Multiple myeloma

A plasma cell is a mature white blood cell whose job is making antibodies — the proteins that tag germs for destruction. Myeloma is a cancer of those cells, and it typically involves many sites within the bone marrow rather than forming one lump in one place.

The abnormal cells all descend from one original cell, and they make the same useless antibody over and over. The NCI calls it M protein: an antibody the body does not need, which does not help fight infection. That is why a very high antibody level on a blood test here does not mean good immunity — quite the opposite.

“Multiple” refers to multiple sites within the marrow. It is a blood and marrow cancer rather than a bone cancer, even though bone is where much of the damage shows up.

Two earlier states are worth knowing the names of. MGUS — monoclonal gammopathy of undetermined significance — means the protein is present without the findings that define myeloma, and it is not cancer. Smouldering myeloma sits between the two: more abnormal cells, but still no organ damage. Both are usually monitored rather than treated.

What starts it in any one person is not established. None of the sources we read attributes myeloma to a specific identified cause, and we are not going to imply a lifestyle or behavioural one.

It is a disease of later life — the median age at diagnosis in US registry data is 69.

What is understood is the sequence. MGUS precedes myeloma, and the annual risk of it progressing to a plasma cell cancer runs from about 0.5% to 1% in population-based groups, higher in people with particular features. Smouldering myeloma carries a higher risk again, and that risk is not uniform — a small high-risk subgroup behaves very differently from the rest.

Changes in the chromosomes of the myeloma cells drive how the disease is expected to behave, and are part of how treatment intensity is decided.

The damage is summarised by four letters, CRAB, and they are laboratory and imaging findings rather than symptoms anyone can check at home.

C is too much calcium in the blood, released as bone breaks down. R is kidney impairment — fragments of the abnormal antibody can damage the kidney’s filtering tubules. A is anemia, because myeloma cells crowd the marrow where red cells are made, bringing tiredness and breathlessness. B is bone lesions: myeloma switches on the cells that dissolve bone, producing pain and fragile bones.

What people actually notice is usually bone pain, often in the back or ribs, bones that break easily, infections that keep coming, fatigue, or easy bruising and bleeding.

Infections are common precisely because the antibody being made in such quantity is useless, and normal antibody production is suppressed alongside it.

Myeloma is generally managed as a relapsing disease — periods of control, then return, then a further line of treatment. None of the sources we read describes standard treatment as curative, and it would be wrong to imply otherwise.

Treatment starts with induction: a combination of drugs given for months to bring the disease down. Three-drug regimens proved better than two, and four-drug regimens adding an antibody against a protein called CD38 are now standard for many people.

Then, for those fit enough, comes an autologous stem cell transplant — and it is worth walking through what that actually involves, because it is what most readers of this page will face.

First, mobilisation: five to ten days of growth factor injections to push blood-forming stem cells out of the marrow into the bloodstream. Then collection, which Cancer Research UK describes as three or four hours with blood cycling through a machine that separates out the stem cells and returns the rest. You are awake throughout. The cells are frozen and stored.

Then conditioning — high-dose melphalan through a central line — followed about a day later by getting your own cells back through a drip. That is the transplant. It is a rescue from the chemotherapy, not a replacement for your immune system.

Recovery is usually three to four weeks as an inpatient, though some centres manage it with daily outpatient visits. Low blood counts, infection risk, fatigue, hair loss and nausea are the expected course.

Afterwards comes maintenance, usually lenalidomide, continued until the disease progresses. So treatment does not finish on a date — many people are on something indefinitely.

When myeloma returns, the newer options are worth understanding because of what they are not. CAR-T uses the patient’s own T cells, collected and re-engineered in a laboratory. Bispecific antibodies are drugs that grab hold of the patient’s own T cells inside the body and bring them onto the myeloma. Neither involves a donor.

Many people arrive at this diagnosis sideways — through back pain, a fracture, an unexplained anemia or an odd kidney result — rather than through anything that looked like cancer.

For those found at the MGUS or smouldering stage, the experience is monitoring: knowing you carry something, and being watched rather than treated. That is its own burden and it is widely under-acknowledged.

Induction runs for months before any transplant, with steroids in nearly every regimen. Then stem cell collection, which is an outpatient day and a very different experience from the admission that follows.

The transplant admission is the hard part: three to four weeks, low counts, infection risk, mouth and gut effects, hair loss, nausea, fatigue. One thing that is genuinely easier here than in a donor transplant — because the cells are your own, there is no graft-versus-host disease to worry about.

And then it continues. Maintenance rather than an ending, successive lines of treatment over years, and bone damage or kidney impairment that can persist even when the myeloma itself is responding.

Almost nothing, and this is the disease that proves the point better than any other in this library.

Myeloma is the single largest reason people have a stem cell transplant in the EBMT reporting region — 13,783 first transplants in 2024, 31.5% of all of them. Of those, 13,694 used the patient’s own cells. Just 89 used anyone else’s, and only 37 of those came from an unrelated donor.

So a transplant is very likely part of your treatment, and a donor is very unlikely to be. If you came to this page braced to start a search, you can stop.

It is worth adding that even the rare donor transplant in myeloma is more often from a relative than from a registry — 52 of those 89 were related donors. And the guidance is cautious about it: there is real uncertainty about which patients benefit, and the benefits are offset by high rates of treatment-related mortality.

The newer treatments for relapsed myeloma do not change that. CAR-T uses your own T cells — the EBMT survey recorded 1,102 CAR-T procedures for myeloma in 2024 and every one of them was autologous. Bispecific antibodies use no cells from anyone at all.