Bad News :-(
That's 3 increases in a row 1.55, 1.69 and 2.12 between March and Sept 2012, which is an indicator of treatment failure or cancer recurrence by at least one standard (1997 ASTRO). The lowest score I've ever gotten following treatment in Sept 2010 was 1.55 in March 2012, so that's apparently my nadir.
My RO at UCSF is now concerned enough to order an E-MRI to see what's going on in there.
Asked him if he would also order a MRSI for additional data based on the following article published by the Prostate Cancer MRI/MRSI Group at UCSF over 10 years ago, which used E-MRIs in their studies but also recommended the use of MRSIs for additional precision. See: http://www.prostate-cancer.org/pcricms/node/169
Will let you all know what the RO decides and what the scan(s) reveal, if anything.
Wish me luck but my "gut" tells me that all of the cancer was never killed w/the CK treatment in Sept 2010 (which I've suspected for some time) and that some form of follow-up treatment will be required.
We'll see . . .
Comments
-
A pain in the neck
Swing
I am sorry for the results. Your PSA tests have been “a pain in the neck” from the start and very stressful for you. The recent three increases could mean recurrence and the way to find the truth is by waiting for another PSA in three months time. Image studies are not that “refined” in cases of small tumours, but it is worth to give it a try with the ones using the latest techniques.
You are an educated patient and know about the types available “in the market”. In the old times a case like yours would have been recommended to Combidex testing. Now you got the USPIO (feraheme MRI). There are several sites in the net discussing its possibilities.
Another test is the PET/CT C11-choline that is now on trials in cases similar to yours.
http://askdrbarken.wordpress.com/2011/12/06/multi-parametric-mri-combidex-and-ferumoxytol-with-dr-j-barentsz/
http://www.diagnosticimaging.com/pet-ct/content/article/113619/1474149
This is two years since your CK treatment. Your PSA at the time was high at 12.3 declining to 1.55 (probable nadir) in 24 months. The last increase rounds the PSADT of 12 month which is higher (longer period) than the critical threshold of < 9 month.
This long period in vPSA may be due to the slow growing type of cancer in your case (Gleason score 6). This is a type that is hard to find with traditional image studies because of possible micromets.
Waiting with periodical testing (PSA) would not alter outcomes from an earlier attack with a salvage treatment. You got time to check for all possibilities and discuss (second opinions) with the professionals.
Many comments about the latest diagnosing tools were talked in the last PCRI gathering. There are newer drugs to fight recurrence and there is also fixed sequential in using them. Get all the information you can and study it. We will be here to help you in this difficult time.
http://csn.cancer.org/node/246671
I hope that the increase is a false positive and that you see it going down for peace of mind.
Be strong and positive.
VGama0 -
SwingBeau2 said:PSA rise
Swing,
Sorry about the PSA rise. You're staying on top of your PCa, and I am sure you will do well. Keep us posted on your choices and progress.
Best of luck in your fight.
I'm sorry of your rise in psa. Since I have been going MDACC the worst I have seem my psa is 2.6 and that was between drugs, which was a requirement to go to Zytiga and now in my 9 months my psa has been at 0.2. My Lymph node tumor's are half the size they there before Zytiga. I still beleive that I will continue for these 9 more months. That mean that I have kept this monster under control for 18 months.
Just check into it, you might fine 18 more months of cancer under control or your psa under control. Once you get into a pattern with the drug the side effect are not so bad.0 -
Thanks, Beau. Will do!Beau2 said:PSA rise
Swing,
Sorry about the PSA rise. You're staying on top of your PCa, and I am sure you will do well. Keep us posted on your choices and progress.
Best of luck in your fight.
Thanks, Beau. Will do!0 -
Will Keep It In Mindralph.townsend1 said:Swing
I'm sorry of your rise in psa. Since I have been going MDACC the worst I have seem my psa is 2.6 and that was between drugs, which was a requirement to go to Zytiga and now in my 9 months my psa has been at 0.2. My Lymph node tumor's are half the size they there before Zytiga. I still beleive that I will continue for these 9 more months. That mean that I have kept this monster under control for 18 months.
Just check into it, you might fine 18 more months of cancer under control or your psa under control. Once you get into a pattern with the drug the side effect are not so bad.
Thanks, Ralph, but it's premature to think about any HT/ADT right now.
What needs to be done now is to determine if there's still any cancer in my prostate or not and, if there is, to then develop a plan to address it. The pending E-MRI/MRSI scans will be the 1st step in that direction.
As I also said above, I hope to avoid any HT/ADT if at all possible. Zytiga is designed for men w/advanced castration hormone resistant prostate cancer (post HT) and, as far as I know, I'm not in that situation yet but will definitely keep it in mind, in the event that I end up in that group.
