Some encouraging news from the good folks at Dana-Farber: researchers there have developed a peptide that seems to help override blood cancer cells' resistance to chemotherapy.
D-F issued a press release yesterday describing the research. In a nutshell, this is how it works:
The body's cells do not last forever. When they are too old, or damaged, they seem to be programmed to die -- to kill themselves, really. The body activates a protein that shuts down the cells' mitochondria (the little power houses within the cell that keeps them going). No mitochondria, no cell life. (Imagine disabling the motor in your freezer; everything melts and spoils.) Lots of cancer treatments work by triggering these proteins in cancer cells, trying to get the cells to shut down and kill themselves.
But, oh, those tricky cancer cells. They find a way to ignore that protein, or intercept it before it can shut down the mitochondria. (Imagine someone screaming, "No! My ice cream!" and holding on to your leg before you can get to the freezer's motor. Now imagine a whole bunch of people holding your leg, because cancer cells develop multiple strategies for survival. Or, better, a whole line of people waiting to grab you once you shake one of them off on your long walk to the freezer.)
This treatment involves "stapling" a chemical to the shut-down protein. The chemical deactivates the cancer cells' signals, allowing the protein to shut down the mitochondria.
(It's too late to turn back now with this ridiculous freezer metaphor, so: imagine, as you approach that line of people ready to grab your leg, you have an 8 year old with a nerf gun and really good aim, riding on your back. As you approach each person in line, the 8 year old shoots them with the nerf gun, distracting them just enough that you can get to the next person in line, who suffers the same fate, until eventually, they all get out of the way and you can disable that freezer motor and ruin all of the ice cream and bags of corn and frozen Swedish meatballs inside. Which, you will remember, is actually cancer in this comparison.)
Anyway, it's a very promising treatment, especially for relapsed blood cancers (including lymphoma), which tend to increase their ability to resist with each recurrence. Still a VERY long ay to go before anything actually happens with it, but it certainly holds a lot of promise.
(And, by the way, this is just the kind of awesome research that gets funded when you give to the Pan Mass Challenge, which, as you may know, my brother will be riding in later in the summer. Feel free to help fund more awesome research.)
Wednesday, May 30, 2012
Sunday, May 27, 2012
What Causes Lymphoma?
A few weeks ago, I mentioned an upcoming podcast called "What Causes Lymphoma?" I was a little critical about it, because I think cancer patients can obsess about causes. That kind of thinking potentially leads to a lot of "What did I do to deserve this?" kind of guilt. And it's often misplaced guilt, because something like Follicular NHL has no definite, known cause. I don't see much point in beating yourself up about something you can't control.
That said, I also fully believe in the power of information, and if being informed about lymphoma empowers you, then learn all you can. (Clearly, it's something that I do myself.)
And, perhaps most importantly, finding answers to "what causes lymphoma?" really is important to researchers, even if it isn't something patients should dwell on.
Anyway, that podcast took place on May 15th, and it's available online now. The show lasts for about 100 minutes, and features interviews with some leading epidemiologists -- medical experts whose focus is on the cause of diseases (specifically lymphoma).
And it's a pretty interesting show. It takes a while to get to the meat of things, but it's worth waiting for. (And in fact, the opening info is worth listening to as well. It includes a plug for a symposium in September to mark World Lymphoma Day; it will focus on Follicular Lymphoma, and is co-sponsored by the excellent organization HOPE for Lymphoma, whose Facebook page is an absolute necessity if you are on FB.)
The show gets a little technical in spots, but the hosts, Charlene McMann-Seaman and Scott Seaman, are pretty good about bringing things back to earth and asking questions that clarify and simplify some issues.
I still think it's easy to let guilt creep in when you're thinking about causes, but if you're past that, it's a show worth listening to.
That said, I also fully believe in the power of information, and if being informed about lymphoma empowers you, then learn all you can. (Clearly, it's something that I do myself.)
And, perhaps most importantly, finding answers to "what causes lymphoma?" really is important to researchers, even if it isn't something patients should dwell on.
Anyway, that podcast took place on May 15th, and it's available online now. The show lasts for about 100 minutes, and features interviews with some leading epidemiologists -- medical experts whose focus is on the cause of diseases (specifically lymphoma).
