Just a quickie, because I’m in the middle of some things.
I’m at a conference for online health advocates (more about that in a few days), but yesterday afternoon, I had the opportunity to meet with a bunch of cancer advocates. A few of them are blood cancer patients and survivors, but they represented a bunch of different types of cancer.
We started by telling our stories. What was so amazing was how similar those stories were. It didn’t matter what type of cancer they had, or how old they were, or where they were from. They all got a cancer diagnosis, and looked for help, and couldn’t find it — at least not from someone who was like them. As one put it, everyone felt “not just fear, but loneliness too — the worst things that can happen at the same time to a person.”
Eventually, they found what they needed (for some of them, that meant creating a community themselves where others could turn — these are online advocates, after all).
But hearing them all speak made me really think about how important it is to connect with other patients, to find a community. It means so much to go online and read about someone else’s experience and think “Hey — it’s not just me that’s going through this.” There’s something really powerful about realizing you’re not alone.
So this is your reminder to find a community, someplace you can share. Or at least listen, if sharing is hard.
Cancer is not easy — we all know that. There’s no need to go through it alone.
And while every cancer is different, Follicular Lymphoma has its own weird things going for it. And one of them is that we can go a long time without having to think too hard about it. At those times, it’s fine to not think about it.
But then, there are times when it’s always there, right in front of us. At diagnosis. At recurrence. After treatment. Or just when it seems like there just might be something going on.
And those are the times we need to make sure we don’t try to go it alone. That’s when we need community.
Don’t forget that.
And if you can’t find someone to share with, just email me. I’ll listen.
Enjoy your day.
Friday, April 27, 2018
Tuesday, April 24, 2018
Exercise for Cancer Survivors
The American Association for Cancer Research held its annual meeting last week. Not too much that I could see about Follicular Lymphoma; maybe the good stuff is coming in another month or so at the ASCO conference
But I did see an article about one interesting study that was presented at the meeting. The presentation was called "The associations of habitual physical inactivity with cancer outcomes: Evidence from the Roswell Park Cancer Institute Data Bank and BioRepositor."
The basic message is simple -- get off your butt if you want to live longer.
The researchers saw that regular physical activity was shown to have a benefit for survivors of a few different types of cancer. But no one really measured physical inactivity and what the implications were.
Patients were given questionnaires asking them about their physical activity for the 10 years before they were diagnosed, and after they were diagnosed. About 17.5% of patients were "habitually inactive" -- no physical activity before or after diagnosis.
Patients who were physically active before and after diagnosis had an overall 40% increase in survival.
It gets interesting when you break things down a little more:
Patients who were active 3 or 4 days a week saw the greatest benefit. Those who were active 1-2 days per week, or 7 days per week, saw a benefit, but not as great as those who were active 3 or 4 days.
The message? Moderation is key. Just like like with ice cream. And scotch.
That's important for cancer patients, I think. If you are planning to run a marathon, great -- I'm cheering for you. But if your physical activity has been slowed down by cancer, or by the side effects of treatment (or by the side effects of the treatment to take care of the side effects of treatment), then a walk around the block might be just fine. Or if that's not possible, some chair aerobics (yes, that's a thing, and it's great for lots of people).
And if you think it's too late to start, then here's some incentive -- the study found that patients who were inactive before their diagnosis, but then became after, had a 25% survival increase.
It's easy to find excuses to not be active, and some of them are legitimate. But most of us can find 30 minutes in the day for a walk (outside, now that the weather is getting warmer). But even three 10 minute walks can be a help.
I have found myself doing this more often. I can usually get to the gym three days a week for at least 30 minutes, but other days, I sit a lot at work. I try to do three 10 minute walks during those days, maybe to get a cup of tea or just do a lap around the building.
(And if I walk fast and carry something in my hands, people think I must be rushing to do something important, which is a nice bonus.)
So find some inspiration. Your spouse or child or friend or pet could use the exercise, too -- drag them along. Tell yourself it will only be 10 minutes. You know you can fit that in somewhere, somehow.
But I did see an article about one interesting study that was presented at the meeting. The presentation was called "The associations of habitual physical inactivity with cancer outcomes: Evidence from the Roswell Park Cancer Institute Data Bank and BioRepositor."
The basic message is simple -- get off your butt if you want to live longer.
