In the last half century, many sciences of science have reached new heights in their field of knowledge, but without as much research and discovery in genetics, there is no precedent for the ascension that has been achieved. Genetics began in 1865 with simple experiments on pea plants by Grey Gomendel, an Australian pastor.
Perhaps if Mendel were asked at this time about the usefulness of these experiments, it is very possible that Mendel’s answer would have been nothing more than quenching the thirst for curiosity, but it is very clear in the speculations about genetics in the twentieth and twenty-first centuries. It is impossible to find the root causes of biological phenomena without genetics.
Where DNA was recognized as the genetic material of animals in 1944, its structure was determined by Whiteson & Creek almost a decade later, and an endless stream of research began, thanks to which biological sciences today Is standing on Genetic science has been responsible for the evolution of living things, the transmission of diseases from generation to generation, and the salivary reality of complex and insidious diseases such as cancer. As a result, not only did new doors of research open up, but these integrity goals were also set. Against which drugs and vaccines can be made.
Even now genetics has reached a point where the complete and permanent correctness of genetic defects is beyond speculation. There are also some of these genetic mutations that make an authentic and effective drug not only ineffective in a patient but can also be harmful and fatal in some cases. These genetic mutations are demanded in Pharma cogenoutics, a branch of genetics. In common parlance, pharmacogenomics is the study of the effects of genetic mutations in organisms on the efficacy of drugs. In order to develop a basic understanding of pharmacougenoumics, it is important to understand how drugs work in the human and animal bodies in general and how they disappear after doing their job.
In general, any drug targets a specific molecule in the body, including humans. These molecules are usually different types of proteins. It is important to note that the structure of all proteins in living things is determined by their genetic material, DNA. However, pharmacological molecules, after binding to their target proteins, either increase or decrease the ability of these proteins to function as desired, or indirectly balance the molecular pathways that became unbalanced during the disease. There are.
As a result, the symptoms and severity of the disease gradually decrease and the disease improves. After doing its job, it is imperative that the medicine either changes its original state in the human body or is completely eliminated, because if the medicine remains in its original state in the human body for more than a certain period of time, it becomes permanent It will continue to increase or decrease the ability of its target proteins to function, or it will continue to run the molecular pathways that were initially balanced by the same drug.
As a result, either the beneficial effects of the drug are lost and the drug begins to show its harmful effects, commonly known as side effects. Direct release of drugs into the body of humans and many living beings is almost impossible, but they can be rendered ineffective by making some changes. In humans and animals, these changes cause some proteins, collectively called cytochromes or P450.
Human genetic material contains approximately 25,000 genes, of which 18 genes make different types of cytochromes proteins. does.
Therefore, these proteins are also made exclusively in liver cells. If there are some genetic changes in the genes of the cytochromes protein, they do not remain active in ineffectiveness of the drug, resulting in side effects of the drug. To further understand this we use two different drugs used in the treatment of diabetes and one drug used in the treatment of breast cancer. Diabetes is a high blood sugar level that is usually caused by a lack of insulin, a protein released from the pancreas.
Diabetes binds to a protein called SUR1 on pancreatic cells, which causes the proteins in the potassium and calcium channels to start working, causing calcium to enter the pancreatic cells and the cells to secrete insulin. ۔ This insulin eventually lowers the amount of sugar in the blood.
As a result, diabetes is controlled, and the drug enters the liver after its work, where a cytochrome called Cyp2C9 breaks it down and increases its effects. However, some diabetic patients have two specific mutations in the Cy2C9 gene, Cy2C9 * 2 and Cy2C9 * 3, and these modified genes have a significantly lower ability to counteract the effects of diabetes medication. As a result, the drug accumulates in the body in its original form and secretly releases insulin from the pancreas, which in this case lowers blood sugar levels to a dangerous level, which can lead to death.
The drug used in breast cancer is a toxic killer for all types of cells, however, because cancer cells divide much faster than normal cells, so the effect of this drug on these cells is greater. Breast cancer drug Cyp3A4 breaks down cytochrome, but in some patients due to genetic changes in Cyp3A4, the drug retains its original form in the body, causing the cancer cells to return to normal after killing the cancer cells. Also starts hitting. As a result, the side effects of chemotherapy begin to appear.
It is important to note that in addition to cytochrome, many other proteins in the human body affect the efficacy of drugs. However, Cytochrome has a hand in reversing about 75% of the drug’s effects. In many Western countries, a patient’s cytochrome is genetically diagnosed before a drug is prescribed, and a drug is chosen based on the results, so that better results can be obtained from a specific drug in controlling the disease. This method is called personalized medicine.