And it's a pretty interesting show. It takes a while to get to the meat of things, but it's worth waiting for. (And in fact, the opening info is worth listening to as well. It includes a plug for a symposium in September to mark World Lymphoma Day; it will focus on Follicular Lymphoma, and is co-sponsored by the excellent organization HOPE for Lymphoma, whose Facebook page is an absolute necessity if you are on FB.)
The show gets a little technical in spots, but the hosts, Charlene McMann-Seaman and Scott Seaman, are pretty good about bringing things back to earth and asking questions that clarify and simplify some issues.
I still think it's easy to let guilt creep in when you're thinking about causes, but if you're past that, it's a show worth listening to.
Friday, May 25, 2012
ASCO: All the Lymphoma News
I can comb through more abstracts from ASCO, but why do that when I can have a Certified Lymphoma Rock Star do it for me?
In a Medscape Today video, Dr. Bruce Cheson of Georgetown University Hospital gives a brief summary of all of the important lymphoma-related abstracts from the conference, including the couple that I have reviewed already. (And yes, he and I agree about some of the significance of some of the research).
The video is called "Blood Cancers: Lymphoma, Myeloma Preview," and in it, Dr. Cheson gives his take on some of the abstracts. (The link also includes a written transcript of what he has to say, if you'd rather read than watch.)
Among the abstracts that he addresses are a study comparing R-CHOP and CHOP + Bexxar (the RadioImmunoTherapy treatment). He promises this one will be controversial.
There will also be an update on the RESORT trial, which recently found that Rituxan Maintenance did not offer significant improvement over watching and waiting after initial treatment.
Another I'll be very interested in: an update on the STIL (Study group of Indolent Lymphomas) trial that compared CHOP and Bendamustine, and which in previous years has gone a long way toward Bendamustine elbowing out CHOP as a preferred fontline treatment for indolent lymphomas like Follicular. We'll get updated information on the trial.
Should be very interesting. As we inch closer to the dates of the conference, we'll start to see some press releases from the sponsors of various studies. We'll see then which studies seem most significant, at least in the sponsors' eyes -- those things that are most worth bragging about.
In a Medscape Today video, Dr. Bruce Cheson of Georgetown University Hospital gives a brief summary of all of the important lymphoma-related abstracts from the conference, including the couple that I have reviewed already. (And yes, he and I agree about some of the significance of some of the research).
The video is called "Blood Cancers: Lymphoma, Myeloma Preview," and in it, Dr. Cheson gives his take on some of the abstracts. (The link also includes a written transcript of what he has to say, if you'd rather read than watch.)
Among the abstracts that he addresses are a study comparing R-CHOP and CHOP + Bexxar (the RadioImmunoTherapy treatment). He promises this one will be controversial.
There will also be an update on the RESORT trial, which recently found that Rituxan Maintenance did not offer significant improvement over watching and waiting after initial treatment.
Another I'll be very interested in: an update on the STIL (Study group of Indolent Lymphomas) trial that compared CHOP and Bendamustine, and which in previous years has gone a long way toward Bendamustine elbowing out CHOP as a preferred fontline treatment for indolent lymphomas like Follicular. We'll get updated information on the trial.
Should be very interesting. As we inch closer to the dates of the conference, we'll start to see some press releases from the sponsors of various studies. We'll see then which studies seem most significant, at least in the sponsors' eyes -- those things that are most worth bragging about.
Wednesday, May 23, 2012
How Doctors Should Treat Us
We interrupt this discussion of ASCO abstracts to bring you an article from the always excellent Mary Elizabeth Williams, cancer patient and Salon writer, called "Listen up, doctors: Here’s how to talk to your patients."
I've linked to Williams before -- I think she is probably the best writer out there is terms of describing what it feels like to be a cancer patient. (And did I mention that I emailed her to tell her how much I liked her work, and she emailed me back? Imagine -- being a groupie at my age.)
