MedicalXpress reports on new research on Vitamin D levels and survival in Follicular Lymphoma patients. It reports on a study from The Journal of Clinical Oncology. I think it's worth discussing both of them. Or, more importantly, my reaction to both of them.
I read the MedicalXpress article last night. Nice headline: "Low vitamin D linked to worse prognosis in type of non-Hodgkin lymphoma." Certainly caught my attention. I've been interested in Vitamin D for a while, and its affect not only on Lymphoma, but on health in general. A few years ago, my doctor (my regular ol' doctor, not my oncologist) recommended I take some every day. It's a controversial supplement, with some studies saying it has a whole lot of health benefits, and others saying those benefits aren't real, or that too much Vitamin D might even be bad for you (the latest in this controversy came out just a few days ago).
So anything about Vitamin D and cancer catches my attention.
The opening sentence was as interesting as the headline: "A new study found that people with lower vitamin D levels prior to
treatment for follicular lymphoma succumb to the disease or face relapse
earlier than patients with sufficient vitamin D levels in their blood."
At this point, I'm thinking, "Woo hoo! I take my Vitamin D every day! I'm covered!"
I scanned the rest of the article, saw that the original research was published in JOC, and made a note to look at it today when I got a chance.
This morning, I read the JOC abstract. My excitement went down a little bit.
The researchers looked at two groups from two separate Follicular Lymphoma trials. Both groups involved patients who had been untreated, and then received CHOP + Rituxan or Zevalin, or just CHOP + Rituxan. They found that the patients who had low levels of Vitamin D had lower Progression Free Survival and Overall Survival.
Reading a little more closely, I could see that the comparison wasn't perfect. Although the researchers tested Vitamin D levels from two different groups, in two different countries, they had slightly different treatments and, if I'm reading correctly, had different levels that were considered "deficient."
The study's conclusion says "Although statistical significance was not reached in the LYSA cohort,
the consistent estimates of association between low
vitamin D levels and FL outcomes in two
independent cohorts suggests that serum vitamin D might be the first
potentially modifiable
factor to be associated with FL survival.
Further investigation is needed to determine the effects of vitamin D
supplementation
in this clinical setting."
Basically, this study doesn't say anything for sure, but it says enough that this should be looked into more deeply by someone else.
I looked back again at the MedicalXpress article, and it said basically the same thing, though without as much emphasis on the lack of statistical significance. So why was I so much happier about reading the MedicalXpress article?
I think part of it is because I read it quickly, but also because of the way it is set up. The good news always comes first in this kind of article. And then it gives some helpful context, talking about the other studies that have shown that Vitamin D is related to better outcomes. When I read a medical journal, that good news (or bad news) usually comes at the end, especially when it's just an abstract. And I always read a little more slowly with a medical journal, because there's so much I don't understand on the first reading.
But mostly, I think I was seeing what I wanted to see in the MedicalXpress piece -- that Vitamin D was going to be a big help, and I was doing the right thing.
So for me, the big take-away doesn't have to do with Vitamin D (though I'm going to keep taking my supplements anyway). It has to do with reading, and remembering that it's easy to see things that aren't there when we read.
I do hope someone does more research on Vitamin D and Follicular Lymphoma. It would nice to have one solid answer about this disease, wouldn't it?
Tuesday, March 31, 2015
Wednesday, March 25, 2015
Watching and Waiting (Including My Own)
NewsmaxHealth has a brief piece out on Watching and Waiting. And I do mean brief -- just a few paragraphs long, written by a survivor of an aggressive Leukemia (not someone who watched and waited herself). This isn't a research article -- I've declared a moratorium on them, and refuse to write about any of those "Is Watch and Wait legitimate?" articles until I see some definitive evidence one way or the other, and that's not happening any time soon.
No, this brief article is a really basic introduction to what W & W is, based on the idea that most of us (probably including that of us who watched and waited) think of cancer as an emergency that needs to be taken care of right away. But, of course, not all cancers are like that, including, of course, Follicular Lymphoma. Some of them don't require immediate treatment.
And that really throws people -- not only patients, but family and friends, too. I had lots of people who questioned the decision, wondering if this was really the right thing to do. It took me a while to rally accept that it was, so I don't blame them for thinking that way. I know that were just worried about me.