The researchers saw that regular physical activity was shown to have a benefit for survivors of a few different types of cancer. But no one really measured physical inactivity and what the implications were.
Patients were given questionnaires asking them about their physical activity for the 10 years before they were diagnosed, and after they were diagnosed. About 17.5% of patients were "habitually inactive" -- no physical activity before or after diagnosis.
Patients who were physically active before and after diagnosis had an overall 40% increase in survival.
It gets interesting when you break things down a little more:
Patients who were active 3 or 4 days a week saw the greatest benefit. Those who were active 1-2 days per week, or 7 days per week, saw a benefit, but not as great as those who were active 3 or 4 days.
The message? Moderation is key. Just like like with ice cream. And scotch.
That's important for cancer patients, I think. If you are planning to run a marathon, great -- I'm cheering for you. But if your physical activity has been slowed down by cancer, or by the side effects of treatment (or by the side effects of the treatment to take care of the side effects of treatment), then a walk around the block might be just fine. Or if that's not possible, some chair aerobics (yes, that's a thing, and it's great for lots of people).
And if you think it's too late to start, then here's some incentive -- the study found that patients who were inactive before their diagnosis, but then became after, had a 25% survival increase.
It's easy to find excuses to not be active, and some of them are legitimate. But most of us can find 30 minutes in the day for a walk (outside, now that the weather is getting warmer). But even three 10 minute walks can be a help.
I have found myself doing this more often. I can usually get to the gym three days a week for at least 30 minutes, but other days, I sit a lot at work. I try to do three 10 minute walks during those days, maybe to get a cup of tea or just do a lap around the building.
(And if I walk fast and carry something in my hands, people think I must be rushing to do something important, which is a nice bonus.)
So find some inspiration. Your spouse or child or friend or pet could use the exercise, too -- drag them along. Tell yourself it will only be 10 minutes. You know you can fit that in somewhere, somehow.
Friday, April 20, 2018
Predicting EFS24 in Follicular Lymphoma
New research from the journal Blood could be an important a step in predicting EFS24 in patients with Follicular Lymphoma.
EFS24 stands for Event Free Survival within 24 months, and it's an important way of predicting how aggressive a FL patient's cancer might be.
The idea is, if a patient has received immunochemotherapy (something like R-CHOP or R-B) and then has an event within 24 months, they tended to have a lower Overall Survival. Events can be things like progression of disease, relapse, or the need for retreatment. About 20% of FL patients seem to fall in this group. Research in the last few years has confirmed that EFS24 is a good predictor.
But here's the problem -- as of now, EFS24 status isn't known until patients have an event. In other words, patients get immunochemotherapy, and then have to wait for a couple of years to see if they have an event to figure out if they are in that 20%. It's a nerve-wracking wait (as some of you know, and as the rest of us can pretty easily imagine).
The next step in research on EFS24 is finding some way to predict, even before treatment starts, whether the patient is in that group.
That's what this research hopes to do, or at least start.
The researchers looked at over 1000 patients in the PRIMA trial, which has been examining the effectiveness of Rituxan Maintenance. They developed an index to predict Progression Free Survival using just two biomarkers: bone marrow involvement and the presence of Beta-2 microglobulin.
We all probably know what bone marrow involvement is (especially if we were unfortunate enough to have a bone marrow biopsy). Beta2m is a protein that is present in the blood when there is increased activity of cancer cells. It's an important predictor for multiple myeloma, another blood cancer -- higher levels usually mean a more aggressive disease and poorer outcomes.
The researchers found that bone marrow involvement and Beta2m levels can predict PFS in FL patients:
High risk: greater than 3mg/L of Beta2m, and a 37% 5 year PFS
Intermediate risk: less that 3mg/L of Beta2m, plus bone marrow involvement, with a 55% 5 year PFS
Low risk: less that 3mg/L of Beta2m, and no bone marrow involvement, with a 69% 5 year PFS
The researchers then looked at whether patients had events with 24 months, and found that the risks for EFS24 matched up well with their PFS index.
They then tested this idea on another group of patients in a different trial, and found that it their risk groups held up: 77% 5 year EFS for the low-risk group, 57% for the intermediate, and 44% for the high.
The researchers admit that this is first step, and it "could serve as a basis for building more sophisticated and integrated biomolecular scores."
