2023-11-05 22:40:20
This type of breast cancer (triple negative) is one of the most dangerous and difficult to treat. Recent research shows that manipulating the metabolism of these cancer cells can both slow tumor growth and activate anti-cancer immunity.
Thanks to the discovery of new drugs such as Herceptin and the improvement of treatment protocols, breast cancer is now one of the cancers with the best prospects for survival, especially when it is diagnosed very early.
The latest data indicates that more than 95% of women affected by early forms of this cancer survive the disease, a resounding success which demonstrates the positive repercussions of cutting-edge scientific research in biochemistry against this cancer.
A complex disease
However, this does not mean that the game is completely won: breast cancer is a complex disease, which brings together several types of diseases and which can vary considerably from one tumor to another, presenting very distinct biochemical characteristics which influence the success of treatments.
This is particularly the case for a class of breast cancers called triple negative: as its name indicates, this type of cancer does not express any of the receptors commonly found on the surface of cancer cells (estrogen receptors, progesterone and growth factor EGF) and therefore does not respond to therapies that have been developed against these receptors.
Approximately 10 to 15% of breast cancers are triple negative and are characterized by very rapid growth as well as an aggressive clinical course which is associated with a low survival rate of affected patients.
The identification of strategies that can reduce the development of this type of breast cancer is therefore particularly important to reduce the burden imposed by this disease.
Alter metabolism
The rapid and uncontrolled growth of cancer cells requires a constant supply of energy and it is for this reason that cancer cells have a different metabolism from normal cells.
This is particularly evident for triple negative breast cancer, as these tumors have been observed to be dependent on a molecule called acetate as a carbon source. It is therefore plausible that interference with acetate metabolism could represent a promising anticancer approach against this cancer.
The validity of this approach has just been confirmed by the results of a study recently published in the very prestigious journal Nature Cancer. (1) In this study, the researchers showed that blocking the enzyme responsible for the transformation of acetate (acetyl-CoA synthetase) profoundly modified the metabolism of cancer cells: instead of using the acetate to reproduce, the tumor cells instead secreted the acetate out of the cells, into the tumor microenvironment, thereby depriving them of an important source of energy for their growth.
Immune activation
An extremely important consequence of this expulsion of acetate towards the outside of the tumor is to potentiate the immune response.
We have known for several years that acetate, produced in very large quantities by the microbial metabolism of dietary fibers in the colon, plays an extremely important role in the functioning of the immune system.
This is particularly crucial in the context of the environment near tumors where glucose is scarce and in insufficient quantities to allow killer T cells to attack and eliminate cancer cells.
By promoting the secretion of acetate by tumors, we at the same time allow killer cells to use this source of energy to accomplish their anti-cancer function.
In other words, interference with acetate metabolism has two distinct but complementary effects: a slowdown in the growth of cancer cells, combined with an activation of immunity directed against tumor cells.
The clinical trials currently underway will provide a better understanding of the clinical potential of this promising new therapeutic approach. An important scientific advance against a dangerously fatal cancer.
♦ (1) Miller KD et al. Acetate acts as a metabolic immunomodulator by bolstering T-cell effector function and potentiating antitumor immunity in breast cancer. Nature Cancerpublished on September 18, 2023.
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