CAR-T therapy

Science: When treatments create new conditions

When the actor Sam Neill died unexpectedly in July this year, media reports emphasized that his death was not due to cancer. Neill was diagnosed in 2022 with angioimmunoblastic T-cell lymphoma […] after four years in remission he stopped responding to chemotherapy. […] Neill seems to have responded well [to CAR-T], and in April 2026 he publicly announced that he was “cancer-free.” Yet only four months later he was dead, and many people were puzzled about what had “gone wrong.”
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The health care of the future may see more and more patients in this ambivalent territory, in which they can be described as free of their original disease but because of their treatment are living in a state of chronic fragility. Yet in many cases there is still a cultural expectation that a “successful” treatment is one that restores the patient to a state of health, without the need of ongoing clinical management.
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The rapidly expanding ability to manipulate the immune system pharmaceutically, increased automation, and the use of artificial intelligence promise to accelerate drug discovery and clinical trials. In this new era of therapeutic development, clarity about goals, outcomes, and realistic expectations is crucial. However successful it is against the primary condition, a therapy that leaves patients in need of continuing and possibly equally demanding health care is not only economically costly, but raises ethical questions about quality of life. Clinicians also need to be able to communicate clearly what “cure” or “disease-free” might mean in different contexts. This need will increase because—as has been the case with CAR T-cell therapy—when an innovative treatment receives regulatory approval and becomes standard care, its use tends to expand from the group of patients with no other treatment options to those in earlier disease stages, or with different diseases.
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I am not sure that it is ominous or unexpected. We knew that CAR-T was cumbdersome and involved problematic steps. There was a hope that it might test the hypothesis that deeper b clonal depletion might induce long term remission in more autoimmune diseases. It may still prove to be true that you can get more long term remissions this way, although what I have seen so far does not look like a quantum leap.

Whatever the result the assumption that Maria and I have tended to make is that what we are really looking for is a safe way of targeting autoimmune B clones specifically and that is more likely to involve monoclonal antibodies or even small molecules like complement inhibitors.

What is disappointing to me is that the community working with these therapies by and large has no detailed understanding of the dynamic bottlenecks they are wanting to attack within B cell dynamics. It is little ore than 'Yeah, let's kill some more B cells'. Most of them have never understood why we developed the approach in the first place. I am not sure what the answer will be but I think it may appear unexpectedly , as these things do, and we were never expecting it to be CAR-T in the long run.

Moreover, it probably has zilch to do with ME/CFS.
 
I meant more in terms of what it means when the definition of recovery becomes slippery and patients continue to suffer from symptoms and illness that current technology cannot make sense of, and cultural memes and ignorant opinions dominate the issue.

It would place them in the same hellpit as us. Not a good outcome. Existing like this can be a far worse outcome than dying, a genuine curse. There have been a few reports of patients dying from CAR-T cell therapy, recognized as a terrible outcome. This here wouldn't, making it all even worse in the end.
 
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