BTW, Dr. Charles Ryan at the UCSF Helen Diller Family Comprehensive Cancer Center (where I am being treated by my RO, Dr. Alexander Gottschalk) was the lead researcher of an international study on the use of Zytiga. See: http://www.medicalnewstoday.com/articles/246365.php and http://www.ucsfhealth.org/charles.ryan
Dr. Eric Small is also the chief of hemotology and oncology at the UCSF HDFCC and "[h]is patient care and research focus is prostate cancer, immunotherapy and the mechanisms of resistance to standard therapies. See: http://www.ucsfhealth.org/eric.small
So, if my situation becomes more serious and negates the further use of radiation treatment, I'll definitely be asking for a referral to Dr. Small (or Dr Ryan) to address my treatment options at that time.0 -
What next?VascodaGama said:A pain in the neck
Swing
I am sorry for the results. Your PSA tests have been “a pain in the neck” from the start and very stressful for you. The recent three increases could mean recurrence and the way to find the truth is by waiting for another PSA in three months time. Image studies are not that “refined” in cases of small tumours, but it is worth to give it a try with the ones using the latest techniques.
You are an educated patient and know about the types available “in the market”. In the old times a case like yours would have been recommended to Combidex testing. Now you got the USPIO (feraheme MRI). There are several sites in the net discussing its possibilities.
Another test is the PET/CT C11-choline that is now on trials in cases similar to yours.
http://askdrbarken.wordpress.com/2011/12/06/multi-parametric-mri-combidex-and-ferumoxytol-with-dr-j-barentsz/
http://www.diagnosticimaging.com/pet-ct/content/article/113619/1474149
This is two years since your CK treatment. Your PSA at the time was high at 12.3 declining to 1.55 (probable nadir) in 24 months. The last increase rounds the PSADT of 12 month which is higher (longer period) than the critical threshold of < 9 month.
This long period in vPSA may be due to the slow growing type of cancer in your case (Gleason score 6). This is a type that is hard to find with traditional image studies because of possible micromets.
Waiting with periodical testing (PSA) would not alter outcomes from an earlier attack with a salvage treatment. You got time to check for all possibilities and discuss (second opinions) with the professionals.
Many comments about the latest diagnosing tools were talked in the last PCRI gathering. There are newer drugs to fight recurrence and there is also fixed sequential in using them. Get all the information you can and study it. We will be here to help you in this difficult time.
http://csn.cancer.org/node/246671
I hope that the increase is a false positive and that you see it going down for peace of mind.
Be strong and positive.
VGama
Vasco: Thanks for the references. My RO has ordered both E-MRI & MRSI scans to determine if there's any cancer still there.
Didn't know anything about C-11 Choline PET/CT scans but the results it yields seems similar to MRSI (Magnetic Resonance Spectroscopic Imaging) which looks for concentrations of choline in the prostate, because cancer cells absorb/store choline. The MRSI not only scans for concentrations of choline but also creatine and citrate which are present in certain established proportions to each other, which give a better basis for comparison between cancerous and non-cancerous focal points.
I'll ask my RO about the C-11 scans but my guess is he'll say that the MRSI already covers that, but will keep it on the back burner as a possible suggestion for further testing in case the MRSI results are inconclusive.
As for drug therapies to "prevent" recurrence, I don't know anything about them either BUT I really do not want to get into HT or ADT of any kind, unless there's no better alternative. The complications of hormone use that I've read about scare me almost as much as the horror stories about surgery. So, I'm not going there until I'm convinced there is no other choice.
I've previously discussed "what if" w/my RO in the event the CK treatment failed (which has now apparently occurred) and he suggested that BT might be an acceptable follow-up to CK. I would not want LDR BT but would consider HDR BT, if that is an option. I also asked if a 2nd CK treatment might be possible. His response suggested that he never considered that before and that that might be possible as well.
We'll see . . .
BTW: The variability in my PSA scores have been a PITA but have not really caused me all that much "stress" because I really haven't given it much thought (except for a short time after the quarterly scores came in).
Now that I am apparently facing treatment failure, I am less concerned about the future PSA scores than I am about the pending MRI/MRSI scan results because they (in combo w/a follow-up biopsy for confirmation) will determine if there actually is cancer still remaining in my prostate or not and, if so, where and how large the remaining tumor(s) is (or are), and (God forbid) whether or not there has been any metastases of the cancer beyond the prostate.
Once we get that that info, we'll then be in a better position to decide what to do.0 -
chronic prostatitis???Swingshiftworker said:Thanks, Beau. Will do!
Thanks, Beau. Will do!
Swing, Here is a discussion from the cyberknife.com web site that I hope is applicable to your situation. I think that I remember that your psa moved around before treatment.
http://cyberknife.com/Forum.aspx?g=posts&t=4818#jumptobottom
Also you might want to post at cyperknife site for inputs.
