Asporin production isn’t supressed in hormone-dependent cancers: in cells, the rate is four times higher than in cells of triple negative or HER2+ background. Examining the survival of 375 patients suffering from triple negative cancer over a period of 25 years showed that the survival rate is 42 % lower in patients with low levels of asporin.

A treatment exists!

The mechanism behind this role played by the triple negative cancer cells was unravelled by the team at the Laboratory of Metastases Research (in particular, Dr. Pamela Maris, the first author of the article) in collaboration with the doctors at CHU Liège (especially Prof. Eric Lifrange and Dr. Pino Cusumano from the senology department; Dr. Sylvie Maweja from the abdominal surgery unit; Prof. Guy Jérusalem from the oncology department; and Prof. Philippe Delvenne from the pathology department). “It’s thanks to this true collaborative effort in translational research that we have been able to do this work”, Prof. Castronovo insists. “Our study reveals that asporin isn’t produced by the fibroblasts in triple negative tumours, because they receive a counter order from the cancer cells transmitted by interleukin-1β (IL-1β). IL-1β is a well-known cytokine involved in the inflammatory mechanisms, which is also produced by the most aggressive cancer cells. Hence, we envisage that by blocking IL-1β, the breast fibroblasts will freely produce asporin, and thus ‘build’ this protective biological wall and significantly slow down the progress of the cancer as well as the formation of metastases”, continues Prof. Castronovo.

The results in mice warrant this approach: mice carrying triple negative cancer cells that were implanted with fibroblast that overexpress asporin, grew twice as slowly and resulted in three times fewer metastases.

The good news is that the treatment, which blocks IL-1β, does exist and is already on the market. It is currently prescribed to people who suffer from inflammatory joint diseases, especially arthritis. “It has already been tested to prove its safety, which means we have a head start in terms of research and therapeutic trials. That said, there’s no point in carrying out studies to compare its efficacy in relation to other treatments because there aren’t any. Therefore, we may soon be able to test this treatment on women with triple negative breast cancer. I think that within six months, we will be able to clearly demonstrate its efficacy in mice, and after that, it may be possible to administer it to patients in a clinical trial.” Negotiations with the pharmaceutical laboratory producing this treatment are underway.

Other avenues, other hopes

Another possibility would consist of administering an asporin peptide that can mimic the action of the full length protein. “The problem is that it has to be stabilised in order to make a new treatment; further difficulty is the polymorphism of cancer cells. Next, there is the required battery of therapeutic trials, which will delay the offer of a possible therapy for one of the most aggressive types of cancer by several years”, concludes Prof. Castronovo.
But this discovery opens other doors: asporin could play a comparable role in other types of cancers, such as lung cancer or lymphoma. New perspectives are therefore on the horizon for aggressive cancers, which kill numerous patients every year.