Cancer found in Lymph and tissue afer DaVinci surgery

live2day

Hi, my name is Jack i am 53yr i am four weeks post operation
my pathology report shows some positive tisue and lymph involvement
i am waiting for six weeks to pass to get blood PSA to establish a baseline
I already know my doctor wants to go with Lupron, this scares the hell out of me
i need to talk to guys who have been down this road before me to help me cope
please contact me, i live in SoCal.
right now i feel good, i can cope with my current condition, surgery went O.K.
but now faced with more treatment that will effect my mind, libido,sex etccc..
this is almost too much to bear, i can have a small erection now and i dont want
to loose what little i have left...
If i go on Lupron will i ever have regular sex again?
i am not interested in implants and extream measures like that...
i dont mind a pil and a pump once in a while, but thats as far as i want to go.
If i go on lupron will the effects of chemical castration be reversable
once i stop?

jack
please contact me.

DaveRN94

Hi Jack
I know of the harshness of PCa first hand. I feel with you as you try so hard to work through this, especially coming at it from being relatively young to start this kind of journey.

Jack, what are some of the details? What was PSA at diagnosis, what were the results of your biopsy: Gleason score, how many core samples did the urologist take and how many reported cancer activity and to what volume?

BTW my understanding is that coming off ADT reverses the "chemical castration."

VascodaGama

DaveRN94 said:

Hi Jack
I know of the harshness of PCa first hand. I feel with you as you try so hard to work through this, especially coming at it from being relatively young to start this kind of journey.

Jack, what are some of the details? What was PSA at diagnosis, what were the results of your biopsy: Gleason score, how many core samples did the urologist take and how many reported cancer activity and to what volume?

BTW my understanding is that coming off ADT reverses the "chemical castration."

Anti-agonists could do the trick
Hi Jack

Welcome to the board.
Sorry to hear about the positive extra capsular extension and metastases. There are a series of ways to deal with the problem. The info Dave requests is essential to determine on a good choice.

Lupron shots are advisable if you present or are at risk of systemic disease. This LHRH agonist is the “heavy duty” drug on the hormonal protocol. It influences the body to stop manufacturing Testosterone. Sex can continue but the low level of testosterone in the body will tend to diminish the appeal for sex (low libido). You will have to work harder for a satisfying accomplishment.
I am on HT since November 2010 with an agonist shot (Eligard = Lupron), got the lowest level of PSA since I took my first test in 2000, and are active in my “lovely nights” but with a low quality in achievements (3-4 o’clock pointed mark).

The good in your treatment is that surgery did not cause you permanent ED. Lupron shots will superimpose but usually all returns to normalcy once one stops taking them and the shots lose its effectiveness action (approximately 2 to 3 months).

Another drug in the hormonal protocol known as anti-agonists (Casodex, Cyproterone, etc.) are less implicated with the libido side effect, hot-flashes or fatigue, because it does not induce the testes to stop manufacturing testosterone (low levels in the body). They can control cancer advancement in considerable long periods by simple closing down the “feeding ports” receptors at the cells, therefore avoiding cancer cells from feeding on testosterone. These anti-agonists mimic the structure of testosterone and attach to the receptors closing the cell’s “mouths”.
In the process some cancer is killed by starvation and other become dormant. Patients can regulate the period on anti-agonists through periodical PSA tests.

The problem with a solo anti-agonists effect in the control of cancer advancement is that after a long period on the drug, cells adapt to the condition and mutate to feed on the anti-androgen itself (hormone resistant prostate cancer).
This “behavioural adaption” of cancer cells is due to random genetic mutations which occur within its genetic code, the beneficial mutations are preserved because they aid survival. This is a process known as "natural selection" from Darwin’s theory. If low testosterone is persistent, the cell to survive will mutate to adapt to the new environment and continue its proliferation uncontrolled.

A treatment with such approach would do better in a protocol of intermittent modalities, to avoid mutations.
I would recommend you to discuss with your doctor the above possibility in your case so that you would not surfer with less sex at your young age.

Wishing you the best.

VGama

tarhoosier

VascodaGama said:

Anti-agonists could do the trick
Hi Jack

Welcome to the board.
Sorry to hear about the positive extra capsular extension and metastases. There are a series of ways to deal with the problem. The info Dave requests is essential to determine on a good choice.

