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Breast Cancer fed mysterious protein Yin Yang

23 July 2018 17:36

Scientists have unveiled details of a mysterious molecule called Yin Yang1, and have shown that it can promote the growth of tumors in breast cancer.

The results obtained by an international team of scientists led by Imperial College London, could pave the way for new treatments and help understand why some tumors become resistant to chemotherapy.

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Importantly, the results show how a tumor can change their "look" to avoid treatment, using a system called epigenetics.

Yin Yang1 - a type of molecule called a transcription factor, which helps to activate the genes. Although each cell contains approximately 25,000 genes, only a certain number of turns at the same time, depending on what function should perform cell.

All body cells need Yin Yang1, but scientists have not known whether they helped or hindered the growth of cancer.

To find out whether it is a friend or enemy team has finished depth genetic profiling of breast tumors in 37 patients using a variety of techniques including a technique CRISPR modify gene.

The results, published in the journal Nature Medicine, showed that cancer cells are much more dependent on Yin Yang1, than normal cells, and that it can stimulate breast cancer growth.

Findings showed that tumors change which genes are switched when they become aggressive, which may affect how they respond to treatment.

This suggests that physicians should adopt new tumor samples when the patient's cancer spreads around the body, said Dr. Luca Magnani, author of the study from the Department of Surgery and Cancer at Imperial College: "At the moment, patients usually undergo a biopsy when they are first diagnosed with cancer breast The doctors then analyzed the tissue sample to determine what type of cancer. the patient, as it will determine the best treatment. "

He continued: "However, our results suggest that tumors change different genes depending on their development and can radically change their" look "Therefore, if the tumor is becoming more aggressive and spreads throughout the body, we recommend to always take a second biopsy. . The cancer may have changed significantly during this time and will respond to different treatments. "

Breast cancer is the most common cancer in the UK, and about 150 people fall ill every day.

The new study, funded by the Wellcome Trust, Cancer Research UK and the European Union, to study the type of breast cancer, called estrogen-receptor positive. It accounts for 70 percent of all cases of breast cancer and treated with hormonal therapy.

In the study, researchers analyzed 34 breast cancer patients whose cancer cells have not spread throughout the body, and another group of 13 cancer patients with more developed mammary tumors which proliferated cells.

The group, which includes researchers from the Oncology European Institute in Milan, the University of Liverpool and University of Western Reserve in Cleveland, studied which genes were turned on and off in tumors.

This process, called epigenetics, allows cancer tumors to adapt to their environment, to avoid treatment and, ultimately, to survive longer.

To help scientists track epigenetics researchers controlled chemical modifications to the DNA regions, called enhancers, types of codes that tell the cell to turn on certain genes when they are activated.

The results showed that two specific enhancer regulating genes SLC9A3R1 and Yin Yang 1, activated at certain stages, when they can help cancer cells grow and evade treatment.

In particular, it was found that Yin Yang1 included SLC9A3R1, who helped tumors grow.

Now the team will examine the increasing number of patient samples and to follow the same group of patients, to track how evolving enhancer activation in these cancers. They explore the type of breast cancer known as triple-negative, which is very difficult to treat.

Dr. Magnani said: "As expected, our work has caused a lot of questions, and now we need to answer them But only through international cooperation and teamwork we can get this vital work We would not have done had it themselves..."



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