One quote from the article is especially important:
“Watchful waiting should be considered an active strategy, as close monitoring can give you reassurance that your cancer is stable, and not aggressively growing. If a cancer is found to be progressing during the monitoring stage, then additional treatment strategies can be started.”
No, this brief article is a really basic introduction to what W & W is, based on the idea that most of us (probably including that of us who watched and waited) think of cancer as an emergency that needs to be taken care of right away. But, of course, not all cancers are like that, including, of course, Follicular Lymphoma. Some of them don't require immediate treatment.
And that really throws people -- not only patients, but family and friends, too. I had lots of people who questioned the decision, wondering if this was really the right thing to do. It took me a while to rally accept that it was, so I don't blame them for thinking that way. I know that were just worried about me.
One quote from the article is especially important:
“Watchful waiting should be considered an active strategy, as close monitoring can give you reassurance that your cancer is stable, and not aggressively growing. If a cancer is found to be progressing during the monitoring stage, then additional treatment strategies can be started.”
Friday, March 20, 2015
Biomarkers in Follicular Lymphoma
I'm feeling guilty because I've been so bad about posting things to the blog. Work is busy and family obligations are abundant. I'm still in physical therapy for my shoulder, which is disrupting my schedule even more.
To be honest, I'm feeling kind of disconnected from my cancer. No time to read and write about it, and I still haven't heard anything from whoever my new oncologist is. I guess that's good, in a way -- it's been a long time since I've obsessed over my health, and I prefer it that way. But I don't want to go too far the other way, either, and put it out of my mind completely. Avoidance is not a coping strategy. I like that happy middle -- learning as much as I can about Follicular Lymphoma and sharing it, and taking comfort from that.
I'll try to get back on track.
*****************************************
OncLive, a web site for the oncology community, posted an interview this week Dr. Randy Gascoyne from the British Columbia Cancer Agency in Canada. Dr. Gascoyne is researching predictive biomarkers in Follicular Lymphoma and DLBCL.
Biomarkers are things like proteins or genes that are present on specific types of cancer cells. There are several already identified for Follicular Lymphoma; Dr. Gascoyne is working on identifying even more. Sometimes this involves finding a biomarker that might disturb a pathway. In other words, something on an FL cell is necessary for something else to happen that keeps the cancer cell alive. Identifying that marker, understanding its role in cell survival, and then finding how to mess with it -- that's what scientists are really excited about (and what they are having some success with recently).
So, for example, Dr. Gascoyne described a study that looks at FLIPI, a tool used by oncologists to measure how aggressive they should be with treatment. (See Lymphomation.org for a nice explanation of FLIPI.) But FLIPI is a very general tool, and about a quarter of patients in his study did worse than predicted. Dr. Gascoyne identified seven genes that, when present, can predict more accurately than FLIPI alone that a patient is probably going to have big problems.
The next step is to use that information to design treatments that take into account those genetic markers. Certain treatments can be targeted to those patients right away (assuming they have been shown to work on those patients).
This kind of work is already happening in Follicular Lymphoma, and Dr. Gascoyne thinks even more will happen in the future. He looks forward to this work being more predictive -- showing a strong connection between particular biomarkers and eventual treatments.
Lots of good stuff on the horizon.
To be honest, I'm feeling kind of disconnected from my cancer. No time to read and write about it, and I still haven't heard anything from whoever my new oncologist is. I guess that's good, in a way -- it's been a long time since I've obsessed over my health, and I prefer it that way. But I don't want to go too far the other way, either, and put it out of my mind completely. Avoidance is not a coping strategy. I like that happy middle -- learning as much as I can about Follicular Lymphoma and sharing it, and taking comfort from that.
I'll try to get back on track.
*****************************************
OncLive, a web site for the oncology community, posted an interview this week Dr. Randy Gascoyne from the British Columbia Cancer Agency in Canada. Dr. Gascoyne is researching predictive biomarkers in Follicular Lymphoma and DLBCL.
Biomarkers are things like proteins or genes that are present on specific types of cancer cells. There are several already identified for Follicular Lymphoma; Dr. Gascoyne is working on identifying even more. Sometimes this involves finding a biomarker that might disturb a pathway. In other words, something on an FL cell is necessary for something else to happen that keeps the cancer cell alive. Identifying that marker, understanding its role in cell survival, and then finding how to mess with it -- that's what scientists are really excited about (and what they are having some success with recently).
