I'm sorry to hear that Figgs. Life can be so
Post# of 148282
Life can be so ironic I guess.
It is so unfortunate that the very disease (amongst many others), of which he studied, would be the one which took his life.
I posted even today about the Hematopoeitic Stem Cell line which gives rise to all our blood cells.
It gives rise to the Myeloid and the Lymphoid cells.
Multiple Myeloma is a cancer of the differentiated B cells which are the Plasma Cells.
The B cells develop antibodies and when a B cell becomes activated to mass produce its antibody, it becomes a Plasma Cell.
Multiple Myeloma is a cancer of the Plasma Cell. Normally, the B and Plasma cells should be able to produce all types of antibodies. MAGED. IGM, IGA, IGG, IGE and IGD. However, with multiple myeloma, one can only produce are the "M" type antibodies. and these don't work anyway, but the patient gets a huge "M" spike when measuring for the type of proteins in the blood.
Multiple Myeloma induces huge osteoclastic activity and therefore leads to lysis of the bone. One can find punched out lesions in the bones because the osteoclasts resorbed too much bone, leading to hypercalcemia and anemia, because, the bone marrow becomes dedicated to producing faulty Plasma cells and not even enough red blood cells.
There are a whole bunch of cells in the Stem Cell line up prior to the Plasma Cell. The development of MM could have come from any one of those progenitor cells. All of these cells use the same interleukins and cytokines to communicate but I'm not sure to what extent CCR5 is employed.
In the Stem Cell line, we have: Pluripotent Hematopoeitic Stem Cell >> Lymphoid Stem Cell >> B Cell Progenitor >> Professional B Cell >> Mature B Cell >> IGM Antibody Secreting B Cell / Switched Plasma Cell Secreting Non-IGM Antibody
Leronlimab might work via chemical cellular communication to prevent MM where ever there is this symbol: >>
Thanks for sharing your dad Figgs. I'm sure he had a wealth of knowledge which I hope he shared.