Lupron shots are advisable if you present or are at risk of systemic disease. This LHRH agonist is the “heavy duty” drug on the hormonal protocol. It influences the body to stop manufacturing Testosterone. Sex can continue but the low level of testosterone in the body will tend to diminish the appeal for sex (low libido). You will have to work harder for a satisfying accomplishment.
I am on HT since November 2010 with an agonist shot (Eligard = Lupron), got the lowest level of PSA since I took my first test in 2000, and are active in my “lovely nights” but with a low quality in achievements (3-4 o’clock pointed mark).

The good in your treatment is that surgery did not cause you permanent ED. Lupron shots will superimpose but usually all returns to normalcy once one stops taking them and the shots lose its effectiveness action (approximately 2 to 3 months).

Another drug in the hormonal protocol known as anti-agonists (Casodex, Cyproterone, etc.) are less implicated with the libido side effect, hot-flashes or fatigue, because it does not induce the testes to stop manufacturing testosterone (low levels in the body). They can control cancer advancement in considerable long periods by simple closing down the “feeding ports” receptors at the cells, therefore avoiding cancer cells from feeding on testosterone. These anti-agonists mimic the structure of testosterone and attach to the receptors closing the cell’s “mouths”.
In the process some cancer is killed by starvation and other become dormant. Patients can regulate the period on anti-agonists through periodical PSA tests.

The problem with a solo anti-agonists effect in the control of cancer advancement is that after a long period on the drug, cells adapt to the condition and mutate to feed on the anti-androgen itself (hormone resistant prostate cancer).
This “behavioural adaption” of cancer cells is due to random genetic mutations which occur within its genetic code, the beneficial mutations are preserved because they aid survival. This is a process known as "natural selection" from Darwin’s theory. If low testosterone is persistent, the cell to survive will mutate to adapt to the new environment and continue its proliferation uncontrolled.

A treatment with such approach would do better in a protocol of intermittent modalities, to avoid mutations.
I would recommend you to discuss with your doctor the above possibility in your case so that you would not surfer with less sex at your young age.

Wishing you the best.

VGama

Terms
In order to clarify the information from VdaG above, the term used in the US for bicalutimide (Casodex), Cyproterone, and similar drugs is Anti-Androgen, sometimes called AA, or A-A. The metaphor used commonly for such drugs is that each cell has a "lock" which allows androgens such as testosterone to enter the cell and complete the cell division cycle. Anti-Androgens (and anti-femogens for women) put gum in this lock and the androgen is unable to "open" the pathway to the cell nucleus.

Lupron is an "agonist" drug in the sense that it causes the release of a flood of hormones that swamp the messaging system of the body and thus causes the cessation of testosterone production until this swamping effect declines as the drug effect subsides. There is a newer drug called Degarelix that is a true "antagonist' because it switches off the production of testosterone by interfering with the chemical messaging system directly and does not swamp the system.
It is true that some doctors and patients prefer, or require the use of both an Anti-Androgen and a hormone agonist (Zoladex/Lupron/equivalent). Occasionally the newer antagonist Degarelix is preferred, usually in recently diagnosed patients with metastases and symptoms because it works almost immediately.
I also wish to make clear that it is my opinion that the mutation of the cells as VdaG explains is not caused by the application of any drug. It is a natural occurrence and will take place with or without any medication.

tarhoosier

Live
Jack, your confusion, frustration, fear and all else is familiar to me. My case is similar to yours. Answering all your questions is a bit premature until you have dealt with the conflicting emotions. You need an excellent listener. Perhaps a local PCa support group can provide a personal experience for you. Someone suggested by that group, or the group experience itself may be the way to go. So. Cal must have many, many groups such as this.
Professional help is always a choice and your doctor can advise you (or should be able to).

After surgery, sexual experience is ALWAYS different. Beyond that, yes, all chemical effects are reversible once the drug is eliminated from the body. Younger, healthy men with active sex lives before treatment tend to respond better after all the treatments you may anticipate.
You are close to one of the most respected Prostate oncologists in the country, Mark Scholz in Marina del Rey. A visit there could be extremely productive.

VascodaGama

tarhoosier said:

Terms
In order to clarify the information from VdaG above, the term used in the US for bicalutimide (Casodex), Cyproterone, and similar drugs is Anti-Androgen, sometimes called AA, or A-A. The metaphor used commonly for such drugs is that each cell has a "lock" which allows androgens such as testosterone to enter the cell and complete the cell division cycle. Anti-Androgens (and anti-femogens for women) put gum in this lock and the androgen is unable to "open" the pathway to the cell nucleus.