So, for example, Dr. Gascoyne described a study that looks at FLIPI, a tool used by oncologists to measure how aggressive they should be with treatment. (See Lymphomation.org for a nice explanation of FLIPI.) But FLIPI is a very general tool, and about a quarter of patients in his study did worse than predicted. Dr. Gascoyne identified seven genes that, when present, can predict more accurately than FLIPI alone that a patient is probably going to have big problems.
The next step is to use that information to design treatments that take into account those genetic markers. Certain treatments can be targeted to those patients right away (assuming they have been shown to work on those patients).
This kind of work is already happening in Follicular Lymphoma, and Dr. Gascoyne thinks even more will happen in the future. He looks forward to this work being more predictive -- showing a strong connection between particular biomarkers and eventual treatments.
Lots of good stuff on the horizon.
Friday, March 13, 2015
CD5 in Follicular Lymphoma
Interesting article in the journal Modern Pathology last week: "CD5-Positive Follicular Lymphoma: Clinicopathologic Correlations and Outcome in 88 Cases."
As the title suggests, researchers looked at patients who had CD5 on their lymphoma cells. CD5 is a protein that is commonly found on cells of some blood cancers, but Follicular Lymphoma isn't usually one of them. We're more likely to find CD10, CD19, CD20 (which is the protein that attracts Rituxan) and CD22. But CD5 is much less common.
So when CD5 does show up, what does that mean?
The purpose of the article is to look at 88 Follicular Lymphoma patients with CD5, describe some trends, and try to figure out what it means.
To be clear: they didn't look at a large sample of FL patients and try to figure out what percentage of them had CD5; they looked specifically for patients who had it, and found 88. That's who they are focusing on.
Here's how it all breaks down:
66 of the patients had FL discovered in their lymph nodes, and 22 had in other places.
81 patients had swollen nodes, 66 had more than one lymph node site affected, 46 had bone marrow involvement, and 7 had enlarged spleens.
Staging information was available for 84 patients: 52 were at stage IV, 18 were at stage III, 12 at stage II, and 2 at stage I.
61 were grade 1 or 2, and 27 were grade 3.
So far, so good; these really aren't that far off from the whole FL population.
So now it gets a little more interesting.
In 64% of the cases, there was some kind of translocation or BCL2-related issue. (BCL2 is related to cancer cells not knowing how to kill themselves off like normal cells.)
43% of the patients also had Diffuse Large B-Cell Lymphoma (DLBCL), either before, after, or at the same time as their FL. All received some kind of chemotherapy, and some had a Stem Cell Transplant.
As for Overall Survival, with a median follow-up of 55 months (one with a follow-up of only 2 weeks, and one with 207 months, or more than 17 years), 15 patients had died, 46 were living with the disease, and 20 were in remission.
When the 88 patients were compared to a matched group of FL patients with CD5, the researchers found that the CD5 patients were more likely to develop DLBCL (about 43% of them did, compared to about 17% of the general FL population). They also had a shorter median Progression Free Survival that the overall FL group (44 months before the disease got worse, versus 89 months -- though this doesn't account for different types of treatment), and the CD5 group was a more likely to have a higher International Prognostic Index (a very general measurement of how aggressive their cancer might be).
It's these last three things (more likely DLBCL, shorter PFL, and higher IPI) that make up their conclusion: if you want to put those things together, they are basically saying that having CD5 means you are more likely to be worse off than most other Follicular Lymphoma patients.
So here's my take on all of this, for what it's worth:
First, I hesitated to put in all of those numbers, because as I've said many times before, numbers don't mean anything to us individually. If anything, they are valuable to researchers because they might give them some clues as to what they might want to look into. In this case, for instance, they might find that it's worth looking into whether or not an anti-CD5 antibody might be valuable for some FL patients. That monoclonal antibody does exist -- remember, CD5 is common in some other blood cancers -- though my understanding is it never took off because those cancers also commonly have CD3, which is more sensitive to antibodies.