My thoughts and prayers are with you0 -
Hang in therehopeful and optimistic said:chronic prostatitis???
Swing, Here is a discussion from the cyberknife.com web site that I hope is applicable to your situation. I think that I remember that your psa moved around before treatment.
http://cyberknife.com/Forum.aspx?g=posts&t=4818#jumptobottom
Also you might want to post at cyperknife site for inputs.
My thoughts and prayers are with you
Swing, sorry to hear about this. Hang in there. Keep focused on this.
Kurt0 -
TestsSwingshiftworker said:Thanks, Beau. Will do!
Thanks, Beau. Will do!
Swing,
Good luck on your tests. Hopefully they will find a small growth in prostate. My thoughts are with you for an easy diagnosis and treatment. I believe in staying in touch with your body. It will tell you more than tests. If anything happens out of the ordinary make sure to inform your doctors. Sometimes little things mean alot.
Good luck,
Mike0 -
I am pretty aware of changes in my body and have had increased urinary urgency/frequency and a burning sensation over the past 2-3 months that I reported to my RO.Samsungtech1 said:Tests
Swing,
Good luck on your tests. Hopefully they will find a small growth in prostate. My thoughts are with you for an easy diagnosis and treatment. I believe in staying in touch with your body. It will tell you more than tests. If anything happens out of the ordinary make sure to inform your doctors. Sometimes little things mean alot.
Good luck,
Mike
He thought it was just a late term reaction to the radiation and only recommended the use of ibubrofen and possibly wheat grass to deal w/the irritation; neither of which helped to resolve the problem. Still dealing with that now.
Reading the CK Forum thread that Hopeful recommended, I picked up the suggestion that perhaps the increase in PSA may be due to these symptom and not to a renewed cancer.
The E-MRI/MRSI scans should determine whether it's residual cancer or "something else" that's causing the PSA scores to escalate.0 -
FightSwingshiftworker said:I am pretty aware of changes in my body and have had increased urinary urgency/frequency and a burning sensation over the past 2-3 months that I reported to my RO.
He thought it was just a late term reaction to the radiation and only recommended the use of ibubrofen and possibly wheat grass to deal w/the irritation; neither of which helped to resolve the problem. Still dealing with that now.
Reading the CK Forum thread that Hopeful recommended, I picked up the suggestion that perhaps the increase in PSA may be due to these symptom and not to a renewed cancer.
The E-MRI/MRSI scans should determine whether it's residual cancer or "something else" that's causing the PSA scores to escalate.
Swing,
Be sure to utilize all your resourses as nessecary. Good luck, and always KTF and fight.
Mike0 -
What Next ?fightn9er said:Fight
Swing,
Be sure to utilize all your resourses as nessecary. Good luck, and always KTF and fight.
Mike
Swing
I think that your next step will be to find a reason for the increase.
Surely many things could be the cause including an infection of the prostate or urethra. Cancer is also possible but difficult to find. Continuous PSA tests are the solution in cases of small size tumours that produce the serum.
You shouldn’t discard any way to find the cause but I would recommend you to follow the best and latest techniques.
I had RT in 2006 and in 2008 I experienced a case of stricture requiring Dilation. I had similar symptoms as those of yours but there were no significant increase in PSA (I have no prostate). An endoscopic test found it and checked latter for cure.
Regarding image studies, they all have limitations of what data they can provide. In 2000 there were must fuse about Prostascint and PET scan, however, these techniques used poor contrast agents that caused many false positives.
After my surgery recurrence became apparent and I wanted to locate the cancer for a hit-radiation. I consulted several specialists at MSKCC, JH and in Japan and were told about the limitations of the equipments. The specialist at MSKCC informed that PET would confuse cancer with the nodes at the spinal so that many false positives were detected in the lower abdominal.
With the resent trials on newer contrast agents and the fusion of systems it has been possible to reach to better outcomes in image studies (lesser cases of false positives).
In saying that, when the aim of the test is to look for small tumours the resolution of the machines become the most important factor for a successful detection. Crisscrossing of information (images) can provide better outcomes. In the combi of PET with CT, PET provides the functional data and the CT (or MRI) provides the anatomical data.
Your test with two MRI is just that. They will crisscross the data to get a better outcome. In any case, the technique is classical and the newer ones are giving better results. PET is more specific than MRSI but it needs representation of the location of the result. CT or MRI can provide that, being MRI better.
http://www.medicalnewstoday.com/articles/154877.php
I believe you will find the reason on the rise of the PSA. I am surprise for your comment that you “haven't given it much thought” but it is and it will be the marker for your treatment success, or for the start of salvage treatment.
As commented in my previous post, image studies may be erroneous in a case of low serum or high but with micromets. A continuous increase in PSA will provide a hint in your status.
