5 ms·
This method is not targeting mutations important for cancer, this is targeting "passenger" somatic mutations. You can't use this mechanism to target important m
by astazangasta 10y ago
This method is not targeting mutations important for cancer, this is targeting "passenger" somatic mutations. You can't use this mechanism to target important mutations because only a minority of patients are going to be able to present an oncogenic mutation (e.g. BRAF V600E) as an antigen (because of differing HLA types). In those rare cases perhaps this therapy might succeed, although the tumor probably still has ways of evading (downregulating the offending HLA for example).
As for the "kitchen sink" approach, so far none of the methods we've developed are free from side effects. Cancer patients are often on the edge of death; each successive therapy will probably do more damage to them. As it is most people fail on current immunotherapies because of autoimmune reactions. So relentless application of therapies is not necessarily going to work, though of course having more weapons in our arsenal is great.
- danieltillett 10y agoI was under the impression that the major reason for the failure of current immunotherapy treatments is due to non-response, not excessive autoimmunity.
- astazangasta 10y agoSorry, you're absolutely right. I should say 'many', not 'most', my comment was hasty. It varies with the therapy and only a minority of patients fail because of adverse immune events, and the drug matters - ipilimumab (anti-CLTA4) had 10-15% severe immune-related adverse events, whereas anti-PD1 is much better tolerated (probably because the immune checkpoint is later). Combination therapies (ipi + nivo) have much higher adverse event rates, unsurprisingly.