Second, I think this emphasizes how difficult it is to pin down a single source for attacking a cancer. I looked at those numbers -- 43% of CD5 FL patients had DLBCL, for example -- and thought, Yeah, but that's less than half. There is some connection, but having CD5 is no guarantee that you'll transform. Heck, one patient was still alive 17 years after diagnosis. So it's not just CD5 that's the problem -- it's CD5 plus....what? I don't know. But it has to be CD5 combined with some other stuff that make that form of FL tougher to handle, and these researchers weren't necessarily looking for that. As I said, it's a reminder of how difficult it is to pin down one source for cancer. We can't attack just one thing and assume everything will be OK. This is the direction that cancer research has been going -- looking for multiple operations, inside and around cancer cells, that work together to keep the cancer cells alive.
Finally, the part for some hope -- they found some information about Follicular Lymphoma patients with CD5! As tough as it's going to be to find all of the operations that work together to keep cancer cells alive, these researchers added their small piece to the big puzzle. And as more and more researchers add their pieces, that big puzzle is going to come into focus, and we're going to have our answer. It's going to take some time, of course, but considering how much we've learned about cancer in the last 10 years, compared to the 10 years before that, we are well on our way.
Stay hopeful, and ignore the numbers.
As the title suggests, researchers looked at patients who had CD5 on their lymphoma cells. CD5 is a protein that is commonly found on cells of some blood cancers, but Follicular Lymphoma isn't usually one of them. We're more likely to find CD10, CD19, CD20 (which is the protein that attracts Rituxan) and CD22. But CD5 is much less common.
So when CD5 does show up, what does that mean?
The purpose of the article is to look at 88 Follicular Lymphoma patients with CD5, describe some trends, and try to figure out what it means.
To be clear: they didn't look at a large sample of FL patients and try to figure out what percentage of them had CD5; they looked specifically for patients who had it, and found 88. That's who they are focusing on.
Here's how it all breaks down:
66 of the patients had FL discovered in their lymph nodes, and 22 had in other places.
81 patients had swollen nodes, 66 had more than one lymph node site affected, 46 had bone marrow involvement, and 7 had enlarged spleens.
Staging information was available for 84 patients: 52 were at stage IV, 18 were at stage III, 12 at stage II, and 2 at stage I.
61 were grade 1 or 2, and 27 were grade 3.
So far, so good; these really aren't that far off from the whole FL population.
So now it gets a little more interesting.
In 64% of the cases, there was some kind of translocation or BCL2-related issue. (BCL2 is related to cancer cells not knowing how to kill themselves off like normal cells.)
43% of the patients also had Diffuse Large B-Cell Lymphoma (DLBCL), either before, after, or at the same time as their FL. All received some kind of chemotherapy, and some had a Stem Cell Transplant.
As for Overall Survival, with a median follow-up of 55 months (one with a follow-up of only 2 weeks, and one with 207 months, or more than 17 years), 15 patients had died, 46 were living with the disease, and 20 were in remission.
When the 88 patients were compared to a matched group of FL patients with CD5, the researchers found that the CD5 patients were more likely to develop DLBCL (about 43% of them did, compared to about 17% of the general FL population). They also had a shorter median Progression Free Survival that the overall FL group (44 months before the disease got worse, versus 89 months -- though this doesn't account for different types of treatment), and the CD5 group was a more likely to have a higher International Prognostic Index (a very general measurement of how aggressive their cancer might be).
It's these last three things (more likely DLBCL, shorter PFL, and higher IPI) that make up their conclusion: if you want to put those things together, they are basically saying that having CD5 means you are more likely to be worse off than most other Follicular Lymphoma patients.
So here's my take on all of this, for what it's worth:
First, I hesitated to put in all of those numbers, because as I've said many times before, numbers don't mean anything to us individually. If anything, they are valuable to researchers because they might give them some clues as to what they might want to look into. In this case, for instance, they might find that it's worth looking into whether or not an anti-CD5 antibody might be valuable for some FL patients. That monoclonal antibody does exist -- remember, CD5 is common in some other blood cancers -- though my understanding is it never took off because those cancers also commonly have CD3, which is more sensitive to antibodies.
