Hello folks - just to let you know I've completed the treatment phase of the trial and - alleluia - I'm clear of cancerous cells in bone marrow and blood.
To read about my experiences on this trial - copy and paste the link below into your browser. It's my Blog of how I survived the trial and other issues - it's a personal view and as such it should be considered (non-medical) and (non-advisory)
I was patient number 6 in this trial and, even though I had extremely bulky disease, it did not work for me at all. On the lowest dose of bispecific antibody, my disease was progressing rapidly. Then my liver gave up so they couldn't increase the dose and I came off the trial after just one week.
This is not an easy trial and requires a huge amount of personal commitment to attend each week for the top up and to have the quite large pump attached to you 24 hours a day. I enjoyed the cognitive tests and being allowed to go out to wander around Hamstead Heath or get coffee/snacks from that lovely little place just across the road. As you say Dr Jasani and Marvie and a fantastic team, so caring and at the top of their professions.
I hope all remains well for you and you are cured
Jackie
PS I'd be interested to know your CLL markers. I am 11qdel, unmated, two BTKi mutations
I should explain to anyone outside the U.K. that Luton was once ( still ? ) the home of hat manufacturing. The Mad Hatter in Alice is supposedly based on the mercury used allegedly making the workers mad ! 🎩
So good to hear of your successful treatment! The new/experimental treatment you were a pioneer in testing, is one more step toward the finding a cure for CLL. I, for one, am grateful for your participation.
Hi Roger, Congratulations & thanks for sharing the GOOD news. If I do venture into any clinical trial, I will copy your trick of singing Hallilujah, at least 3 times a day.
(I'm not getting a medical degree from reading this stuff , I just am happy to read that this method of targeting is successful)
NVG-111 is a bispecific antibody drug, having two "arms", one arm attaches to a substance on cancer cells called ROR1, the other arm attaches to the body's immune cells directing them to kill the cancer cells.
. . .
Receptor tyrosine kinase-like Orphan Receptor 1 (ROR1) is a protein which is expressed at high levels on many types of haematological cancers but is absent or expressed at low levels in normal adult organs. NVG-111 is a bispecific antibody T cell engager, comprising tandem single chain variable fragments (scFv), one arm binding to ROR1 on cancer cells, the other to cell surface CD3 on lymphocytes. Dual binding of NVG-111 causes MHC-independent immunological synapse formation, releasing perforins, granzyme B and cytokines, resulting in targeted killing of the cancer cells.
81ue, great summary of NVG-111! In an earlier post Jackie Jm954 posted a figure showing how BiTEs work to bring cancer cells and T-cells together. healthunlocked.com/cllsuppo...
Since some folks have reported that figures can aid their understanding of cell & molecular biology, I slightly modified the figure that Jackie posted to make it NVG-111-specific. The link to the original figure is researchgate.net/publicatio...
Great - I'm afraid - I was kicked off O Level Chemistry (although I have O Level biology!) I'm happy to leave it to the clever scientists. It gives me confidence that despite all the bad things happening - we are still seeking and finding solutions to some big problems - shame we've taken our ey off the ball with the planet and economics!
Roger, what an inspiring story! Congratulations to you and Kym!
Somehow I missed an earlier link to your “Significantly Average - Assorted rambling thoughts!” webpage, but today I read all of your posts and listened to your music.🤗 All I can say is that you are definitely anything but significantly average! Your posts were incredibly engaging! Not only are you a musician but you are a polished journalist as well as a mystery writer! A composer of music as well as a composer of the written word.
I encourage anyone reading this to check out Roger’s website at:kymandroger.co.uk
Now, back to the topic of NVG-111, there is an ASH abstract (#1810) reporting results from the first few months of the NVG-111 101 Clinical Trial. I believe the abstract was written before you, Roger, even started the trial. They may update data at the meeting, including your excellent results.
Objective clinical responses were observed in 66% of subjects and included 2 MRD4 negative clinical remissions (CR). These two subjects remained in MRD4 negative CRs at 6 months after completion of treatment. ash.confex.com/ash/2022/web...
This the first CLL treatment I know of that specifically hopes to target the cancerous B cells while sparing healthy, maturing B cells., because of the high degree of overabundance in ROR-1 expression in CLL cells. To a lesser extent BCL-2 and BTK also tend to be higher in CLL cells, so treatments targeting these proteins (venetoclax and the many 'brutininbs') can also spare healthy maturing B cells.
Thank you for sharing your experiences and for writing about them at length on your blog.
Thank you for continuing to share your knowledge and wisdom. I've read many of your posts over the 7 years of my CLL experience. I'm not a regular on HU - but I lurk , look and learn.
Ha ha - I never thought that of myself - there were a few scary moments - but such a great team. Thanks for your kindness - life goes on! Still on Ibrutinib - but those days may be numbered! R
Well done Roger, I'm so pleased for you, but reading some of your blog I'm not sure I would have had the strength and perseverance to complete the treatment. I really admire you.
I hope to speak to Parag next week, and if it's OK with you I would like to congratulate him on your success. I'm sure he must be thrilled.
Fabulous - Parag is a good, clever man. He was up all hours during a few of my bad nights. They will learn from experiences of crazy folk such as me. R to R Roger and out!
Hi RogerHappy, wonderful news! Yay & so grateful to you for sharing~ Took a quick look at your website (my husband plays guitar too). And I will be enjoying more as I sip my coffee.
You're so kind - make sure he plays every day! I'm showing my age when I write - I learned to play with a book by Bert Weedon called "play in a day" - it's taken me over 50 years!
Many thanks - let's encourage one another to keep on with this CLL business - I've been fortunate to have asked the right question to someone who knew Dr Jasani and I was able to participate - I'm trying to find some normality now!!!
Second, pardon my ignorance here, but this treatment, is it a new class of CLL drug--meaning, we have the 'brutinibs, we have Venetoclax, and we have the forthcoming pirtobrutinib, each of which works in different ways; was your treatment something entirely new, hence a fourth class, or a variation on one of the three classes we already have?
(I shamefully admit I didn't carefully read the more technical-looking posts above ...
Yes Dave - it's brand new. Check out on the WWW. This trial is the first human trial of it - I'm blessed to have been able to participate. It was a bit of a "trial" too - but I was well-supported. R
Targeted therapies do not affect CLL DNA, so they do not cause mutations. What happens is that when CLL cells divide, it is inevitable that some errors in the DNA occur during the DNA copying process. Cancer cells aren't good at checking their DNA when the cells divide - that's how the cancer began! So what can happen, is that during CLL cell division, an error in the DNA responsible for the production of the BTK enzyme in CLL can occur and not be corrected. If the BTKi can no longer inhibit the enzyme, that sub-clone has a selective advantage. So over time, it becomes the dominant clone and the CLL becomes resistant to treatment with that class of BTKi. Currently approved BTKi drugs (acalabrutinib, ibrutinib and zanubrutinib (for MCL, but CLL FDA approval is imminent)), covalently bond to the BTK. There's a third generation of BTKi drugs which non-covalently bond to the BTK. These should still work when resistance develops to the covalently bonding BTKi. So switching to one of the BTKi drugs in this class should give you an extension of the control of your CLL by BTKi treatment. FDA approval for the first non-covalently bonding BTKi, pirtobrutinib, is imminent!
Neil
PS When resistance develops on BTKi treatment, it tends to occur slowly. It's important to stay on the failing BTKi until you can transition to your next treatment. If you cease treatment, there's a risk of tumour flare, the treatment for which is to resume BTKi treatment. Tumour flare is best avoided.
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