Class material:cancer

Cancer has traditionally been understood as a disease caused by genetic mutations.
However, through this course, I have come to realize that epigenetics also plays a crucial role in the development of cancer. 

Epigenetics involves the regulation of gene expression without changes in the DNA sequence itself.
It is noteworthy that gene expression can be regulated through mechanisms
such as DNA methylation, histone modification, and chromatin remodeling. Changes in gene expression patterns can lead to the development of cancer cells.

Understanding that there are causes of cancer beyond genetic mutations is important.
If we consider only genetic mutations as the cause of cancer, treatments would focus solely on analyzing DNA sequences.
However, if the cause lies in epigenetics, simply examining DNA sequences would not suffice to uncover
the reasons for the cancer. Knowing that epigenetics can also be a cause of cancer broadens the horizons of cancer treatment, enabling more diverse approaches for treating patients.

Numerous studies have been conducted to demonstrate how epigenetics can explain cancer. Among them, research
on the epigenetic regulatory factor known as the Polycomb group protein has been significant.
Polycomb proteins play a role in repressing genes during development. Abnormalities in these proteins can disrupt gene expression
and completely alter the future of cells.

The mechanism of cancer development by methylation in epigenetics is as follows.
In normal cells, CpG islands located in the promoter regions of tumor suppressor genes are largely unmethylated.
In cancer cells, the same CpG islands are hypermethylated.
inhibition of expression of tumor suppressors by hypermethylation and overexpression of oncogenes by hypomethylation might occur.

inhibition of expression of tumor suppressors by hypermethylation is as follow.
When CpG islands are unmethylated, the gene is activated and can function normally. Chromatin in this state has an ‘open’ structure, making it easy for genes to express. However, when the chromatin structure changes to a ‘closed’ form, gene expression is suppressed.
These changes cause cells to escape the normal cell cycle, divide indefinitely, escape the suicide program apoptosis, and develop defects in DNA repair mechanisms. All these changes lead to tumor formation

overexpression of oncogenes by hypomethylation is as follow.
the DNA becomes hypomethylated, resulting in an 'open' or 'relaxed' chromatin structure, which increases the expression of other genes and leads to abnormal cell proliferation.
Abnormal activation of genes can lead to pathological proliferation of cells.

The mechanism of cancer development by histone modification in epigenetics is as follows.
Histone modification Histones are important in regulating gene expression and cell death, DNA replication and repair, chromosome condensation and segregation, and are reported to cause diseases such as cancer when problems occur.
In particular, what is being actively studied in cancer is histone methylation, which occurs at arginine and lysine, and regulates transcriptional activity (H3K4, H3K36, H3K79) and transcriptional repression (H3K9, H3K27, H3K20) depending on the location and degree of methylation. It has been found to affect chromatin structure and transcription.

So, how should our approach to treatment expand in the future?
Firstly, both genetic and epigenetic factors should be considered in cancer diagnosis.
This could allow for the detection of early signs of cancer that have not been discovered previously, enabling prompt action. 

Additionally, we could consider methods such as artificially introducing proteins that regulate genes,
similar to how hormone injections are administered when there is a deficiency. Using proteins to properly
regulate gene expression could potentially prevent cells from developing into cancer cells. 

By embracing a broader understanding of the genetic and epigenetic factors involved in cancer,
we open up new possibilities for early detection, prevention, and more personalized treatments, enhancing
the efficacy of our approaches against this complex disease.