Scientists unveiled clues to a mysterious molecule called Yin Yang1 – and revealed that it could stimulate tumor growth in breast cancer – ScienceDaily



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Scientists unveiled clues to a mysterious molecule called Yin Yang1 – and revealed that it could fuel tumor growth in breast cancer.

The findings of a group of international scientists led by Imperial College London could open new perspectives. In addition, the results also reveal how tumors can change their "appearance" to escape cancer treatments, using a system called epigenetics.

Yin Yang1 is a type of cancer. molecule, called transcription factor, that helps activate genes. Although each cell contains about 25,000 genes, only a certain number of them are activated at the same time, depending on the functions that the cell must fulfill.

All body cells need Yin Yang1, but scientists did not know To determine whether it is a friend or an enemy, the team completed a thorough genetic profile of breast tumors of 37 patients, using a variety of different techniques, including CRISPR gene editing technique.

The results, published in the journal Nature Medicine revealed that cancer cells are much more dependent on Yin Yang1 than normal cells and that they can promote the growth of breast cancer.

turn on when they become aggressive – which may affect the way they respond to treatment.

This suggests that doctors should take new tumor samples when a patient's cancer is spread in the body, said Dr. Luca Magnani or the Department of Surgery and Cancer of Imperial : "At the present time, patients usually have a biopsy at the time of breast cancer diagnosis. Doctors then analyze this tissue sample to identify the type of breast cancer in a patient, as this dictates the best treatment for them.

He continues, "However, our findings suggest that tumors activate and deactivate different genes as they progress, and can fundamentally change their appearance." Therefore, if a tumor becomes more aggressive and spreads around the body, we always recommend taking a second biopsy. The cancer may have changed significantly at this time, and respond to different treatments. Although a second biopsy is performed when the relapses of a patient become more common, this does not always happen.

Breast cancer is the most common cancer in the UK, with about 150 people diagnosed each day.

The new research, funded by the Wellcome Trust, Cancer Research UK and the European Union, has studied a type of breast cancer called estrogen-receptor positive, accounting for 70% of all breast cancers and treated with hormone therapy.

In the trial, researchers analyzed 34 breast tumors of patients whose cancer had not spread in the body, and 13 tumors of another group of patients with breast tumors more advanced, whose cancer had spread.

Researchers at the European Institute of Oncology of Milan, University of Liverpool and Case Western Reserve University in Cleveland, have studied activated and deactivated genes in tumors [19659013]. The allied epigenetic allows cancerous tumors to adapt to their environment, escape treatment and survive longer.

To help scientists follow epigenetics, researchers monitored chemical changes on DNA regions called amplifiers. on certain genes when they are activated.

The results revealed that two particular activators, regulating the SLC9A3R1 and Yin Yang 1 genes, are activated at specific stages when they could help cancer cells to develop and escape treatment

. was found to light up SLC9A3R1, which helped the tumors grow.

The team will now study a larger number of patient samples, and follow the same group of patients to follow the evolution of the activation of these cancers. They will also investigate a type of breast cancer known as the triple negative, which is very difficult to treat.

Dr. Magnani said, "As expected, our work has raised a lot of questions – and we have to respond to them – but it's only through international collaboration – and working as a team – that we can doing this essential work and, hopefully, helping more patients to conquer the disease. We could never have done it on our own. "

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