There is also another image technique you should explore with C11 acetate. This is reported as being better than the C11 choline to identify PCa. The tracer trial has been conclusive of that and I would recommend you to read about it. Here are the words of the doctor involved and the trial which you could try to participate;
http://www.healingwell.com/community/default.aspx?f=35&m=2217367&p=2
http://clinicaltrials.gov/ct2/show/NCT01304485
About C11 choline PET;
http://www.health-forums.com/alt-support-cancer-prostate/c-11-choline-pet-scan-192202.html
Best.
VGama0 -
Thanks!VascodaGama said:What Next ?
Swing
I think that your next step will be to find a reason for the increase.
Surely many things could be the cause including an infection of the prostate or urethra. Cancer is also possible but difficult to find. Continuous PSA tests are the solution in cases of small size tumours that produce the serum.
You shouldn’t discard any way to find the cause but I would recommend you to follow the best and latest techniques.
I had RT in 2006 and in 2008 I experienced a case of stricture requiring Dilation. I had similar symptoms as those of yours but there were no significant increase in PSA (I have no prostate). An endoscopic test found it and checked latter for cure.
Regarding image studies, they all have limitations of what data they can provide. In 2000 there were must fuse about Prostascint and PET scan, however, these techniques used poor contrast agents that caused many false positives.
After my surgery recurrence became apparent and I wanted to locate the cancer for a hit-radiation. I consulted several specialists at MSKCC, JH and in Japan and were told about the limitations of the equipments. The specialist at MSKCC informed that PET would confuse cancer with the nodes at the spinal so that many false positives were detected in the lower abdominal.
With the resent trials on newer contrast agents and the fusion of systems it has been possible to reach to better outcomes in image studies (lesser cases of false positives).
In saying that, when the aim of the test is to look for small tumours the resolution of the machines become the most important factor for a successful detection. Crisscrossing of information (images) can provide better outcomes. In the combi of PET with CT, PET provides the functional data and the CT (or MRI) provides the anatomical data.
Your test with two MRI is just that. They will crisscross the data to get a better outcome. In any case, the technique is classical and the newer ones are giving better results. PET is more specific than MRSI but it needs representation of the location of the result. CT or MRI can provide that, being MRI better.
http://www.medicalnewstoday.com/articles/154877.php
I believe you will find the reason on the rise of the PSA. I am surprise for your comment that you “haven't given it much thought” but it is and it will be the marker for your treatment success, or for the start of salvage treatment.
As commented in my previous post, image studies may be erroneous in a case of low serum or high but with micromets. A continuous increase in PSA will provide a hint in your status.
There is also another image technique you should explore with C11 acetate. This is reported as being better than the C11 choline to identify PCa. The tracer trial has been conclusive of that and I would recommend you to read about it. Here are the words of the doctor involved and the trial which you could try to participate;
http://www.healingwell.com/community/default.aspx?f=35&m=2217367&p=2
http://clinicaltrials.gov/ct2/show/NCT01304485
About C11 choline PET;
http://www.health-forums.com/alt-support-cancer-prostate/c-11-choline-pet-scan-192202.html
Best.
VGama
Thanks for the additional advice, Vasco.
I am pretty confident that the E-MRI and MRSI scans will pinpoint the existence of any residual cancer that may exist in or around the prostate.
The E-MRI identifies suspect tissues and the MRSI will pinpoint the existence of choline molecules and other metabolites indicative of cancer, if any, within those suspect tissues, that can be confirmed by biopsy to rule out any false positive results.
If nothing is found, only further PSA increases and later scans will reveal that the result was a false negative. In the meantime, we can focus on whether the current urinary frequency, urgency and irritation issues that I'm experiencing may be causing the PSA increase instead.
On the other hand, if the scans do find a residual cancer, we can then develop a plan to address it.
I hope it's "just" prostatitis but am prepared if it's residual cancer. I haven't given my cancer much thought in the past 2 years following my treament (other than anticipating and reacting to the quarterly PSA scores) because there wasn't anything else I could do about it and there was no point in dwelling on it.
I am focused on it now because there is an apparent problem w/the 3 PSA increases that are indicative of treatment failure and/or cancer recurrence. Even so, the problem doesn't stress me out because I think that whatever we find can be addressed by current treatment methods to insure my longevity indefinitely; ie., I don't think I'm going to die from it.
My attitude obviously would change if it is determined that I now have an advanced form of prostate cancer that has metastasized and is no longer amenable to treatment.
In that case, I would definitely give it A LOT of thought and would take action to prepare for my eventual death while maintaining the quality of the remainder of my life as best possible.0 -
See belowhopeful and optimistic said:chronic prostatitis???