But it seems like a pretty good first step. Better models could build on this one and figure out other biomarkers that can make EFS24 easier to predict and, hopefully, treat more effectively.
Hope comes in small stages sometimes, but it builds up if you let it....
EFS24 stands for Event Free Survival within 24 months, and it's an important way of predicting how aggressive a FL patient's cancer might be.
The idea is, if a patient has received immunochemotherapy (something like R-CHOP or R-B) and then has an event within 24 months, they tended to have a lower Overall Survival. Events can be things like progression of disease, relapse, or the need for retreatment. About 20% of FL patients seem to fall in this group. Research in the last few years has confirmed that EFS24 is a good predictor.
But here's the problem -- as of now, EFS24 status isn't known until patients have an event. In other words, patients get immunochemotherapy, and then have to wait for a couple of years to see if they have an event to figure out if they are in that 20%. It's a nerve-wracking wait (as some of you know, and as the rest of us can pretty easily imagine).
The next step in research on EFS24 is finding some way to predict, even before treatment starts, whether the patient is in that group.
That's what this research hopes to do, or at least start.
The researchers looked at over 1000 patients in the PRIMA trial, which has been examining the effectiveness of Rituxan Maintenance. They developed an index to predict Progression Free Survival using just two biomarkers: bone marrow involvement and the presence of Beta-2 microglobulin.
We all probably know what bone marrow involvement is (especially if we were unfortunate enough to have a bone marrow biopsy). Beta2m is a protein that is present in the blood when there is increased activity of cancer cells. It's an important predictor for multiple myeloma, another blood cancer -- higher levels usually mean a more aggressive disease and poorer outcomes.
The researchers found that bone marrow involvement and Beta2m levels can predict PFS in FL patients:
High risk: greater than 3mg/L of Beta2m, and a 37% 5 year PFS
Intermediate risk: less that 3mg/L of Beta2m, plus bone marrow involvement, with a 55% 5 year PFS
Low risk: less that 3mg/L of Beta2m, and no bone marrow involvement, with a 69% 5 year PFS
The researchers then looked at whether patients had events with 24 months, and found that the risks for EFS24 matched up well with their PFS index.
They then tested this idea on another group of patients in a different trial, and found that it their risk groups held up: 77% 5 year EFS for the low-risk group, 57% for the intermediate, and 44% for the high.
The researchers admit that this is first step, and it "could serve as a basis for building more sophisticated and integrated biomolecular scores."
But it seems like a pretty good first step. Better models could build on this one and figure out other biomarkers that can make EFS24 easier to predict and, hopefully, treat more effectively.
Hope comes in small stages sometimes, but it builds up if you let it....
Sunday, April 15, 2018
Frankenstein Lymphoma: Can It Be Cured?
This is kind of a follow-up to my recent post on the ViPOR trial, but not exactly a follow-up, because I'm going to talk about something from a couple of months ago.
Dr. Bruce Cheson wrote a piece for the ASCO Post a couple of months ago called "Releasing Follicular Lymphoma From the Curse of Frankenstein."
If you've been reading this blog for a while, you know I'm fond of Dr. Cheson. I've never met him, but I've read plenty of what he's written and watched plenty of the videos he's made. He's smart and funny, and he's very hopeful about Follicular Lymphoma and its future. As an FL patient, I really appreciate that.
That hopefulness is the point of the "Frankenstein" article. He wrote it because the ASCO Post editor had read that Dr. Cheson had mentioned the possibility of a cure for FL, and challenged Dr. Cheson to defend that possibility.
Dr. Cheson says he has a number of patients who have received treatments that have put them in remission for more than 10 years -- maybe enough to consider them cured.
(For the record, it's been 10 years since I was diagnosed, 8 years since treatment with Rituxan, and while I'd love to think of myself as cured, I've never had a completely clean scan. Bummer. But I'm still going strong anyway....)
The next step, he says, if to release FL from the Frankenstein approach. As he describes it: "Lovely nose from here, great heart from there, sturdy arms from elsewhere, decent torso, very good brain. But, when you stitch them all together, the result is reminiscent of a line by Dr. Victor -Frankenstein from the classic eponymous novel: 'How can I describe my emotions at this catastrophe, or how delineate the wretch whom with such infinite pains and care I had endeavoured to form?'."
