mpn

Intense itching, prickling or burning of the skin within minutes of contact with water, typically after a shower. It affects a large minority of people with polycythaemia vera and can be the most disabling symptom.

Aspirin is not a cancer drug but sits in cancer care in two places: low doses prevent clots in polycythaemia vera and essential thrombocythaemia, and long-term use lowers colorectal cancer in people with Lynch syndrome, while a trial in the healthy elderly found no benefit and possible harm.

Led COMFORT-II, which established ruxolitinib as the first drug for myelofibrosis, and most UK MPN trials since.

Today's PV drugs control blood counts but leave the mutant cells in place. Interferon is the one treatment that shrinks the clone, and the first JAK2 V617F-selective inhibitors have entered trials; combining the two could aim at molecular remission, the way imatinib did for CML.

CYTO-PV settled the most basic question in PV: keeping the haematocrit under 45 percent gives far fewer serious clots and cardiovascular deaths than a looser target.

Too many red cells. In polycythaemia vera the marrow itself is at fault (primary); far more often the cause is something else driving it, such as smoking, low oxygen, sleep apnoea, a kidney tumour or testosterone (secondary).

Burning pain, redness and heat in the hands or feet, brought on by warmth. In polycythaemia vera and essential thrombocythaemia it comes from platelets clumping in tiny vessels and often disappears with low-dose aspirin.

Essential thrombocythaemia is a slow blood cancer in which the marrow makes too many platelets. Most people need only aspirin and monitoring; those at higher risk of clots take a drug to lower the platelet count, usually hydroxyurea or interferon, with anagrelide in reserve.

The share of blood volume made up of red cells. Normal is roughly 40 to 50 percent; in polycythaemia vera treatment aims to keep it under 45 percent, because above that clots become much more likely.

The liver hormone that controls how much iron the body absorbs and releases. Drugs that mimic it lock iron away so the marrow cannot make excess red cells, the idea behind rusfertide.

Rusfertide replaced phlebotomy in patients who needed it often. The open question is whether hepcidin control from diagnosis, in low-risk patients who today get phlebotomy alone, prevents the iron deficiency, the count swings and perhaps the clots that phlebotomy leaves behind.

A single letter change in the JAK2 gene that jams the growth signal for blood cells in the on position. Almost everyone with polycythaemia vera has it, as do about half of those with essential thrombocythaemia or myelofibrosis.

Low-PV asked whether even low-risk patients gain from interferon: more of them stayed at the haematocrit target without progression when ropeginterferon was added to phlebotomy.

MAJIC-ET found that ruxolitinib was no better than the usual second-line drugs at controlling platelets in ET, although it eased itching and other symptoms.

MAJIC-PV, a UK academic trial, found that ruxolitinib gave more complete responses than best available therapy and, for the first time, that a complete response went with fewer clots and progressions.

Removing about a pint of blood through a vein, as in a blood donation, to bring the red cell count down. It is the oldest treatment in polycythaemia vera and still the first.

Polycythaemia vera is a slow blood cancer in which a single faulty gene, JAK2, makes the bone marrow produce too many red cells. Thick blood causes clots, so treatment thins it (blood removal, aspirin) and, for higher-risk patients, calms the marrow with hydroxyurea, interferon or ruxolitinib; a hepcidin mimic, rusfertide, now controls red cell counts without regular blood removal.

The late stage some people with polycythaemia vera reach after many years, when the marrow scars over, the red count falls and the spleen swells. It is treated as myelofibrosis.

PROUD-PV and its extension showed that ropeginterferon matches hydroxyurea in the first year and then pulls ahead, with more complete responses and far more molecular responses by three years.

PT-1 is the trial that made hydroxyurea the first-line drug in high-risk ET: anagrelide gave more arterial clots, more serious bleeding and more progression to myelofibrosis.

New York haematologist who led MANIFEST-2, the trial testing whether adding the BET inhibitor pelabresib to ruxolitinib helps people with myelofibrosis more than ruxolitinib alone.

RESPONSE showed that ruxolitinib controls the haematocrit and shrinks the spleen in PV patients hydroxyurea has failed, and won the first drug approval specific to that setting.

RESPONSE-2 extended ruxolitinib's benefit to PV patients without an enlarged spleen: three times as many reached haematocrit control.

Haematologist who led the COMFORT-I trial that established ruxolitinib, the first drug approved for myelofibrosis, and MOMENTUM, which established momelotinib for patients with anaemia.

VERIFY showed that weekly rusfertide, a hepcidin mimetic, freed most PV patients from phlebotomy and improved their symptoms, leading to the drug's approval in 2026.