Swing, Here is a discussion from the cyberknife.com web site that I hope is applicable to your situation. I think that I remember that your psa moved around before treatment.
http://cyberknife.com/Forum.aspx?g=posts&t=4818#jumptobottom
Also you might want to post at cyperknife site for inputs.
My thoughts and prayers are with you
Thanks for the link & your prayers, Hopeful.
I did pick up a suggestion that the PSA variation could be due to post-CK urinary prostatis, which I've been experiencing for the past 2-3 months. See more on that below. Would be "nice" if that's the only reason for the rising PSA but won't that w/any certainty until the E-MRI/MRSI results come in.
I've lurked around the CK Patient Forum before, but have never posted there. May post there after I get the E-MRI/MRSI scans to get some other opinions from the docs there, if I don't like my RO's assessment and suggested treatments.0 -
C-11 Choline vs C-11 Acetate PET/CT imagingVascodaGama said:What Next ?
Swing
I think that your next step will be to find a reason for the increase.
Surely many things could be the cause including an infection of the prostate or urethra. Cancer is also possible but difficult to find. Continuous PSA tests are the solution in cases of small size tumours that produce the serum.
You shouldn’t discard any way to find the cause but I would recommend you to follow the best and latest techniques.
I had RT in 2006 and in 2008 I experienced a case of stricture requiring Dilation. I had similar symptoms as those of yours but there were no significant increase in PSA (I have no prostate). An endoscopic test found it and checked latter for cure.
Regarding image studies, they all have limitations of what data they can provide. In 2000 there were must fuse about Prostascint and PET scan, however, these techniques used poor contrast agents that caused many false positives.
After my surgery recurrence became apparent and I wanted to locate the cancer for a hit-radiation. I consulted several specialists at MSKCC, JH and in Japan and were told about the limitations of the equipments. The specialist at MSKCC informed that PET would confuse cancer with the nodes at the spinal so that many false positives were detected in the lower abdominal.
With the resent trials on newer contrast agents and the fusion of systems it has been possible to reach to better outcomes in image studies (lesser cases of false positives).
In saying that, when the aim of the test is to look for small tumours the resolution of the machines become the most important factor for a successful detection. Crisscrossing of information (images) can provide better outcomes. In the combi of PET with CT, PET provides the functional data and the CT (or MRI) provides the anatomical data.
Your test with two MRI is just that. They will crisscross the data to get a better outcome. In any case, the technique is classical and the newer ones are giving better results. PET is more specific than MRSI but it needs representation of the location of the result. CT or MRI can provide that, being MRI better.
http://www.medicalnewstoday.com/articles/154877.php
I believe you will find the reason on the rise of the PSA. I am surprise for your comment that you “haven't given it much thought” but it is and it will be the marker for your treatment success, or for the start of salvage treatment.
As commented in my previous post, image studies may be erroneous in a case of low serum or high but with micromets. A continuous increase in PSA will provide a hint in your status.
There is also another image technique you should explore with C11 acetate. This is reported as being better than the C11 choline to identify PCa. The tracer trial has been conclusive of that and I would recommend you to read about it. Here are the words of the doctor involved and the trial which you could try to participate;
http://www.healingwell.com/community/default.aspx?f=35&m=2217367&p=2
http://clinicaltrials.gov/ct2/show/NCT01304485
About C11 choline PET;
http://www.health-forums.com/alt-support-cancer-prostate/c-11-choline-pet-scan-192202.html
Best.
VGama
Vasco,
I don't understand your comment pertaining to the C-11 Choline PET/CT (Mayo) vs the C-11 Acetate (So Cal, Arizona, etc). You indicate re the C-11 acetate imaging: "There is also another image technique you should explore with C11 acetate. This is reported as being better than the C11 choline to identify PCa."
I'm wondering what information there might be to indicate that the Acetate is "better" than the Choline. What advantage might it have? Why is it better? How do the two contrast agents differ? As I understand it, they're both carbon based, yet different. Thx for sharing any add'l info.0 -
Similar but differentlewvino said:Best wishes as you continue
Best wishes as you continue on your journey. Knock the beast out for good on this round!
Larry (lewvino)
Mrs PJD
As far as I know the contrast agents C11 acetate and C11 choline in PET scans have been on study for the past ten years. These are substances that have shown to be more reliable than the traditional FDG PET based on glucose metabolism to detect prostate cancer in tissues (soft and bone). Even the F18 fluorocholine has not performed as well as the similar substance C11 choline.
It is hard to say that one is better than the other because the results differ from patient to patient. C11-Acetate is a radioisotope tagged nutrient that prostate cancer cells take up to feed their growth.
This is an uptake tracer that responds well in cases where radiosensitive tumours favour oxidative metabolism. It is a good agent for differentiation in low levels of PSA. Choline seems to work better in cases where hormonal ablation took place. Do not ask me why.
In Swings case, the former seems to be better in my lay view.