He's seen it done with different combinations of traditional chemotherapy, and now he's seeing it done with non-chemo agents like inhibitors and monoclonal antibodies. Like with the Frankenstein monster, we take good things and try to combine them into something better. Sometimes that works a little, sometimes it doesn't work at all, and sometimes the combo just makes things worse.
That's where the ViPOR follow-up comes in. Five agents combined into one treatment. Will it save us all? Or will it be a monster?
For Dr. Cheson, the road to a cure will come with more knowledge and a smarter, more deliberate approach. There are a lot of combinations that are possible from the agents that are already approved and close to being approved. Too many, really. He gives us the math: if you take just 8 agents and combine them with one another in pairs, you have 36 treatments. Combine each of those 8 in triplets, testing combinations of 3 at a time, and you have 84 combinations.
In some ways, that's kind of cool -- 84 possible things to try. For a patient, that could be a hopeful thing.
But Dr. Cheson's point is less hopeful -- that's 84 combinations that have to be tested, and that means recruiting patients for trials and hoping for the right combo (and hoping to avoid the monsters).
He thinks a cure will come when we know more about biomarkers and other genetic clues that will cut down on the guessing. We'll be able to predict the right combinations and do less guessing. Fewer possible treatments, but fewer monsters, too.
So what does this mean for us as Follicular Lymphoma patients?
Well, first, there isn't much we can do to figure out the right combinations -- that's going to need to come from researchers.
But we can participate in clinical trials when we have the chance to. Especially trials that seem to have more of a basis that "Hey, let's try this combo!" Not that I'm completely against that approach, but with limited resources, at some point we need to have good reasons for running and choosing which trials to support.
Second, as I have written before, the idea of combining agents makes a lot of sense to me. Cancer is sneaky, and if we can attack in different ways, maybe we can cut off some of its escape routes. Obviously, Dr. Cheson sees this as a promising path to a cure.
But that doesn't mean it's the only path. RIT and CAR-T are two examples of approaches that don't require multiple agents in combinations like ViPOR, and they may not be the only ones to come in the next few years. The path to a cure might not even be in our sites yet.
The bigger point is, as much as we need to rely on researchers to do most of the work for us, we can still do our part by staying informed and being open to clinical trials to help test out new, promising agents.
No one is saying there's a cure for us all just yet. But there's no reason to give up hope, either.
Dr. Bruce Cheson wrote a piece for the ASCO Post a couple of months ago called "Releasing Follicular Lymphoma From the Curse of Frankenstein."
If you've been reading this blog for a while, you know I'm fond of Dr. Cheson. I've never met him, but I've read plenty of what he's written and watched plenty of the videos he's made. He's smart and funny, and he's very hopeful about Follicular Lymphoma and its future. As an FL patient, I really appreciate that.
That hopefulness is the point of the "Frankenstein" article. He wrote it because the ASCO Post editor had read that Dr. Cheson had mentioned the possibility of a cure for FL, and challenged Dr. Cheson to defend that possibility.
Dr. Cheson says he has a number of patients who have received treatments that have put them in remission for more than 10 years -- maybe enough to consider them cured.
(For the record, it's been 10 years since I was diagnosed, 8 years since treatment with Rituxan, and while I'd love to think of myself as cured, I've never had a completely clean scan. Bummer. But I'm still going strong anyway....)
The next step, he says, if to release FL from the Frankenstein approach. As he describes it: "Lovely nose from here, great heart from there, sturdy arms from elsewhere, decent torso, very good brain. But, when you stitch them all together, the result is reminiscent of a line by Dr. Victor -Frankenstein from the classic eponymous novel: 'How can I describe my emotions at this catastrophe, or how delineate the wretch whom with such infinite pains and care I had endeavoured to form?'."
He's seen it done with different combinations of traditional chemotherapy, and now he's seeing it done with non-chemo agents like inhibitors and monoclonal antibodies. Like with the Frankenstein monster, we take good things and try to combine them into something better. Sometimes that works a little, sometimes it doesn't work at all, and sometimes the combo just makes things worse.
That's where the ViPOR follow-up comes in. Five agents combined into one treatment. Will it save us all? Or will it be a monster?
