Northern California Blood Cancer Conference

Hey there folks, haven’t forgotten your queries. In due time the conference organisers will send out copies of the slides shown in the various sessions, so I’ll be able to share any useful data then. In the meantime, I thought I’d share some notes that may be of interest that relate to MPNs. They’re a bit fragmented.

Firstly, I attended 3 sessions/lectures. The first one was from a locally famous cancer survivor, Stephanie Chuang, who set up The Patient Story so others could tell their cancer stories. It’s a bit like StoryCorps, if you know that, but for cancer. Her presentation was interesting but upon reading some of the information on The Patient Story website I noticed a few too many inaccuracies which put me off wanting to use it as a resource or share a link to it here. I’m sure the personal stories shared on there are fascinating. I think there’s only one Myeloproliferative neoplasms (MPN) survivor’s story.

Session 2 was Cognitive Concerns and Cancer with Dr Charles Windon of UCSF Memory and Aging Center (a fancy research hospital in San Francisco). Dr Windon spoke of his work studying how cancer survivor’s memories are affected by cancers and their treatments.

Chemotherapy causes neuroinflammation in the central nervous system. Neurons, which carry brain signals, can become injured from neuroinflammation. The body-brain barrier can weaken or doesn’t stop chemotherapy from entering the central nervous system via the brain. This affects memories and recalling them.

Ginkgo biloba shows benefits to memory/cognition impairment from cancer. Melatonin also helps, as does improving sleep generally.

Session 3 was MPNs with Dr Jason Gotlib of Stanford Cancer Institute (a fancy research university in the San Francisco Bay Area). Dr Gotlib shared so much information that his session ran over! He’s written over 200 scientific papers about blood cancer and is considered a world expert. I’d never heard of him but a fellow Polycythaemia vera (PV) survivor I chatted with at lunch is his patient and raved about his expertise in a slightly annoying way.

95-98 % of people with Polycythaemia vera (PV) have the JAK2 gene mutation. 50-60 % of Essential thrombocythemia (ET) and MF survivors have the JAK2 gene mutation. JAK2, CALR and the many other blood cancer-related gene mutations are known as driver mutations, as in they promote cancer development. JAK2 is by far the most common driver mutation.

Ropeginterferon treatment is better over time at molecular response on JAK2 than hydroxyurea. Less than 5 % of patients on interferon needed to stop due to side effects.

Some patients taking hydroxyurea can have iron added back in if anaemia is an issue (thank goodness!).

Ruxolitinib treatment is more effective at relieving fatigue and achieving overall benefits than hydroxyurea or interferon. It’s also better for complete response and event-free survival from thrombosis, haemorrhage, transformation (from one cancer to another), and death.

A new medicine being trialled, rusfertide, helps eliminate the need for phlebotomy and improves symptoms. Also better than others at eliminating iron deficiency as fewer bloodletttings are needed. It has a possible increased risk of basal cell carcinoma. May be introduced as treatment within 2-3 years.

A treatment currently called INCB160058 affects and inhibits only mutated JAK2, not all JAK2 gene mutations. No information about its medical approval.

In the womb, a foetus’ spleen makes its blood, whereas once born the bone marrow takes over producing blood.

Essential thrombocythemia (ET) can morph into Polycythaemia vera (PV) and can be considered masked Polycythaemia vera (PV). However, Polycythaemia vera (PV) won’t change into Essential thrombocythemia (ET). Polycythaemia vera (PV) can transform into Acute myeloid leukaemia (AML), or into Myelofibrosis (MF) and then into Acute myeloid leukaemia (AML), over 20 years.