Dr. Mushtaq Hussain
(Vice Principal, Dow College of
Biotechnology, Dewey University of Health Sciences)
This branch of genetics studies the
effects of genetic modifications on the efficacy of drugs in living things.
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 an Australian pastor, Greeley Goe Mendel.
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. To develop a basic understanding of pharmacogenomics, 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 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 was 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 the ineffectiveness of the
drug, resulting in the 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 medicine 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 stays in its original form in the
body and is permanently absorbed by the pancreas