Here is a very comprehensive presentation on “Molecular Imaging of Prostate Cancer”, done by Dr. Hossein Jadvar, Associate Professor of Radiology and Biomedical Engineering in the University of Southern California;
http://www.wrsnm.org/presentations_v2/oct22/Hossein Jadvar MD 2.pdf
In one study they say this; “Kato et al. recently presented results with 11C-acetate not only in prostate tumors but also in normal prostate glands and benign prostate hyperplasia (12). Interestingly, the authors emphasized that normal accumulation occurred in the normal prostate gland of patients”
This is contrary to a positive recurrence and it could indicate a false positive, but it would indicate the area in conflict and provide a target for further biopsy.
http://jnm.snmjournals.org/content/44/4/556.full
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3129631/
Multitracer studies using C-acetate and F-choline are on the agenda by many researchers. In fact they all recommend such approach which should include genetics. (How?)
In this site they explain details about PET C11 acetate;
http://www.ob-ron.org/2012/05/tidbits-about-c11-acetate-petct-and.html
Here is a book on PET scans using the several contrast agents; http://books.google.pt/books?id=dZIBbLhTOoQC&pg=PA205&lpg=PA205&dq=c+11+choline+vs+c+11+acetate&source=bl&ots=SWcSXiCU2W&sig=Af8rqc0cflPGqQfHv5ktULBNZh4&hl=en&sa=X&ei=2MNcUKDYM4WThgeVzICAAg&redir_esc=y#v=onepage&q=c 11 choline vs c 11 acetate&f=false
Regards.
VGama0 -
Agree (somewhat)VascodaGama said:Similar but different
Mrs PJD
As far as I know the contrast agents C11 acetate and C11 choline in PET scans have been on study for the past ten years. These are substances that have shown to be more reliable than the traditional FDG PET based on glucose metabolism to detect prostate cancer in tissues (soft and bone). Even the F18 fluorocholine has not performed as well as the similar substance C11 choline.
It is hard to say that one is better than the other because the results differ from patient to patient. C11-Acetate is a radioisotope tagged nutrient that prostate cancer cells take up to feed their growth.
This is an uptake tracer that responds well in cases where radiosensitive tumours favour oxidative metabolism. It is a good agent for differentiation in low levels of PSA. Choline seems to work better in cases where hormonal ablation took place. Do not ask me why.
In Swings case, the former seems to be better in my lay view.
Here is a very comprehensive presentation on “Molecular Imaging of Prostate Cancer”, done by Dr. Hossein Jadvar, Associate Professor of Radiology and Biomedical Engineering in the University of Southern California;
http://www.wrsnm.org/presentations_v2/oct22/Hossein Jadvar MD 2.pdf
In one study they say this; “Kato et al. recently presented results with 11C-acetate not only in prostate tumors but also in normal prostate glands and benign prostate hyperplasia (12). Interestingly, the authors emphasized that normal accumulation occurred in the normal prostate gland of patients”
This is contrary to a positive recurrence and it could indicate a false positive, but it would indicate the area in conflict and provide a target for further biopsy.
http://jnm.snmjournals.org/content/44/4/556.full
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3129631/
Multitracer studies using C-acetate and F-choline are on the agenda by many researchers. In fact they all recommend such approach which should include genetics. (How?)
In this site they explain details about PET C11 acetate;
http://www.ob-ron.org/2012/05/tidbits-about-c11-acetate-petct-and.html
Here is a book on PET scans using the several contrast agents; http://books.google.pt/books?id=dZIBbLhTOoQC&pg=PA205&lpg=PA205&dq=c+11+choline+vs+c+11+acetate&source=bl&ots=SWcSXiCU2W&sig=Af8rqc0cflPGqQfHv5ktULBNZh4&hl=en&sa=X&ei=2MNcUKDYM4WThgeVzICAAg&redir_esc=y#v=onepage&q=c 11 choline vs c 11 acetate&f=false
Regards.
VGama
Vasco,
I think we are both in agreement that the use of C-11 contrast agents may be proven advantageous with PET/CT imaging as a new modality in the near future. However, my question wasn’t so much about the possible advantages of the imaging with either of the two carbon agents, the C-11 Choline or the C-11 Acetate in PET/CT imaging, as much as it was about the differences between the two agents and if one is "better" than the other.
You indicate: “It is hard to say that one is better than the other because the results differ from patient to patient.” That’s pretty much always the case with txs, imaging, test results & tx side effects, etc. related to PCa. In a previous post above you also stated the Acetate was “better” than the Choline. It may turn out to be a case of ½ dozen of one and 6 of the other. With either of the two Carbon agents, the patient can’t be on ADT for the imaging since the study is “reading” the functional activity of the cancer. Frankly, I don’t know if one contrast agent is better than the other. I was curious to understand (curious minds want to know...) the differences and why you indicated the Acetate was reported to be a better agent. Maybe I missed something but, I was unable to find any info in the sources you provided that pointed to the C-11 Choline Acetate (used by a clinic in Arizona) being a better contrast agent than the C-11 Choline (used by Mayo clinic). Nevertheless, thanks for the interesting sources.