For Dr. Cheson, the road to a cure will come with more knowledge and a smarter, more deliberate approach. There are a lot of combinations that are possible from the agents that are already approved and close to being approved. Too many, really. He gives us the math: if you take just 8 agents and combine them with one another in pairs, you have 36 treatments. Combine each of those 8 in triplets, testing combinations of 3 at a time, and you have 84 combinations.
In some ways, that's kind of cool -- 84 possible things to try. For a patient, that could be a hopeful thing.
But Dr. Cheson's point is less hopeful -- that's 84 combinations that have to be tested, and that means recruiting patients for trials and hoping for the right combo (and hoping to avoid the monsters).
He thinks a cure will come when we know more about biomarkers and other genetic clues that will cut down on the guessing. We'll be able to predict the right combinations and do less guessing. Fewer possible treatments, but fewer monsters, too.
So what does this mean for us as Follicular Lymphoma patients?
Well, first, there isn't much we can do to figure out the right combinations -- that's going to need to come from researchers.
But we can participate in clinical trials when we have the chance to. Especially trials that seem to have more of a basis that "Hey, let's try this combo!" Not that I'm completely against that approach, but with limited resources, at some point we need to have good reasons for running and choosing which trials to support.
Second, as I have written before, the idea of combining agents makes a lot of sense to me. Cancer is sneaky, and if we can attack in different ways, maybe we can cut off some of its escape routes. Obviously, Dr. Cheson sees this as a promising path to a cure.
But that doesn't mean it's the only path. RIT and CAR-T are two examples of approaches that don't require multiple agents in combinations like ViPOR, and they may not be the only ones to come in the next few years. The path to a cure might not even be in our sites yet.
The bigger point is, as much as we need to rely on researchers to do most of the work for us, we can still do our part by staying informed and being open to clinical trials to help test out new, promising agents.
No one is saying there's a cure for us all just yet. But there's no reason to give up hope, either.
Tuesday, April 10, 2018
Priority Review for Duvelisib
The FDA has granted Priority Review for Duvelisib for Relapsed or Refractory Follicular Lymphoma (and for another blood cancer, CLL).
Duvelisib is a PI3K inhibitor (Phosphoinositide 3-kinase inhibitor). It works (as all inhibitors work) by stopping something from happening, in this case, some signals that cancer cells receive that allow them to live and grow and not die.
Duvelisib is different from other PI3K inhibitors in that it works on two different isoforms of PI3K, the delta and gamma isoforms. (An isoform is a different type of a protein -- the different isoforms do the same job, but they might be controlled by different genes. So an inhibitor that works on more than one isoform should, at least in theory, do a better job than one that works on just one isoform.) It is taken by mouth twice a day -- no ports, no infusions, no visits to the treatment room.
FDA Priority Review basically means the application will be looked at faster -- usually within 6 months. Regular Review usually takes about 10 months. Priority Review is given to treatments that seem to show an improvement in effectiveness or safety over other available treatments.
The FDA decision is based on results from the phase 2 DYNAMO clinical trial. In the trial, there was a 46% Overall Response Rate for indolent NHL patients, inlcuding a 41% ORR for Follicular Lymphoma patients.
OncLive has a nice, brief video from Dr. Lori A. Leslie that discusses some of the good and bad of Duvelisib and other kinase inhibitors. They are effective, though they have side effects that need to be considered. And while they are effective on their own, a better strategy might be to combine them with other agents, which seems to increase overall effectiveness.
As a patient, I am always happy to see another treatment move up the pipeline. Dr. Leslie discusses these in terms of eventually replacing traditional chemotherapy, which is also a great thing -- targeting lymphoma cells and keeping them in check.
As always, we'll keep an eye for the news of this the FDA's decision.
Duvelisib is a PI3K inhibitor (Phosphoinositide 3-kinase inhibitor). It works (as all inhibitors work) by stopping something from happening, in this case, some signals that cancer cells receive that allow them to live and grow and not die.
Duvelisib is different from other PI3K inhibitors in that it works on two different isoforms of PI3K, the delta and gamma isoforms. (An isoform is a different type of a protein -- the different isoforms do the same job, but they might be controlled by different genes. So an inhibitor that works on more than one isoform should, at least in theory, do a better job than one that works on just one isoform.) It is taken by mouth twice a day -- no ports, no infusions, no visits to the treatment room.
FDA Priority Review basically means the application will be looked at faster -- usually within 6 months. Regular Review usually takes about 10 months. Priority Review is given to treatments that seem to show an improvement in effectiveness or safety over other available treatments.
