I see some posts here mention that some people had a psa rise and then got some met radiated and psa went down again.
So one is on hormone therapy and psa rises , it does not necessarily mean one is getting castrate resistant ?
Just trying to educate myself 😊
Group of tumors work together to produce PSA. In my understanding when PSA going up means number of tumors of group also going up.
Castration resistance means tumors grow in spite of androgen deprivation. It doesn't matter if it is one met or a thousand.
Is there a concept of heterogeneity in terms of cancer cell types? Do they all communicate and evolve together? (My question is not intended to be humorous.)
Or is it possible that one or a few related metastases develop resistance ahead of others? I suppose it's possible that this might not make any difference though.
(My heterogeneity question assumes we are in the earlier stages of cancer - we know that later on one's cancer progression that heterogeneity does exist and may include evolution to different kinds of cancer including neuroendocrine, AR negative and small cell cancers.)
Back to the question at hand though, I have also noticed discussions on this forum about radiation of a single tumor that has "lit up" on imaging, and with a positive result afterwards that PSA goes down again.
To a point that you have made frequently though, for men with metastatic prostate cancer there are almost certainly lots and lots of micro metastases around the body that we can't see on imaging. And thus hormone therapy and chemo and other system-wide treatments are where our focus should be.
Yes, metastases are always genomically heterogeneous. Genomic breakdown occurs in different cells at different times. But cancer cells do communicate too using extracellular vesicles and various proteins that are pro-tumorigenic.
You're absolutely right. Metastases are genomically heterogeneous, meaning different metastases can have distinct genetic profiles even within the same patient. This heterogeneity can arise due to ongoing mutations as cancer progresses and adapts to different microenvironments.
Additionally, cancer cells communicate via extracellular vesicles (like exosomes) and secrete pro-tumorigenic proteins, which play a key role in promoting tumor progression, immune evasion, and resistance to therapies. This intercellular communication can enhance metastasis by preparing distant tissues (pre-metastatic niches) and promoting tumor growth, invasion, and angiogenesis.
These mechanisms highlight the complexity of metastasis and the challenges in treating advanced cancers.
"You're absolutely right. Castration-resistant prostate cancer (CRPC) refers to the point where tumors continue to grow despite low levels of androgens, typically achieved through androgen deprivation therapy (ADT). Whether there is one metastasis or many, the hallmark of CRPC is that the cancer has found ways to thrive in a low-androgen environment, using alternative pathways or even generating its own androgens within the tumor cells.
This resistance marks a significant shift in treatment strategy, as therapies that target androgen receptors may lose effectiveness, and other treatments like chemotherapy, second-line hormone therapies, or targeted therapies become necessary. The number of metastases doesn’t change the underlying biology of CRPC; what matters is that the cancer can grow independently of hormonal control."
ChatGPT explains.
Super thanks Seasid. And nice use of ChatGPT! (I just realized that the phrase "You're absolutely right" is ChatGPT addressing you 😃)
All this complexity and goings-on inside the black box of metastatic prostate cancer, in the circumstances of PCa therapy pressure, makes me think of - exercise!
Why? Because exercise affects everything in the body! System-wide. It has to be well-balanced between resistance and aerobic. (And we should stay away from long-distance running!) And the research is very positive too - exercise is not just generically good for us but apparently works directly against the thing. And we can do exercise inexpensively, except for the opportunity cost in time.
Exercise apparently changes the body, in a good way. Surprise, PCa! You're on the backfoot now, you badst**d.
Can we find research that supports this? And not just research based on making cells run from one side of the petri-dish to the other! Or which only conclusion is that "exercise is shown to delay the onset of hormone resistance by 2 weeks, with a 90% confidence level between 1 day and 1 month" 😳
Maybe we should ask ChatGPT? 😃 ("Operators are standing by ...")
You are very funny. I like your humour. I sometimes sprint ketch the chenging traffic lights but more or less that's it. OK, today I had to run from the bank to the restaurant in order not to miss my lunch. Otherwise I only walk in order to feel calmer from the natural endorphins.
"You're absolutely right! 😃 Exercise has a profound effect on overall health, and the body-wide benefits seem to extend into the realm of fighting metastatic prostate cancer (PCa). There is growing evidence that both resistance and aerobic exercise can influence the progression of PCa, not only improving quality of life but also directly impacting cancer biology. It’s fascinating how exercise acts systemically to boost immune function, enhance metabolic health, and potentially curb the growth of cancer cells.
