There are of course many mechanisms that are proposed which bridge the cancer or the cancerous cell and the neuronal activity and more recently even what made this link even more interesting is novel data that points to the fact that the neurons itself the activity can also contribute to change the cancer cell behavior. This has been demonstrated in glioblastoma tumors, and it has been shown that by activating the neurons surrounding the tumor, these tumors can grow...
There are of course many mechanisms that are proposed which bridge the cancer or the cancerous cell and the neuronal activity and more recently even what made this link even more interesting is novel data that points to the fact that the neurons itself the activity can also contribute to change the cancer cell behavior. This has been demonstrated in glioblastoma tumors, and it has been shown that by activating the neurons surrounding the tumor, these tumors can grow. So there is here a bridge that goes, or a link that goes in both directions. For us, of course, it’s more important how this tumor triggers epilepsy, and the gap is, of course, to target all the mechanisms at once. So we know that these mechanisms can be non-cell autonomous or paracrine. So this means that the cells can release some factors that are able to alter the neurons. And we have proved this with in vitro experiments. So this happens during development. These cells are very active, they release factors, and they alter the surrounding neurons by altering this activity. But this is not the only mechanism. This, of course, brings up several candidates, but there are more. Cells can also modify the environment physically. Even though these tumors don’t grow very much, they trigger a strong glial reaction that in the end alters the microenvironment and the milieu. And of course, this is also or triggers also changes in the neuronal activity. So I would say that at the moment, the main gap is to find the best treatment candidate in order to tackle all these mechanisms at once. So we suggest that instead of doing this, the option may be adjuvant treatment, which of course has been done in the past very frequently. And we think that this will be the way to really describe how the cells communicate with the neurons and to find out the most important candidates or targets to tackle. But we don’t think that there is only one, let’s say one problem, but there are several. And I would say that this, to answer your question, it’s the major gap.
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