The FDA decision is based on results from the phase 2 DYNAMO clinical trial. In the trial, there was a 46% Overall Response Rate for indolent NHL patients, inlcuding a 41% ORR for Follicular Lymphoma patients.
OncLive has a nice, brief video from Dr. Lori A. Leslie that discusses some of the good and bad of Duvelisib and other kinase inhibitors. They are effective, though they have side effects that need to be considered. And while they are effective on their own, a better strategy might be to combine them with other agents, which seems to increase overall effectiveness.
As a patient, I am always happy to see another treatment move up the pipeline. Dr. Leslie discusses these in terms of eventually replacing traditional chemotherapy, which is also a great thing -- targeting lymphoma cells and keeping them in check.
As always, we'll keep an eye for the news of this the FDA's decision.
Saturday, April 7, 2018
The ViPOR Trial for B Cell Lymphoma
A few weeks ago, the National Cancer Institute released information about the ViPOR trial. It's a phase I trial, and a really interesting combination.
ViPOR is the name for a combination of 5 different FL treatments that make up this new treatment. They are:
Venetoclax (also known as Venclexta -- this blocks the protein that keeps lymphoma cells from dying the way they are supposed to)
Ibrutinib (also known as Imbruvica -- a BTK inhibitor that messing with things the cell needs to do to stay alive. Not sure why Ibrutinib gets a small "I" when everyone else gets a capital letter. Seems kind of mean).
Prednisone (a steroid that is very common in cancer combinations -- it is the P in CHOP, for example)
Obinutuzumab (a monoclonal antibody, like Rituxan, but created from human cells. not mouse cells)
Revlimid (also known as Lenalidomide, the second R in R-squared, along with Rituxan).
The thinking behind this combination is the same as with so many other combinations -- let's attack the the cancer in different ways so it doesn't have anywhere to escape.
It's a really common approach these days, as we recognize how sneaky cancer can be (block one of its paths and it will find a way around it). It's also an approach that makes a lot of sense to me personally. I remember, years ago, before I even had my first treatment, reading about a study that used Rituxan, then CHOP, then RadioImmunoTherapy (RIT), with the same logic -- three different ways to attack the cancer cells has to better than one, right?
Of course, there are potential problems.
Every treatment has side effects. And so it make sense that a treatment with 5 different agents has the potential to have many different side effects, some of which could be made worse because more than one of the agents can cause the same problem.
This is a phase I clinical trial, and one of the main purposes of a phase I trial is to figure out safety problems -- the Maximum Tolerated Dose -- how much of the agents you can give before the problems outweigh the benefits.
And that will be a challenge. I remember seeing this all discussed on Twitter a few weeks ago, and the folks at Lymphomation pointed out that one of the challenges is going to be to figure out which of the agents is causing which of the side effects. I'm going to give the researchers the benefit of the doubt and assume they have a plan for that, but the comment does show how complex this might be.
Of course, the benefits might outweigh the problems in the end. The combination could be the one that finally does the trick. We won't know until the trials run their course.
Another issue -- it might work well for another B Cell Lymphoma, but not Follicular Lymphoma. That's another goal of lots of phase I trials -- a kind of "throw it against the wall and see what sticks" approach. All of these 5 agents have shown some effectiveness in different types of lymphoma, including FL. So the trial is open to almost anyone with a B Cell Lymphoma. It could find that the combo works great for CLL and DLBCL, but not so much for Follicular.
Like with all trials, it will be a long time before we see the results of this one, but it's worth keeping an eye on.
ViPOR is the name for a combination of 5 different FL treatments that make up this new treatment. They are:
Venetoclax (also known as Venclexta -- this blocks the protein that keeps lymphoma cells from dying the way they are supposed to)
Ibrutinib (also known as Imbruvica -- a BTK inhibitor that messing with things the cell needs to do to stay alive. Not sure why Ibrutinib gets a small "I" when everyone else gets a capital letter. Seems kind of mean).
Prednisone (a steroid that is very common in cancer combinations -- it is the P in CHOP, for example)
Obinutuzumab (a monoclonal antibody, like Rituxan, but created from human cells. not mouse cells)
Revlimid (also known as Lenalidomide, the second R in R-squared, along with Rituxan).