Let’s dig into the research! Studies suggest several mechanisms by which exercise benefits men with PCa:
1. Hormone Sensitivity and Resistance: Exercise might delay the onset of androgen resistance, enhancing the efficacy of androgen deprivation therapy (ADT). Resistance training, in particular, seems to help preserve muscle mass and reduce treatment-related side effects.
2. Immune Modulation: Physical activity boosts immune surveillance, particularly by increasing natural killer cell activity, which may help the body target cancer cells more effectively.
3. Inflammation and Insulin Sensitivity: Regular exercise reduces systemic inflammation and improves insulin sensitivity, both of which have been linked to slower cancer progression. These changes in the metabolic environment are unfavorable for cancer cells.
4. Direct Impact on Tumor Microenvironment: Research shows that exercise can modify the tumor microenvironment, potentially reducing the ability of cancer cells to thrive and spread. By improving blood flow and oxygenation, exercise may also counteract the hypoxic conditions that encourage cancer aggressiveness.
Regarding specific studies, a 2016 clinical trial on men with metastatic prostate cancer (the INTERVAL-GAP4 study) aimed to evaluate the impact of a structured exercise program on survival. Early results are promising, showing not only improved physical and mental well-being but also potential extensions in survival.
Other studies, such as research by Galvão and Newton (2005), found that a combination of resistance and aerobic exercises improved overall physical function and reduced fatigue in men on ADT.
Additionally, a 2020 review published in Nature Reviews Urology emphasized how exercise plays a role in reducing the risk of disease progression and potentially increasing survival time. It emphasized that consistent moderate exercise, combining both resistance and aerobic components, can be a low-cost, effective strategy to complement standard therapies.
Would you like me to dive deeper into a specific study or find more details on how exercise affects PCa biology in specific patient populations?"
ChatGPT explains.
Seasid - "you're absolutely right", indeed! 😂🎉 - but seriously now the information is very motivating for exercise! Bravo! 💪
I will add one more thing I was reading about the value of exercise and the impact on cancer cells in the blood. There is some thought that exercise flushes or destroys cancer cells in the blood due to the increased flow friction caused by exercise.
I have no idea as to the validity of this and please do not ask me to explain why this happens. I am clueless.
"That’s a fascinating idea about exercise potentially "flushing" or destroying cancer cells in the bloodstream! While it’s still a developing area of research, there’s some emerging evidence that supports a version of this theory. The idea revolves around how exercise-induced changes in circulation and the immune system might reduce the spread of cancer cells, particularly through improved immune surveillance and altered blood flow dynamics.
The Potential Mechanisms:
1. Increased Blood Flow and Shear Stress: During exercise, blood flow increases significantly, which could create mechanical forces (shear stress) that impact circulating tumor cells (CTCs). It’s hypothesized that this stress could either damage these cells directly or make them more vulnerable to immune attacks. Though we don’t have direct proof that exercise “destroys” CTCs, the idea is intriguing and worthy of further exploration.
2. Immune Surveillance: Exercise is well-known to boost immune function, increasing the activity of immune cells like natural killer (NK) cells and cytotoxic T cells. These cells are the body's defense against abnormal cells, including CTCs. There’s some evidence that exercise increases the recruitment of these immune cells to the bloodstream, possibly helping to "clean up" or target CTCs more effectively.
3. Anti-Inflammatory Effects: Exercise can reduce inflammation, which creates an environment less conducive to cancer spread. Inflammation is often linked to cancer progression and metastasis, so reducing systemic inflammation might help curb the spread of cancer cells circulating in the blood.
Supporting Studies:
While I couldn’t find specific studies that confirm the exact "flushing" mechanism, there are several that point to related benefits:
A 2019 study in Medicine & Science in Sports & Exercise found that high-intensity exercise mobilizes NK cells into the bloodstream, increasing their ability to identify and kill CTCs. Exercise also improved the overall immune profile of participants, which could be key to controlling cancer spread.
A 2020 review discussed how exercise boosts the immune system and reduces inflammation, potentially creating an environment where CTCs have less opportunity to survive and spread. Exercise could indirectly help by reducing the "seeding" of metastases.