BTW, the FDA just approved the Mayo Clinic as the first facility to manufacture the Choline C-11 Injection:
http://www.fda.gov/NewsEvents/Newsroom/PressAnnouncements/ucm319201.htm
The Arizona clinic has an open clinical trial, for a fee, as I understand. Although both contrast agents may prove to be equal (unknown?), in my lay opinion it would be a wiser, if not safer, approach to consider the Mayo Clinic venue (similar fee involved) for advanced, yet still experimental, C-11 Choline PET/CT imaging for cases where more standard forms of imaging--bone scan, CT’s, F-18 (FDG), MRI, EMRI, etc--have been unable to identify mets in the context of a recurrence with rising PSA after failed primary and/or secondary PCa txs. FWIW, I’m open to be persuaded to change my mind if you or other CSN members provide information to the contrary.
Be well.
mrs pjd0 -
Cell’s chemistry and Trial’s ratesmrspjd said:Agree (somewhat)
Vasco,
I think we are both in agreement that the use of C-11 contrast agents may be proven advantageous with PET/CT imaging as a new modality in the near future. However, my question wasn’t so much about the possible advantages of the imaging with either of the two carbon agents, the C-11 Choline or the C-11 Acetate in PET/CT imaging, as much as it was about the differences between the two agents and if one is "better" than the other.
You indicate: “It is hard to say that one is better than the other because the results differ from patient to patient.” That’s pretty much always the case with txs, imaging, test results & tx side effects, etc. related to PCa. In a previous post above you also stated the Acetate was “better” than the Choline. It may turn out to be a case of ½ dozen of one and 6 of the other. With either of the two Carbon agents, the patient can’t be on ADT for the imaging since the study is “reading” the functional activity of the cancer. Frankly, I don’t know if one contrast agent is better than the other. I was curious to understand (curious minds want to know...) the differences and why you indicated the Acetate was reported to be a better agent. Maybe I missed something but, I was unable to find any info in the sources you provided that pointed to the C-11 Choline Acetate (used by a clinic in Arizona) being a better contrast agent than the C-11 Choline (used by Mayo clinic). Nevertheless, thanks for the interesting sources.
BTW, the FDA just approved the Mayo Clinic as the first facility to manufacture the Choline C-11 Injection:
http://www.fda.gov/NewsEvents/Newsroom/PressAnnouncements/ucm319201.htm
The Arizona clinic has an open clinical trial, for a fee, as I understand. Although both contrast agents may prove to be equal (unknown?), in my lay opinion it would be a wiser, if not safer, approach to consider the Mayo Clinic venue (similar fee involved) for advanced, yet still experimental, C-11 Choline PET/CT imaging for cases where more standard forms of imaging--bone scan, CT’s, F-18 (FDG), MRI, EMRI, etc--have been unable to identify mets in the context of a recurrence with rising PSA after failed primary and/or secondary PCa txs. FWIW, I’m open to be persuaded to change my mind if you or other CSN members provide information to the contrary.
Be well.
mrs pjd
Mrs PJD
It will require some expertise in biotechnology and chemistry to fully satisfy your question. As a layman on the matter I can just tell that PET using the tracer acetate seems to have better outcomes in RT failed cases with well differentiated type of cells. However the answer is subjective to the chemistry in one’s cell’s structure. It would help if you consider in obtaining an explanation from the people (biologists) involved in the studies or reading and trying interpreting their reports.
Just like other methods and techniques in testing with contrast agents, the preferences for something fall in past experiences of similar situations. The highest rated is usually taken as the appropriated method. You may lay down the number of successful cases in both PET tests and get an average rate. This is the way doctors explain about their preferences and it is the bases of my understanding.
Regarding the C11 tracers, you may be surprised for the huge number of varieties and known results in their chemistry. The Molecular Imaging and Contrast Agent Database (MICAD) from the American National Center for Biotechnology Information (the same author, Kam Leung, PhD) writes this in 2004;
“Acetate is readily taken up by cells and is activated to acetyl-CoA in both the cytosol and mitochondria by acetyl-CoA synthetase. Acetyl-CoA is a common metabolic intermediate for synthesis of cholesterol and fatty acids, which are then incorporated into membrane (1). Acetyl-CoA is also oxidized in mitrochondria by the tricarboxylic acid (TCA) cycle to carbon dioxide and water. Some of the acetate is converted to amino acids. In normal myocardium, acetate is metabolized to CO2 via the TCA cycle as the dominant pathway. In contrast, tumor cells convert most of the acetate into fatty acids by a key enzyme fatty acid synthetase (FAS), which is over-expressed in cancer cells (2). Acetate is predominantly incorporated into intracellular phosphatidylcholine membrane microdomains that are important for tumor growth and metastasis (3). [11C]Acetate are used as a positron emission tomography (PET) tracer for studying myocardial oxidative metabolism and regional myocardial blood flow (4). [11C]Acetate is a promising PET tracer for renal, pancreatic, and prostate tumors (5)”.