This article offers some advice to doctors for how they should talk to patients. All of us -- cancer patients or not -- have dealt with doctors with nasty bedside manners; it gets worse when the situation involves cancer, or some other dire (or seemingly dire) situation. Williams' practical advice for doctors would help all of them, whatever their specialty, and whatever their patients' situation.
It's blunt, too: the first piece of advice is "Get your hand off the goddamn doorknob already." As in: we know you're in a hurry. We can see how crowded the waiting room is. But if you're already focused on the next patient, you aren't paying attention to us. Plus, it makes us feel less than valued, as if our problems don't matter. So have a seat and hear what I have to say.
There's other good advice, too. And the comments from readers are also worth reading.
I've linked to Williams before -- I think she is probably the best writer out there is terms of describing what it feels like to be a cancer patient. (And did I mention that I emailed her to tell her how much I liked her work, and she emailed me back? Imagine -- being a groupie at my age.)
This article offers some advice to doctors for how they should talk to patients. All of us -- cancer patients or not -- have dealt with doctors with nasty bedside manners; it gets worse when the situation involves cancer, or some other dire (or seemingly dire) situation. Williams' practical advice for doctors would help all of them, whatever their specialty, and whatever their patients' situation.
It's blunt, too: the first piece of advice is "Get your hand off the goddamn doorknob already." As in: we know you're in a hurry. We can see how crowded the waiting room is. But if you're already focused on the next patient, you aren't paying attention to us. Plus, it makes us feel less than valued, as if our problems don't matter. So have a seat and hear what I have to say.
There's other good advice, too. And the comments from readers are also worth reading.
Tuesday, May 22, 2012
ASCO: Transformation
Another abstract from the ASCO conference to be held in a couple of weeks.
This one is called "Transformation of follicular lymphoma in the era of immunochemotherapy: A population-based study from British Columbia."
There was some encouraging news from it (though, of course with the usual "yeah, but..."). The study aimed to find out whether Rituxan, which has had such a positive impact on fNHL in general, has had any impact on transformation -- when Follicular turns into a more aggressive form of lymphoma.
As the abstract notes, most studies put transformation risk at about 3%. In other words, about 3% of Follicular patients will transform every year, and about 15-20% will transform over 5 years. (This abstract doesn't say it, but depending on who you ask, the risk is anywhere from 30-50% over 15 years, and the risk seems to disappear after that time.) The researchers looked at 261 patients with Follicular NHL from the Lymphoid Cancer Database of the British Columbia Cancer Agency. All had been treated with either CVP + Rituxan or Fludarabine + Rituxan. Some also received Rituxan Maintenance (infusions of Rituxan every 6 months after the initial treatment).
According to the study, the risk of transformation for the entire group was 2% per year -- lower than the 3% from other studies. This suggests that Immunochemotherapy (that is, combining chemo and Rituxan) lowers the risk of transformation.
The study also found, though, that the rate of transformation for patients who received R-Maintenance was even lower: about 1.5% per year.
They seem careful not to make too many promises in their abstract. It's a relatively small study of a very geographically limited population. (I have no idea if geography, or environment, has anything to do with transformation, but it seems like a broader study would be more trustworthy.) But it's significant enough to justify further exploration. Some kind of relief for transformation would certainly make Follicular patients happy.
This one is called "Transformation of follicular lymphoma in the era of immunochemotherapy: A population-based study from British Columbia."
There was some encouraging news from it (though, of course with the usual "yeah, but..."). The study aimed to find out whether Rituxan, which has had such a positive impact on fNHL in general, has had any impact on transformation -- when Follicular turns into a more aggressive form of lymphoma.
As the abstract notes, most studies put transformation risk at about 3%. In other words, about 3% of Follicular patients will transform every year, and about 15-20% will transform over 5 years. (This abstract doesn't say it, but depending on who you ask, the risk is anywhere from 30-50% over 15 years, and the risk seems to disappear after that time.) The researchers looked at 261 patients with Follicular NHL from the Lymphoid Cancer Database of the British Columbia Cancer Agency. All had been treated with either CVP + Rituxan or Fludarabine + Rituxan. Some also received Rituxan Maintenance (infusions of Rituxan every 6 months after the initial treatment).
