proteins in food. Actually, it is a simple test where you put 5% sodium hydroxide into food sample and copper(II) sulphate drop by drop. If the solution turns purple, it meant that the food sample contains protein and if the sample contain polypeptide, the solution turns pink.

The mechanism behind it is the ability of nitrogen in peptide bonds to form a complex with copper(II). This complex is the reason why the solution turns purple. Sodium hydroxide is to make the solution alkaline and the only reason I can think of why we have to put it drop by drop is to save cost. Thus, if anybody found the reason why, please feel free to write a comment.

That's all.... I'm dead beat. Shall continue tomorrow on my tumour lecture notes.