The thinking behind this combination is the same as with so many other combinations -- let's attack the the cancer in different ways so it doesn't have anywhere to escape.
It's a really common approach these days, as we recognize how sneaky cancer can be (block one of its paths and it will find a way around it). It's also an approach that makes a lot of sense to me personally. I remember, years ago, before I even had my first treatment, reading about a study that used Rituxan, then CHOP, then RadioImmunoTherapy (RIT), with the same logic -- three different ways to attack the cancer cells has to better than one, right?
Of course, there are potential problems.
Every treatment has side effects. And so it make sense that a treatment with 5 different agents has the potential to have many different side effects, some of which could be made worse because more than one of the agents can cause the same problem.
This is a phase I clinical trial, and one of the main purposes of a phase I trial is to figure out safety problems -- the Maximum Tolerated Dose -- how much of the agents you can give before the problems outweigh the benefits.
And that will be a challenge. I remember seeing this all discussed on Twitter a few weeks ago, and the folks at Lymphomation pointed out that one of the challenges is going to be to figure out which of the agents is causing which of the side effects. I'm going to give the researchers the benefit of the doubt and assume they have a plan for that, but the comment does show how complex this might be.
Of course, the benefits might outweigh the problems in the end. The combination could be the one that finally does the trick. We won't know until the trials run their course.
Another issue -- it might work well for another B Cell Lymphoma, but not Follicular Lymphoma. That's another goal of lots of phase I trials -- a kind of "throw it against the wall and see what sticks" approach. All of these 5 agents have shown some effectiveness in different types of lymphoma, including FL. So the trial is open to almost anyone with a B Cell Lymphoma. It could find that the combo works great for CLL and DLBCL, but not so much for Follicular.
Like with all trials, it will be a long time before we see the results of this one, but it's worth keeping an eye on.
Wednesday, April 4, 2018
Improving Clinical Trials
I've always tried to be an advocate for clinical trials. They are important -- we can't get any new treatments unless there are patients who are willing to try them out first to see if they work (that is, they do a better and safer job than the treatments we have now).
I also understand the difficulties that patients have with trials. I am, after all, a lymphoma patient of 10 years who has never participated in one himself. I've only needed treatment once in those 10 years, and my doctor and I decided that an available treatment was my best option. But one of the things I do now as an informed patient is prepare myself for my next treatment, if and when I need it. And for me, that means being aware of the clinical trials that are open to me.
Now, there are lots of reasons why patients don't get involved with trials. Sometimes, that's personal choice, as it was with mine.
But there are lots of other reasons why that might not be about personal choice at all. Sometimes, people are excluded for socioeconomic reasons -- for example, they can't afford to travel the 100 miles to the nearest trial for the treatment that seems appropriate.
Sometimes it's a matter of the way the trial was designed; a patient might me all of the criteria but one, whatever it might be -- a previous treatment, or a seemingly unrelated health issue.
In February, I attended a conference that looked at some of the policy issues surrounding cancer, including clinical trials. One of the speakers was the President-elect of the American Medical Association. She is a community oncologist -- one who has a private practice, rather than working in a large research hospital where trials are likely to take place. She talked about her frustration with trials -- some patients could not get to the closest research hospital, and the trial design did not allow doctors outside of the hospital to give the treatment.
That's understandable, in a way, since for the trial to be useful, it needs to carefully control which patients are allowed to be a part of it. On the other hand, if community oncologists aren't allowed to participate, there is a large population of patients who might want to participate, but who cannot. That's bad for everyone. Patients don't get potentially life-saving treatments, and trial researchers potentially can't get enough patients to participate. (About 20% of publicly-funded cancer clinical trials don't get enough patients enrolled to complete the trial.)
One possible piece of good news is that the FDA, the government agency that oversees trials, is holding a public meeting in a couple of weeks to address this issue. The purpose of the meeting is to get as many people involved as possible who can give their opinions on how to make clinical trials easier for patients to enroll in.
It's a complicated issue -- the FDA plays an important roll in making sure that trials are safe, that the measure the things they say they are measuring, and that the treatments actually improve on what is already available.
While I personally get happy when I see new treatments approved for Follicular Lymphoma, I also get happy (maybe a little less, but still happy) when I read about a treatment that didn't make it out of a trial, or didn't get approved. That might seem strange, but it lets me know the system is working -- treatments aren't being approved without being rigorously tested first. I can trust that new treatments have been shown to work for certain patients.