“Choline is an important component of phospholipids in the cell membranes. Tissues with increased metabolism will lead to an increased uptake of choline. Choline is phosphorylated by choline kinases (CHK) to phosphorylcholine within cells, and, after several biosynthetic processes, finally is integrated into phospholipids (1). Because tumor cells have a high metabolic rate, choline uptake is high in order to keep up with the demands with the synthesis of phospholipids in their cellular membranes (2). Positron emission tomography (PET) with [11C]Choline has been reported to be useful for the detection and differential diagnosis of brain tumors, prostate cancer, lung cancer, and esophageal cancer (3, 4), whereas [18F]2-fluoro-2-deoxyglucose (FDG) lacks of specificity or sensitivity (3).
Here is the list of contrast agent’s data base. Search for C11 (11C) for details;
http://www.ncbi.nlm.nih.gov/books/NBK5330/
I hope the materials can lead you to a satisfying conclusion.
Be well.
VGama0 -
Our very satisfying conclusionVascodaGama said:Cell’s chemistry and Trial’s rates
Mrs PJD
It will require some expertise in biotechnology and chemistry to fully satisfy your question. As a layman on the matter I can just tell that PET using the tracer acetate seems to have better outcomes in RT failed cases with well differentiated type of cells. However the answer is subjective to the chemistry in one’s cell’s structure. It would help if you consider in obtaining an explanation from the people (biologists) involved in the studies or reading and trying interpreting their reports.
Just like other methods and techniques in testing with contrast agents, the preferences for something fall in past experiences of similar situations. The highest rated is usually taken as the appropriated method. You may lay down the number of successful cases in both PET tests and get an average rate. This is the way doctors explain about their preferences and it is the bases of my understanding.
Regarding the C11 tracers, you may be surprised for the huge number of varieties and known results in their chemistry. The Molecular Imaging and Contrast Agent Database (MICAD) from the American National Center for Biotechnology Information (the same author, Kam Leung, PhD) writes this in 2004;
“Acetate is readily taken up by cells and is activated to acetyl-CoA in both the cytosol and mitochondria by acetyl-CoA synthetase. Acetyl-CoA is a common metabolic intermediate for synthesis of cholesterol and fatty acids, which are then incorporated into membrane (1). Acetyl-CoA is also oxidized in mitrochondria by the tricarboxylic acid (TCA) cycle to carbon dioxide and water. Some of the acetate is converted to amino acids. In normal myocardium, acetate is metabolized to CO2 via the TCA cycle as the dominant pathway. In contrast, tumor cells convert most of the acetate into fatty acids by a key enzyme fatty acid synthetase (FAS), which is over-expressed in cancer cells (2). Acetate is predominantly incorporated into intracellular phosphatidylcholine membrane microdomains that are important for tumor growth and metastasis (3). [11C]Acetate are used as a positron emission tomography (PET) tracer for studying myocardial oxidative metabolism and regional myocardial blood flow (4). [11C]Acetate is a promising PET tracer for renal, pancreatic, and prostate tumors (5)”.
“Choline is an important component of phospholipids in the cell membranes. Tissues with increased metabolism will lead to an increased uptake of choline. Choline is phosphorylated by choline kinases (CHK) to phosphorylcholine within cells, and, after several biosynthetic processes, finally is integrated into phospholipids (1). Because tumor cells have a high metabolic rate, choline uptake is high in order to keep up with the demands with the synthesis of phospholipids in their cellular membranes (2). Positron emission tomography (PET) with [11C]Choline has been reported to be useful for the detection and differential diagnosis of brain tumors, prostate cancer, lung cancer, and esophageal cancer (3, 4), whereas [18F]2-fluoro-2-deoxyglucose (FDG) lacks of specificity or sensitivity (3).
Here is the list of contrast agent’s data base. Search for C11 (11C) for details;
http://www.ncbi.nlm.nih.gov/books/NBK5330/
I hope the materials can lead you to a satisfying conclusion.
Be well.
VGama
My and my husband's conclusion is that if it ever becomes necessary to consider C-11 Choline PET/CT imaging and we had to choose between the two, we're going to Kwon @ Mayo--for the reasons I stated and many other reasons pertaining to the overall center of excellence that Mayo & it's doctors offer.0
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