According to the study, the risk of transformation for the entire group was 2% per year -- lower than the 3% from other studies. This suggests that Immunochemotherapy (that is, combining chemo and Rituxan) lowers the risk of transformation.
The study also found, though, that the rate of transformation for patients who received R-Maintenance was even lower: about 1.5% per year.
They seem careful not to make too many promises in their abstract. It's a relatively small study of a very geographically limited population. (I have no idea if geography, or environment, has anything to do with transformation, but it seems like a broader study would be more trustworthy.) But it's significant enough to justify further exploration. Some kind of relief for transformation would certainly make Follicular patients happy.
Sunday, May 20, 2012
ASCO: Follicular Treatment Options
And so it begins: the abstracts and press releases for papers at the upcoming ASCO conference. ASCO is the American Society of Clinical Oncology, and their annual conference takes place in Chicago June 1-4. There are a whole bunch of lymphoma-related conferences throughout the year, but one reason I like ASCO so much is that it's devoted to clinical oncology -- the doctors who work directly with patients. All lymphoma research is valuable; there's no question about that. But the clinical stuff appeals to my pragmatic nature.
I'll try to review as many of the Follicular NHL abstracts as possible over the next few weeks. This first one is from a group of researchers in Italy. Their aim was to try to establish a standard for treating advanced fNHL. This represents a serious problem: there are lots of treatments available, but no real agreement over which one should be used, or which should be preferred, or in which order they should be given.
The presentation is called "R-CVP versus R-CHOP versus R-FM as first-line therapy for advanced-stage follicular lymphoma: Final results of FOLL05 trial from the Fondazione Italiana Linfomi (FIL)," and, as the named implies, they attempted to compare three widely-used treatments: CHOP, CVP, and Fludarabine (with Rituxan added to all of them). The study took place over 5 years, and involved 504 patients, divided between the three treatments. The patients were measured for Time to Treatment Failure (evidence that the treatment didn't work, or evidence that the disease had returned or gotten worse).
Overall, 91% of patients responded to the treatment they were given. (Which is very good -- and further evidence of why it's so hard to establish one treatment as the best). After 3 years, Time to treatment Failure (that is, the percentage of patients who had no progression) for the three treatments were 46% for R-CVP, 64% for R-CHOP, and 61% for R-FM. But while CVP seemed less effective than the others, R-FM also resulted in a greater number of secondary cancers (probably leukemias, from what I've read of Fludarabine when Dr. R mentioned it to me as a possibility long ago).
That would seem to make CHOP the winner, but, interestingly, the abstract does not some right out and say so.
My guess, then, is that clinicians will continue to choose whichever of the three has been most appealing to them up until now.
Of course, the study didn't include Bendamustine, which might have come out as successful as CHOP, but with less toxicity. Which doesn't do anything to clear things up.
Two ways to look at this: 1) There's still lots of confusion, and no one knows what the best thing to do is. Or 2) We have lots of options, and they all seem very good, so if one doesn't work, we can try another.
I choose the latter.
I'll try to review as many of the Follicular NHL abstracts as possible over the next few weeks. This first one is from a group of researchers in Italy. Their aim was to try to establish a standard for treating advanced fNHL. This represents a serious problem: there are lots of treatments available, but no real agreement over which one should be used, or which should be preferred, or in which order they should be given.
The presentation is called "R-CVP versus R-CHOP versus R-FM as first-line therapy for advanced-stage follicular lymphoma: Final results of FOLL05 trial from the Fondazione Italiana Linfomi (FIL)," and, as the named implies, they attempted to compare three widely-used treatments: CHOP, CVP, and Fludarabine (with Rituxan added to all of them). The study took place over 5 years, and involved 504 patients, divided between the three treatments. The patients were measured for Time to Treatment Failure (evidence that the treatment didn't work, or evidence that the disease had returned or gotten worse).
Overall, 91% of patients responded to the treatment they were given. (Which is very good -- and further evidence of why it's so hard to establish one treatment as the best). After 3 years, Time to treatment Failure (that is, the percentage of patients who had no progression) for the three treatments were 46% for R-CVP, 64% for R-CHOP, and 61% for R-FM. But while CVP seemed less effective than the others, R-FM also resulted in a greater number of secondary cancers (probably leukemias, from what I've read of Fludarabine when Dr. R mentioned it to me as a possibility long ago).
