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Sima Lev Prof. of the Weizmann Institute of Science aims to defeat a particularly threatening type of breast cancer

Prof. Sima Lev of the Weizmann Institute of Science aims to defeat a particularly threatening type of breast cancer. Of course, cancer diagnosis is never good news, but the particular type of malignant breast tumor that Prof. Lev is dealing with makes it particularly difficult to treat. This type is called triple negative, because the cells do not have the same three receptors that other types of breast cancer serve as targets for drugs. With no targets to which drugs can bind, treatment options are extremely limited, and even when chemotherapy does work - the cancer is so aggressive that it sometimes returns. Even when the tumor is discovered at a very early stage, there is a great chance that it has already been able to sneak into distant limbs, eventually causing metastasis

In a new study published in the scientific journal Nature Communications, Prof. Sima Lev and postdoctoral researcher Dr. Nandini Verma, from the Department of Cell Molecular Biology, have provided new insights into triple-deficiency breast cancer that may help treat these malignant tumors in the future. Focus on the process that takes place in all the cancer cells to create a metastasis, which is a relatively steady transition, in which the cells maintain regular contact with neighboring cells and the intercellular pattern, into a more invasive state - during which their shape, the structural components that allowed them to connect to the environment, To spread in the body.

Scientists have identified a kind of molecular switch - an enzyme called PYK2 - that plays a key role in switching to the invasive state. About two decades ago, when Professor Lev discovered this enzyme, it showed that it transmits signals that lead to cell growth, distribution, and mobility. In a healthy state, when the cell grows, for example in the embryo or during wound healing, these signals are essential. In the new study, Dr. Verma - in collaboration with Omar Keenan and Michael Slitternik, also from Prof. Lev's group - revealed how this enzyme promotes the formation of breast cancer metastases.

In the first stage, scientists found that the enzyme causes the cells to invade by extending the normal signal it produces, and it starts to act like a stuck doorbell that doesn't stop ringing. They later found out that in triple deficiency cancer two different mechanisms lead to this
First - by weakening the switch that usually stops the signal - the enzyme causes the signal leading to the invasive state to remain long in the activated state. At the same time, the enzyme acts as a kind of continuous positive feedback - it transmits a signal that promotes the transition to an invasive state, while at the same time increasing the very production of the enzyme itself, so that its level in the cell continues to rise. These two mechanisms lead to the fact that the signal that leads to the cells to invade continues to work for a long time, causing more damage.

Scientists examined nearly 100 tissue samples from breast cancer patients, and found that the enzyme levels were higher in more aggressive tumors. Furthermore, in patients whose lymphoma spreads the enzyme level was higher than in patients whose cancer did not spread to these vessels. When the scientists engineered the cells in the laboratory to evade the enzyme, the invasive cells returned to their normal state - evidence that indeed, this enzyme acts as a switch to enable the invasive state.
 
In light of these findings, the enzyme PYK2 may, in the future, serve as a target for new treatment of triple deficiency breast cancer, through the development of small molecules that block its deleterious signal. Such molecules may, in the future, be used as a drug, in combination with other anti-breast cancer drugs.
Prof. Sima Lev of the Weizmann Institute of Science aims to defeat a particularly threatening type of breast cancer. Of course, cancer diagnosis is never good news, but the particular type of malignant breast tumor that Prof. Lev is dealing with makes it particularly difficult to treat. This type is called triple negative, because the cells do not have the same three receptors that other types of breast cancer serve as targets for drugs. With no targets to which drugs can bind, treatment options are extremely limited, and even when chemotherapy does work - the cancer is so aggressive that it sometimes returns. Even when the tumor is discovered at a very early stage, there is a great chance that it has already been able to sneak into distant limbs, eventually causing metastasis

In a new study published in the scientific journal Nature Communications, Prof. Lev and postdoctoral researcher Dr. Nandini Verma, from the Department of Cell Molecular Biology, have provided new insights into triple-deficiency breast cancer that may help treat these malignant tumors in the future. Focus on the process that takes place in all the cancer cells to create a metastasis, which is a relatively steady transition, in which the cells maintain regular contact with neighboring cells and the intercellular pattern, into a more invasive state - during which their shape, the structural components that allowed them to connect to the environment, To spread in the body.

Scientists have identified a kind of molecular switch - an enzyme called PYK2 - that plays a key role in switching to the invasive state. About two decades ago, when Professor Lev discovered this enzyme, it showed that it transmits signals that lead to cell growth, distribution, and mobility. In a healthy state, when the cell grows, for example in the embryo or during wound healing, these signals are essential. In the new study, Dr. Verma - in collaboration with Omar Keenan and Michael Slitternik, also from Prof. Lev's group - revealed how this enzyme promotes the formation of breast cancer metastases.

In the first stage, scientists found that the enzyme causes the cells to invade by extending the normal signal it produces, and it starts to act like a stuck doorbell that doesn't stop ringing. They later found out that in triple deficiency cancer two different mechanisms lead to this
First - by weakening the switch that usually stops the signal - the enzyme causes the signal leading to the invasive state to remain long in the activated state. At the same time, the enzyme acts as a kind of continuous positive feedback - it transmits a signal that promotes the transition to an invasive state, while at the same time increasing the very production of the enzyme itself, so that its level in the cell continues to rise. These two mechanisms lead to the fact that the signal that leads to the cells to invade continues to work for a long time, causing more damage.

Scientists examined nearly 100 tissue samples from breast cancer patients, and found that the enzyme levels were higher in more aggressive tumors. Furthermore, in patients whose lymphoma spreads the enzyme level was higher than in patients whose cancer did not spread to these vessels. When the scientists engineered the cells in the laboratory to evade the enzyme, the invasive cells returned to their normal state - evidence that indeed, this enzyme acts as a switch to enable the invasive state.
 
In light of these findings, the enzyme PYK2 may, in the future, serve as a target for new treatment of triple deficiency breast cancer, through the development of small molecules that block its deleterious signal. Such molecules may, in the future, be used as a drug, in combination with other anti-breast cancer drugs.
Last modified onWednesday, 01 April 2020 06:56

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