Second, I think this emphasizes how difficult it is to pin down a single source for attacking a cancer. I looked at those numbers -- 43% of CD5 FL patients had DLBCL, for example -- and thought, Yeah, but that's less than half. There is some connection, but having CD5 is no guarantee that you'll transform. Heck, one patient was still alive 17 years after diagnosis. So it's not just CD5 that's the problem -- it's CD5 plus....what? I don't know. But it has to be CD5 combined with some other stuff that make that form of FL tougher to handle, and these researchers weren't necessarily looking for that. As I said, it's a reminder of how difficult it is to pin down one source for cancer. We can't attack just one thing and assume everything will be OK. This is the direction that cancer research has been going -- looking for multiple operations, inside and around cancer cells, that work together to keep the cancer cells alive.
Finally, the part for some hope -- they found some information about Follicular Lymphoma patients with CD5! As tough as it's going to be to find all of the operations that work together to keep cancer cells alive, these researchers added their small piece to the big puzzle. And as more and more researchers add their pieces, that big puzzle is going to come into focus, and we're going to have our answer. It's going to take some time, of course, but considering how much we've learned about cancer in the last 10 years, compared to the 10 years before that, we are well on our way.
Stay hopeful, and ignore the numbers.
Monday, March 9, 2015
Case Study: Transformed Follicular Lymphoma
Lymphoma Hub, a site aimed at health care professionals, posted a nice case study a week ago describing a the process for deciding on how to treat a patient with transformed Follicular Lymphoma. The patient described is a 59 year old male, and the oncologist discussing the case is Dr. Nathan Fowler from M. D. Anderson Cancer Center in Texas.
The post, which includes both a video and a transcript, takes us through the whole process. First we see a brief history of the patient, who had an indolent, slow-growing form of Follicular Lymphoma, with no symptoms. Dr. Fowler favors watching and waiting for patients like this, since there is no Overall Survival benefit to treating early (as he points out).
In a follow-up a few months later, the patient complained of abdominal pain. We get to see his biopsy and PET scan results, and based on them, Dr. Fowler concluded he had transformed.
From here, Dr. Fowler goes through the options available. He is careful to point out that there are no studies that compare treatments for transformed FL, so most of what we know is retrospective, looking back at patients after to see how things worked out. Not ideal, since researchers can't control who is in the studies, so there might not be an accurate comparison. But, it's all we have.
Among the options he discusses are Autologous Stem Cell Transplants, where a patient's own stem cells are removed and then put back in, and Allogeneic Stem Cell Transplants, where a donor's cells are put in. There's more to these transplants, and each has strengths and weaknesses -- enough weaknesses that neither can really be said to be a better choice than the other. If you want to read more on Stem Cell Transplants of both kinds, Lymphomation.org has lots of good description and links.)
Dr. Fowler also discusses chemotherapy options like R-CHOP, which he would recommend if the patient has not had CHOP or a similar anthracycline treatment before (since too much can cause heart damage).
Overall, it's an interesting look at how an oncologist makes decisions. I don't think any of us like to think about the possibility of transforming, but I like to know my options if it ever comes to that. This video/transcript is a good way to remind us of those options.
The post, which includes both a video and a transcript, takes us through the whole process. First we see a brief history of the patient, who had an indolent, slow-growing form of Follicular Lymphoma, with no symptoms. Dr. Fowler favors watching and waiting for patients like this, since there is no Overall Survival benefit to treating early (as he points out).
In a follow-up a few months later, the patient complained of abdominal pain. We get to see his biopsy and PET scan results, and based on them, Dr. Fowler concluded he had transformed.
From here, Dr. Fowler goes through the options available. He is careful to point out that there are no studies that compare treatments for transformed FL, so most of what we know is retrospective, looking back at patients after to see how things worked out. Not ideal, since researchers can't control who is in the studies, so there might not be an accurate comparison. But, it's all we have.
Among the options he discusses are Autologous Stem Cell Transplants, where a patient's own stem cells are removed and then put back in, and Allogeneic Stem Cell Transplants, where a donor's cells are put in. There's more to these transplants, and each has strengths and weaknesses -- enough weaknesses that neither can really be said to be a better choice than the other. If you want to read more on Stem Cell Transplants of both kinds, Lymphomation.org has lots of good description and links.)
Dr. Fowler also discusses chemotherapy options like R-CHOP, which he would recommend if the patient has not had CHOP or a similar anthracycline treatment before (since too much can cause heart damage).
