Behind the genome

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DNA, RNA and protein research is advancing medicine on the way to solving the mystery of cancer. Although the journey is just beginning, researchers in various parts of the world are constantly working. Success will come one day through their overall efforts. Sajeeb Chakraborty, a Bangladeshi researcher and associate professor of biochemistry and biopsy at Dhaka University, is working with the world to fight cancer. He is representing Bangladesh in the world court. Recently, the statements of the world's best cancer researchers including Chakraborty have been published in the journal Nature. The magnetic part of it has been transformed for the readers of science thought.

An important revolution in current cancer research has come at the hands of genomics. Cancer is divided into different categories depending on the affected tissue or organ. Again the disease can be divided into several subcategories based on the specific genetic changes or mutations responsible for it. Although its effect on cancer cure has not been as successful as expected, it is still questionable. Andrea Califano, a systems biologist at Columbia University in the United States, said: After most of them, the symptoms of cancer returned. The number of patients who fully recover from this procedure is very low.

Discovering and implementing a treatment based on a particular genetic trait is not an easy task. In the case of cancer, it is difficult to identify which genetic mutations are responsible for cancer. However, researchers have focused on mutations in the driver of various oncogenes (genes responsible for cancer) to develop specific therapies. But there are many other genes that play a role in the spread of cancer. Bert Vogelstein, a cancer researcher at Johns Hopkins University in the United States, said:

These genetic changes invalidate the tumor suppressor gene. But these genes help protect us from cancer. Such as genes that modify damaged DNA or genes that control cell death (apoptosis). In many cases, proteins made from these defective genes are not found in cancer cells, so it is difficult to study them. Vogelstein added, "If there is no protein in the cell, it is not possible to use any medicine against it."

Different types of mutations occur in different cells of the tumor. Due to this, the cancer comes back after a lot of treatment. "A cancerous tumor is made up of multiple clones," said Tamar Geiger, a biochemist at Tel Aviv University in Israel. A clone is a group of cells that carry the same type of mutation. "Even if the treatment doesn't work against a small amount of these cells, they can take over the entire tumor, leading to a recurrence of the cancer," Geiger said.

Because of these limitations, researchers are being forced to think beyond cancer genomic replicas. Therefore, research is underway on the epigenetic mechanism of the gene. The epigenetic mechanism is a mechanism influenced by the environment and adaptation. This method can change the nature of genes without changing the genetic code. It can play a role in tumor formation. Sequencing technology is much more advanced now. Using RNA sequencing, researchers measured RNA made from genes. Then you can understand the ongoing epigenetic status of the gene. In addition, recent advances have made it easier for researchers to study proteins made from genes. So scientists have been able to easily create a picture of the internal activity of cancer cells.

In 2006, the US National Cancer Institute (NCI) and the National Human Genome Research Institute launched a program called The Cancer Genome Atlas (TCGA). So far, more than 20,000 samples of 33 types of cancer have been collected through this. Different characteristics of those samples have been identified, such as epigenome, RNA and proteins. Each of these is part of Amicus, one of the branches of science. Using data from these branches of Amicus, researchers continue to try to identify and treat cancer. For example, mutations in tumor suppressor genes are difficult to resist directly. However, as a result of these mutations, action can be taken against the activities that start in the cell. "If we could learn about the movement of a tumor suppressor gene, we would know about the next steps," Vogelstein said.

By analyzing the interactions between different biological elements, it is possible to know their role in conducting physical activities. It is possible to create and invent different therapies. These methods may be able to work simultaneously against multiple mutations at the same time. Protein analysis shows why some therapies are not effective for all people. However, the most effective study is to combine different branches of the amygdala to create a complete picture of cancer cells. Hopefully, this will help us learn more about the diversity and dynamics of cancer.

Tie in the same formula

How genetic traits can affect proteins using RNA data and computational modeling methods. Califano is trying to learn more about how it can transform a normal cell into a cancer cell. "DNA is the predictor of our genetic results, RNA is its reflection," he said. It paints a picture of the activity of our cells. '

He called the idea a "tumor checkpoint." There are even many variations of the same type of cancer. As is often the case, there is only one mutation between two subcategories of the same cancer. Multiple mutations can cause similar diseases. That is, they are affecting similar proteins. From this idea, Califano created a mathematical algorithm. Through this algorithm, the activity of genes can be inferred from numerous RNA data. From this it is possible to identify proteins that are affected by multiple mutations. These proteins can be enzymes. These can affect RNA through epigenetic mechanisms. Or it could be a transcription factor capable of making proteins directly from RNA. "These proteins regulate the basic function of cancer cells," said Califano. These are called master regulators in the language of science. '

Califano and his colleagues searched 10,000 cancer samples and identified 406 master regulators. These provide an idea of ​​the effects of all mutations in cancer samples. Their study was published in Bioprint, a server at Piprint. These master regulators are influenced by mutations in other genes. But mutations themselves are rare. That is why their identification method depends on genomics.

Multiple mutations can inhibit the activity of altered cells by inhibiting only one master regulator. "Only by identifying the key vulnerabilities can a complete shutdown of a 'tumor checkpoint,'" Califano said. The approach has already been effective. In 2015, Califano and colleagues conducted a study on breast cancer patients. Patients with mutations in the HER2 gene. But a large portion of these patients are given the antibody-based drug trastuzumab (herceptin). These drugs are made in a mutation-based manner. But this medicine did not work well in the body of the patients.

High levels of a type of cytokine protein called IL-6 are secreted from HER2 positive cells. This activates a transcription factor called STAT3. This results in the formation of a type of protein called calprotectin, which helps in cell proliferation. For this reason, the idea is that STAT3 is a master regulator. It inhibits the action of the breast cancer antibody drug trastuzumab. A drug called Ruxlitinib has been developed to overcome this obstacle. These drugs are being tested in the second phase of the trial. The drug ruxlitinib has already been approved for blood cancer and sister marrow cancer. As soon as the master regulator was identified, Califano and his colleagues developed various mathematical algorithms. This allows them to predict effective treatment. This algorithm is able to turn off the more active master regulator and increase the activation of the less active master regulator. The method has been piloted in Colombia with the goal of healing more than 3,000 patients over the next three years. Along with genomic research, physicians are also emphasizing the results of California's mathematical algorithm.

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