Hi EveryoneMy husband starts his Venetoclax on Thursday this week.
His consultant sent a letter to his GP saying he is starting treatment. However it also says he has progressing CLL with complex genetics. SF3B1 mutated with genetic complexity
Can anyone tell me what this means? As you can imagine I am fearing the worst
Thank you
Hi Sanders9,
There are several clinical trial results on our modern targeted therapies that indicate some folks with complex genetics are likely to progress slightly faster than other CLL patients.
This is not a strong negative indication, and does not predict serious complications, it may mean that instead of having a 5 year remission after completing venetoclax/Venclexto, his remission may be 4 years.
But please remember that each CLL patient has different results, and the trials only measure the averages for a large number of people.
In a few years, your husband will still have many other treatments to choose from, if and when his CLL starts to progress again.
My CLL progresses much faster than others with my genetic profile. I have had 5 different targeted therapies since 2012 and completed 15 years since my diagnosis.
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Len
Thank you Len. I appreciate your response. Dr Google is not my friend
Hello Sanders. Cll is very heterogeneous. That means we can all have different types of cll that can act a bit differently. Even if we have the same genetic type cll, it can act differently.
The four main types of cll, as defined by the location on a chromosome where we have genetic abnormalities, are 11q cll, 13q cll, trisomy (on the 12th chromosome) and 17p cll.
It’s confusing, but basically if one has 11q cll, it means they have a genetic abnormality on the q arm of the 11th chromosome. One with 17p cll has a genetic abnormality on the p arm of the 17th chromosome.
Our chromosomes are loaded with genes like the ATM gene on the 11th chromosome and the TP53 gene on the 17th chromosome. To my understanding, a lot is known about these genes and how they contribute to our cll.
I am no expert at all, but to my understanding the sf3b1 is a gene located on the 2nd chromosome and is implicated in several cancers, including cll. I dont think they know as much about the role the sf3b1 gene plays in our cll as compared to some other genes.
Many people with cll only have one chromosome or genetic defect, a simple case of cl. Each of these carry a varying prognosis, for example, people with only 13 q usually stay out of treatment longer than those with 17p.
Others among us with cll have so called complex cases where more than one defect is involved. As a very general rule, those with complex cll start treatment earlier.
If your husbands doctor described his cll as complex, it might be that in addition to some abnormality with the sf3b1 gene, he might have other damaged genes.
So while I can imagine that if your doctor throws out all this gene and chromosome stuff at you, it must sound like scary mumbo-jumbo. It did, and still does, to me.
But the big picture is that lots of people on here have complex cll of all types and are doing quite well with their treatment. Len gave a great example of how he has dealt with that for 15 years now. Your husband likely has some advantage over Len and I, in that there are a lot better drugs now with less side effects for cll than there was even 5 years ago.
The venetoclax your husband is about to start is only one of the new drugs and it generally works very well on all types of cll, simple and complex. Venetoclax kills cll cancer cells very efficiently with relatively mild side effects for most people. We have a variety of btk type medicines we can take that can be just as efficient for cll as venetoclax.
And there are many more drugs in development for cll. Most cancers are faster growing than cll and having new drugs in development might not help people if they dont live long enough to see the drugs. Thats not the case for most of us with cll where we can live with our cll, even decades for some. We are seeing newer and better drugs every year it seems.
Good luck to you. I hope I haven’t overloaded you with confusing terms. While I am no expert, I have read a lot of what cll experts have written, and a lot of it recently is very encouraging that people diagnosed with cll in this day in age have an excellent chance to manage their Cll indefinitely.
Thanks cajunjeff. You haven't overloaded me 🙂 I kepp myself informed and know about TP53 17pdel 11q etc but hadn't heard of SF3b1 until it appeared on his notes so it threw me. Not sure if it is a consequence of FCR as he didn't have it on pre FCR tests. Alternatively as we become more capable of testing for things we find them. You response has lifted me. Thank you
As lankisterguy and cajunjeff gave you great answers, I hope this eases your concerns, these are becoming less worrisome because of the advancements in the medicines the specialists work with now.
Think of them more as indicators as to what choices in medicines your doctors will offer you when the time comes.
Thanks Spark Plug that is a good way of looking at it.
My wife was diagnosed in 2015 with CLL, 13Q 2x, 17p and TP53 complex karyotype. Venetoclax after one year gave her 3 and 1/2 years of clinical mission. She was recently on Calquence for about a year and has taken another vacation from treatment and has been in clinical remission 8 months.
There are so many good treatments for the worse diagnosis that we hear it said from some of the best minds in the CLL community that like diabetes's, CLL is treatable if not curable. Also, that the CLL patients will in all probability die with CLL and not from CLL.
Shepherd777 I am so pleased to hear your wife is doing well. Thank you for your reply
I have SF3B1 and several other mutations and have done well on venetoclax plus obinutuzumab. I respond really well to treatment, and am already in a complete remission before the treatment is even over. It is good to have information about his risk profile just to make sure he is followed more closely. I was diagnosed 11 years ago and still see my dr every 3-4 months.
He’s home! Hurrah!
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