Lupron is an "agonist" drug in the sense that it causes the release of a flood of hormones that swamp the messaging system of the body and thus causes the cessation of testosterone production until this swamping effect declines as the drug effect subsides. There is a newer drug called Degarelix that is a true "antagonist' because it switches off the production of testosterone by interfering with the chemical messaging system directly and does not swamp the system.
It is true that some doctors and patients prefer, or require the use of both an Anti-Androgen and a hormone agonist (Zoladex/Lupron/equivalent). Occasionally the newer antagonist Degarelix is preferred, usually in recently diagnosed patients with metastases and symptoms because it works almost immediately.
I also wish to make clear that it is my opinion that the mutation of the cells as VdaG explains is not caused by the application of any drug. It is a natural occurrence and will take place with or without any medication.

Tarhoosier, Thanks for correcting the terminology

Anti-androgens NOT anti-agonists is what I meant in my above comments.

In regards to cell’s mutations, it happens naturally independently of the drugs. However, the problem of mutations involving anti-androgens in the treatment of prostate cancer is that at one time cells which supposedly are dormant become active theoretically due to “feeding” on the anti-androgens. In such status doctors usually recommend stopping the administration of anti-androgens (continuing with the agonists, if any) which results in a significant drop of cancer activity as verified in a drop of PSA. This condition is referred to as the Anti-Androgen Withdrawal Response (AAWR). Here is an overview on the matter at PCRI publications;
http://www.prostate-cancer.org/education/andeprv/aawr.html

Cancer that have mutated are not all hormone refractory. Cancer can be androgen insensitive but not hormone independent. This is where cancer is found to produce its own testosterone to “survive”. Drugs such as Abiraterone are targeted to this sort of intratumoral condition inhibiting cells from producing its own testosterone.
Hormone Refractory Prostate Cancer (HRPC), which is the type in many advanced cases, is diagnosed when a PSA test shows an increase after six weeks of withdrawing of anti-androgens, in a confirmed castrate level of testosterone at <50ng/ml.

Regards
VGama

mrspjd

tarhoosier said:

Terms
In order to clarify the information from VdaG above, the term used in the US for bicalutimide (Casodex), Cyproterone, and similar drugs is Anti-Androgen, sometimes called AA, or A-A. The metaphor used commonly for such drugs is that each cell has a "lock" which allows androgens such as testosterone to enter the cell and complete the cell division cycle. Anti-Androgens (and anti-femogens for women) put gum in this lock and the androgen is unable to "open" the pathway to the cell nucleus.

Lupron is an "agonist" drug in the sense that it causes the release of a flood of hormones that swamp the messaging system of the body and thus causes the cessation of testosterone production until this swamping effect declines as the drug effect subsides. There is a newer drug called Degarelix that is a true "antagonist' because it switches off the production of testosterone by interfering with the chemical messaging system directly and does not swamp the system.
It is true that some doctors and patients prefer, or require the use of both an Anti-Androgen and a hormone agonist (Zoladex/Lupron/equivalent). Occasionally the newer antagonist Degarelix is preferred, usually in recently diagnosed patients with metastases and symptoms because it works almost immediately.
I also wish to make clear that it is my opinion that the mutation of the cells as VdaG explains is not caused by the application of any drug. It is a natural occurrence and will take place with or without any medication.

Degarelix (aka Firmagon) vs Lupron
The data from a 2009 phase III pivotal trial compared one study group receiving the one month dosing of Lupron (WITHOUT the use of a bicalutamide to prevent T flare) with two other study groups each receiving the one month dosing of Firmagon. (Each of the two groups receiving the Firmagon had different initial loading doses.)

It appears that since no bicalutamide was given along with the Lupron to prevent T flare in the group receiving the Lupron alone, study data showed a faster rate in PSA decline within the first few weeks of the study (as expected) in the group receiving the Firmagon compared to that of the group receiving the Lupron. However, at the end of one year, the study authors reported no significant difference between the two groups. Also, the Firmagon group had more transient injection-site reactions/complications (such as pain and erythema). Most often, Lupron is injected intramuscularly while Firmagon is injected sub-q (under the skin). Monthly Firmagon injections may also be more costly/expensive than the 3, 4, or 6 month Lupron injections.

Just some of the many factors to consider when evaluating the risks and benefits of available AD therapies, especially in first line tx of intermediate/advanced PCa.