Overall, it's an interesting look at how an oncologist makes decisions. I don't think any of us like to think about the possibility of transforming, but I like to know my options if it ever comes to that. This video/transcript is a good way to remind us of those options.
anthracylines
Thursday, March 5, 2015
Immunotherapy Basics
I've linked a few times to a site called Yale Cancer Center Answers, and I'm going to give you another one.
"Answers" is a local radio show, sponsored and produced by the Smilow Cancer Center at Yale-New Haven Hospital. The show is hosted by oncologists, and every week, they have a different cancer-related topic, and interview an expert in that area who is affiliated with Yale. Shows range from specific types top cancer to information for caregivers to nutrition and exercise advice.
A recent show was titled "Using Immunotherapy to Fight Cancer," and that title certainly caught my eye. If you have kept up with cancer news in the last couple of years, you know how important immunotherapy is for our future. As researchers have learned more about cancer, they have come to understand how it resists attempts by the immune system to control it. In other words, cancer doesn't belong in the body, and the immune system is supposed to take care of stuff that doesn't belong. Immunotherapy involves the many ways that researchers are trying to fix that situation, training the body to recognize and eliminate cancer cells. Think PD-1, which has been in the news. PD-1 stands for "Programmed Death"; it appears on the surface of cells and prevents T-cells from killing the cancer cells. One class of cancer treatments making lots of news is PD-1 Inhibitors, which shut down PD-1 and let T-cells do their job and wipe out the cancer cells. Immunotherapy -- allowing the body's natural immune system to take care of the cancer.
The Yale show features an interview with Dr. Tarek Fahmy, who teaches Biomedical Engineering and Immunology at Yale. In the interview, he describes Immunotherapy in general, using vaccines as an example. A vaccine for something like measles works because it trains the immune system to recognize measles and attack it. Immunotherapy engineers try to build the pieces that go into that reaction and get the various parts to talk to each other.
It works the same way with cancer cells, as Dr Fahmy discusses, though it's a little tougher because cancer cells are so tricky.
Overall, it's an interesting interview. Yale always does a nice job on this show of explaining difficult ideas in easy-to-understand ways. In this interview, you'll find comparisons to brewing beer, Pac Man, and hair follicles, among other things.
You can find a recording of the show here and clicking in the January 25 link, and a written transcript of it here.
Enjoy.
"Answers" is a local radio show, sponsored and produced by the Smilow Cancer Center at Yale-New Haven Hospital. The show is hosted by oncologists, and every week, they have a different cancer-related topic, and interview an expert in that area who is affiliated with Yale. Shows range from specific types top cancer to information for caregivers to nutrition and exercise advice.
A recent show was titled "Using Immunotherapy to Fight Cancer," and that title certainly caught my eye. If you have kept up with cancer news in the last couple of years, you know how important immunotherapy is for our future. As researchers have learned more about cancer, they have come to understand how it resists attempts by the immune system to control it. In other words, cancer doesn't belong in the body, and the immune system is supposed to take care of stuff that doesn't belong. Immunotherapy involves the many ways that researchers are trying to fix that situation, training the body to recognize and eliminate cancer cells. Think PD-1, which has been in the news. PD-1 stands for "Programmed Death"; it appears on the surface of cells and prevents T-cells from killing the cancer cells. One class of cancer treatments making lots of news is PD-1 Inhibitors, which shut down PD-1 and let T-cells do their job and wipe out the cancer cells. Immunotherapy -- allowing the body's natural immune system to take care of the cancer.
The Yale show features an interview with Dr. Tarek Fahmy, who teaches Biomedical Engineering and Immunology at Yale. In the interview, he describes Immunotherapy in general, using vaccines as an example. A vaccine for something like measles works because it trains the immune system to recognize measles and attack it. Immunotherapy engineers try to build the pieces that go into that reaction and get the various parts to talk to each other.
It works the same way with cancer cells, as Dr Fahmy discusses, though it's a little tougher because cancer cells are so tricky.
Overall, it's an interesting interview. Yale always does a nice job on this show of explaining difficult ideas in easy-to-understand ways. In this interview, you'll find comparisons to brewing beer, Pac Man, and hair follicles, among other things.
You can find a recording of the show here and clicking in the January 25 link, and a written transcript of it here.
