• Welcome to Phoenix Rising!

    Created in 2008, Phoenix Rising is the largest and oldest forum dedicated to furthering the understanding of, and finding treatments for, complex chronic illnesses such as chronic fatigue syndrome (ME/CFS), fibromyalgia, long COVID, postural orthostatic tachycardia syndrome (POTS), mast cell activation syndrome (MCAS), and allied diseases.

    To become a member, simply click the Register button at the top right.

Scientists can now make leukemia cells kill each other

lansbergen

Senior Member
Messages
2,512
http://www.pnas.org/content/early/2015/10/20/1519079112

Abstract
An attractive, but as yet generally unrealized, approach to cancer therapy concerns discovering agents that change the state of differentiation of the cancer cells. Recently, we discovered a phenomenon that we call “receptor pleiotropism” in which agonist antibodies against known receptors induce cell fates that are very different from those induced by the natural agonist to the same receptor. Here, we show that one can take advantage of this phenomenon to convert acute myeloblastic leukemic cells into natural killer cells. Upon induction with the antibody, these leukemic cells enter into a differentiation cascade in which as many as 80% of the starting leukemic cells can be differentiated. The antibody-induced killer cells make large amounts of perforin, IFN-γ, and granzyme B and attack and kill other members of the leukemic cell population. Importantly, induction of killer cells is confined to transformed cells, in that normal bone marrow cells are not induced to form killer cells. Thus, it seems possible to use agonist antibodies to change the differentiation state of cancer cells into those that attack and kill other members of the malignant clone from which they originate.
 

alex3619

Senior Member
Messages
13,810
Location
Logan, Queensland, Australia
An antiibody can change a cell to do something totally different than it usely does.
I think this is probably limited in what it can do, but changing a B cell to an NK cell? What are we trying to get rid of using Rituximab? The proximate target is B cells, though arguably the final target is plasma cells. What innate cell type do we have that does not work? NK cells. This approach is intriguing to say the least. I think a pilot study might be a good idea at some point, presuming that the research can stand up to scrutiny.

On psychobabble I am content with just academic suicide. The PACE trial is an Achilles heel - touted as miraculous but so flawed it should be investigated for retraction. The latest article, still being published in parts by David Tuller, highlights just some of the issues we have been talking about, presumably those he has currently been able to verify independently. The argument that actions in the trial might have been unethical has surfaced again. Consideration that it is so fatally flawed that it has no value have also been cited. This could get interesting. While its not clear we are talking scientific fraud, it is clear that much of the argument is deceptive and misleading. For the most part they say what they did (but not always, hence the need for FOI requests), but their argument relies heavily on nobody actually reading and understanding what they did, just reading the reviews, or abstract, or bits and pieces of the papers.

This might be academic suicide in progress: http://forums.phoenixrising.me/inde...he-pace-chronic-fatigue-syndrome-study.40664/
 

lansbergen

Senior Member
Messages
2,512
What innate cell type do we have that does not work? NK cells.
This approach is intriguing to say the least. I think a pilot study might be a good idea at some point, presuming that the research can stand up to scrutiny.

I agree.