The FDA has a thankless job -- patients want access to treatments, researchers and pharma companies want their treatments to be approved, and doctors want to be able to give their patients more options. The FDA has to balance all of that and make sure things are safe and effective. The new push for Right-To-Try laws seems to try to go around the process and push for treatments that haven't been tested enough. (The FDA already has a process in place that lets patients ask for treatments that aren't approved yet, but also allows for some oversight.)
If you are interested in viewing the FDA meeting, it will be available online afterwards (see the link for more information). Some advocacy here would be a good thing -- contact your elected representatives and tell them your opinion about clinical trials.
And, of course, as patients, we can do our part by talking to our oncologists about trials that are available and that might be work for us. If you're in between treatments right now, it's the perfect time to have that conversation, so you can both be ready if and when the time comes.
(Of course, I hope none of us need treatment, ever, but that doesn't mean I'm not keeping myself informed about my options.....)
I also understand the difficulties that patients have with trials. I am, after all, a lymphoma patient of 10 years who has never participated in one himself. I've only needed treatment once in those 10 years, and my doctor and I decided that an available treatment was my best option. But one of the things I do now as an informed patient is prepare myself for my next treatment, if and when I need it. And for me, that means being aware of the clinical trials that are open to me.
Now, there are lots of reasons why patients don't get involved with trials. Sometimes, that's personal choice, as it was with mine.
But there are lots of other reasons why that might not be about personal choice at all. Sometimes, people are excluded for socioeconomic reasons -- for example, they can't afford to travel the 100 miles to the nearest trial for the treatment that seems appropriate.
Sometimes it's a matter of the way the trial was designed; a patient might me all of the criteria but one, whatever it might be -- a previous treatment, or a seemingly unrelated health issue.
In February, I attended a conference that looked at some of the policy issues surrounding cancer, including clinical trials. One of the speakers was the President-elect of the American Medical Association. She is a community oncologist -- one who has a private practice, rather than working in a large research hospital where trials are likely to take place. She talked about her frustration with trials -- some patients could not get to the closest research hospital, and the trial design did not allow doctors outside of the hospital to give the treatment.
That's understandable, in a way, since for the trial to be useful, it needs to carefully control which patients are allowed to be a part of it. On the other hand, if community oncologists aren't allowed to participate, there is a large population of patients who might want to participate, but who cannot. That's bad for everyone. Patients don't get potentially life-saving treatments, and trial researchers potentially can't get enough patients to participate. (About 20% of publicly-funded cancer clinical trials don't get enough patients enrolled to complete the trial.)
One possible piece of good news is that the FDA, the government agency that oversees trials, is holding a public meeting in a couple of weeks to address this issue. The purpose of the meeting is to get as many people involved as possible who can give their opinions on how to make clinical trials easier for patients to enroll in.
It's a complicated issue -- the FDA plays an important roll in making sure that trials are safe, that the measure the things they say they are measuring, and that the treatments actually improve on what is already available.
While I personally get happy when I see new treatments approved for Follicular Lymphoma, I also get happy (maybe a little less, but still happy) when I read about a treatment that didn't make it out of a trial, or didn't get approved. That might seem strange, but it lets me know the system is working -- treatments aren't being approved without being rigorously tested first. I can trust that new treatments have been shown to work for certain patients.
The FDA has a thankless job -- patients want access to treatments, researchers and pharma companies want their treatments to be approved, and doctors want to be able to give their patients more options. The FDA has to balance all of that and make sure things are safe and effective. The new push for Right-To-Try laws seems to try to go around the process and push for treatments that haven't been tested enough. (The FDA already has a process in place that lets patients ask for treatments that aren't approved yet, but also allows for some oversight.)
If you are interested in viewing the FDA meeting, it will be available online afterwards (see the link for more information). Some advocacy here would be a good thing -- contact your elected representatives and tell them your opinion about clinical trials.
And, of course, as patients, we can do our part by talking to our oncologists about trials that are available and that might be work for us. If you're in between treatments right now, it's the perfect time to have that conversation, so you can both be ready if and when the time comes.
(Of course, I hope none of us need treatment, ever, but that doesn't mean I'm not keeping myself informed about my options.....)
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