Enjoy.
Monday, March 2, 2015
Watching and Waiting is OK (And Now It's Time to Move On)
The British Journal of Haematology has an article coming out that focuses on Watching and Waiting in advanced stage, asymptomatic Follicular Lymphoma patients. Patients who are kind of like I was -- stage III, some swollen inguinal nodes, but otherwise feeling fine. The study looked at 286 stage III or 4 Follicular Lymphoma patients (in Denmark, I think, since that is where the researchers are from).
I'll spare you the suspense -- the conclusion of the article is "advanced stage FL managed by WAW had a favourable outcome and abandoning this strategy could lead to overtreatment in some patients."
There are a bunch of statistics, too, though they don't mean much without comparing them to patients who had other treatments. Also, they don't mean much because they are statistics, and statistics might give us a sense of trends for a group of people, they say nothing about us as individuals. I've said it before, and I'll say it here again -- any time I've gotten depressed about my cancer, it has been because of statistics. So I'm not going to say anything about them here.
The important thing is that conclusion -- that Watching and waiting is still a valid strategy. Having been a watch-and-waiter myself, I appreciate hearing that I made an acceptable choice. If I had chosen differently, that would probably be OK, too -- there's nothing I can do to change the past. We all make out choices best on the best information we have available to us. I'm guessing if I hadn't chosen Watch and Wait, I wouldn't spend so much time reading and writing about it. I'd just have moved on.
And moving on is just what I think we should do with the question of whether Watching and Waiting is a valid strategy for this FL population. It seems pretty clear to me that we aren't going to have a clear answer to the question. We have some studies that say it's not worth doing, because we have a clear alternative in Rituxan (and may have a few more in the next few years as more monoclonal antibodies become available). And we have some studies that say there isn't enough of a difference between Watch-and-Waiters and patients who are treated immediately to say Watch and Wait isn't valid. The most recent was a study from Japan, presented at this year's ASH conference a few months ago.
So I'm using my power as Lympho Bob to demand an end to this debate. It's time to move on. Let's focus on those exciting new treatments in the pipeline, train oncologists to get a sense of the whole patient at diagnosis -- her emotional state as well as her physical state -- and involve the patient in deciding the best course of treatment.
Having lots of options is one of our strengths. Let's do our best to make sure patients get all the options they can, and choose the one that they need.
There. It's decided.
I'll spare you the suspense -- the conclusion of the article is "advanced stage FL managed by WAW had a favourable outcome and abandoning this strategy could lead to overtreatment in some patients."
There are a bunch of statistics, too, though they don't mean much without comparing them to patients who had other treatments. Also, they don't mean much because they are statistics, and statistics might give us a sense of trends for a group of people, they say nothing about us as individuals. I've said it before, and I'll say it here again -- any time I've gotten depressed about my cancer, it has been because of statistics. So I'm not going to say anything about them here.
The important thing is that conclusion -- that Watching and waiting is still a valid strategy. Having been a watch-and-waiter myself, I appreciate hearing that I made an acceptable choice. If I had chosen differently, that would probably be OK, too -- there's nothing I can do to change the past. We all make out choices best on the best information we have available to us. I'm guessing if I hadn't chosen Watch and Wait, I wouldn't spend so much time reading and writing about it. I'd just have moved on.
And moving on is just what I think we should do with the question of whether Watching and Waiting is a valid strategy for this FL population. It seems pretty clear to me that we aren't going to have a clear answer to the question. We have some studies that say it's not worth doing, because we have a clear alternative in Rituxan (and may have a few more in the next few years as more monoclonal antibodies become available). And we have some studies that say there isn't enough of a difference between Watch-and-Waiters and patients who are treated immediately to say Watch and Wait isn't valid. The most recent was a study from Japan, presented at this year's ASH conference a few months ago.
So I'm using my power as Lympho Bob to demand an end to this debate. It's time to move on. Let's focus on those exciting new treatments in the pipeline, train oncologists to get a sense of the whole patient at diagnosis -- her emotional state as well as her physical state -- and involve the patient in deciding the best course of treatment.
Having lots of options is one of our strengths. Let's do our best to make sure patients get all the options they can, and choose the one that they need.
There. It's decided.
Subscribe to:
Posts (Atom)