That would seem to make CHOP the winner, but, interestingly, the abstract does not some right out and say so.
My guess, then, is that clinicians will continue to choose whichever of the three has been most appealing to them up until now.
Of course, the study didn't include Bendamustine, which might have come out as successful as CHOP, but with less toxicity. Which doesn't do anything to clear things up.
Two ways to look at this: 1) There's still lots of confusion, and no one knows what the best thing to do is. Or 2) We have lots of options, and they all seem very good, so if one doesn't work, we can try another.
I choose the latter.
Thursday, May 17, 2012
Antibodies for Follicular Lymphoma
The May 2012 issue of Hematologic Malignancies reports on results of a phase II clinical trial comparing Rituxan with Obinutuzumab, and Obinutuzumab wins!
This seems like a pretty big deal. It's the first time the two monoclonal antibodies went head-to-head in a clinical trial. Both antibodies target the CD20 protein on the surface of B-cell lymphocytes, but there are some key differences. Obinutuzumab (also known as GA101) is a humanized antibody, unlike Rituxan, which was derived from mice. It is also glyco-engineered. (Which is apparently important, but honestly, I've read a dozen different explanations of what glyco-engineering is, and I can't get a handle on it. Sorry. We'll just say it's a good thing and leave it at that.) Obinutuzumab also seems to bring on death of cancer cells more directly.
As for results: 149 Follicular Lymphoma patients took part in the study. Of those given Obinutuzumab, 44.6% had a response, compared to 33.3% who were given Rituxan. That seems like a pretty good improvement.
We need to step back a little bit, though.
First of all, these results aren't new; they were presented at the 2011 ASH conference. Even then, they were seen as exciting, but not earth-shattering; in a sample of 149 patients, which is fairly small, an 11 percentage point difference is not statistically significant (which means it can't actually be attributed to Obinutuzumab).
But what is encouraging is that we have enough data to justify a phase III trial, which will mean a larger sample.
Rituxan has been a miracle for so many people -- I'll include myself -- but despite a dozen or more attempts at improving on it, there has yet to be a monoclonal antibody that can do much better. Maybe Obinutuzumab will prove to be the one, and the trial will show that. Like Rituxan, it won't be a cure. At best, it might prove to be an alternative for patients who are sensitive to Rituxan, or who become Rituxan-resistant.
At worst, it's another arrow in the quiver. Not too bad.
This seems like a pretty big deal. It's the first time the two monoclonal antibodies went head-to-head in a clinical trial. Both antibodies target the CD20 protein on the surface of B-cell lymphocytes, but there are some key differences. Obinutuzumab (also known as GA101) is a humanized antibody, unlike Rituxan, which was derived from mice. It is also glyco-engineered. (Which is apparently important, but honestly, I've read a dozen different explanations of what glyco-engineering is, and I can't get a handle on it. Sorry. We'll just say it's a good thing and leave it at that.) Obinutuzumab also seems to bring on death of cancer cells more directly.
As for results: 149 Follicular Lymphoma patients took part in the study. Of those given Obinutuzumab, 44.6% had a response, compared to 33.3% who were given Rituxan. That seems like a pretty good improvement.
We need to step back a little bit, though.
First of all, these results aren't new; they were presented at the 2011 ASH conference. Even then, they were seen as exciting, but not earth-shattering; in a sample of 149 patients, which is fairly small, an 11 percentage point difference is not statistically significant (which means it can't actually be attributed to Obinutuzumab).
But what is encouraging is that we have enough data to justify a phase III trial, which will mean a larger sample.
Rituxan has been a miracle for so many people -- I'll include myself -- but despite a dozen or more attempts at improving on it, there has yet to be a monoclonal antibody that can do much better. Maybe Obinutuzumab will prove to be the one, and the trial will show that. Like Rituxan, it won't be a cure. At best, it might prove to be an alternative for patients who are sensitive to Rituxan, or who become Rituxan-resistant.
At worst, it's another arrow in the quiver. Not too bad.
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