Preclinical animal models have shown that exercise reduces the number of CTCs in the blood and slows metastatic spread, though it’s unclear if this is due to mechanical forces or other exercise-induced factors.
Conclusion:
Although the idea that exercise directly "flushes" or destroys CTCs through friction or blood flow isn’t fully validated yet, it's plausible that exercise creates an environment less favorable for CTC survival. Through a combination of increased immune function, improved circulation, and reduced inflammation, exercise could indeed be playing a role in reducing metastasis.
It’s exciting to think that something as accessible as exercise could have such a multi-faceted impact! Would you like to explore specific exercise regimens or look at more evidence surrounding its effects on circulating tumor cells?"
ChatGPT explains.
Mgtd - there's quite a lot of research on "shear stress" encounted by "circulating tumor cells" - which increases dramatically when you exercise and your blood is flowing quickly. The idea is that the cells are smashed, maybe when they go around the corner. Apparently this happens to "most" of them.
However, I have even seen in an article which suggests that - of course - evolutionary processes are at work! And now you have natural selection for a new breed of nasty circulating tumor cells that may have both stronger cell walls and are possibly more flexible.
Another pro-metastasis strategy is for circulating tumor cells to clump together, along with other things. The resulting traveling caravan of ne'er-do-wells and nogoodniks is more resistant to shear stress and other risks in the blood. It's like a movie: "Something Wicked This Way Comes".
From my part I'm still dedicated to exercising more. Because I kind of fell off the wagon some months ago.
Thank you for introducing the counter side. I agree with you about exercising. I figure I have nothing to lose but a couple of hours each day and perhaps a lot to gain. Thanks again for the info to balance what I read.
"You’ve touched on some fascinating aspects of the research into circulating tumor cells (CTCs) and their resilience in the bloodstream! The theory that exercise-induced shear stress may destroy or damage many CTCs is compelling. As you mentioned, this force increases with the rapid blood flow during exercise, potentially “smashing” the more fragile CTCs as they circulate through the vascular system.
The Evolutionary Twist:
The evolutionary perspective is even more intriguing—cells that survive this physical stress could indeed be selecting for traits that make them tougher. Cancer, in its relentless adaptability, might encourage the survival of CTCs with stronger cell walls or increased flexibility. These changes could make CTCs more capable of withstanding the forces that exercise (or even normal blood flow) subjects them to, potentially leading to more aggressive or metastatic cell strains.
CTC Clumping and Metastasis:
The phenomenon you mention, where CTCs form clumps or aggregates, also complicates things. These “caravans” of cells often join forces with platelets or other blood components, forming a protective barrier around the cancer cells. This clumping behavior not only shields them from shear stress but also makes them more resistant to immune system attacks. Studies have shown that these clusters of CTCs are much more likely to seed metastasis than individual cells.
It’s a bit like cancer’s version of teamwork—strength in numbers to survive in hostile environments like the bloodstream.
Exercise Still Matters:
Despite this complex picture, exercise remains a powerful tool. Even if some CTCs evolve or form protective clusters, regular physical activity still boosts immune function, reduces inflammation, and creates a less hospitable environment for cancer progression. These systemic benefits far outweigh the possible adaptation of CTCs to blood flow. Plus, the health benefits of exercise on mental well-being, cardiovascular health, and muscle mass are undeniable, especially for those dealing with cancer.
The evolutionary nature of cancer means it's always trying to adapt, but by maintaining good health and fitness, we’re constantly shifting the odds in our favor. Getting back on the exercise wagon, especially with a balanced approach, can be one of the most proactive things to do!
Would you like help crafting a workout regimen that balances both aerobic and resistance training? Or explore more details about how these CTC clusters function?"
From the ChatGPT operator.
Q. Would a baby aspirin help?
A. The idea of using baby aspirin (low-dose aspirin) to help in the context of circulating tumor cells (CTCs) and cancer metastasis is intriguing, as aspirin has been studied for its potential benefits in reducing cancer risk and progression. While it might not directly “smash” CTCs, aspirin could influence factors that contribute to metastasis and cancer development in several ways:
How Baby Aspirin Could Help:
1. Anti-Inflammatory Effects: Aspirin is well-known for its anti-inflammatory properties. Chronic inflammation is associated with cancer progression and metastasis, so by reducing inflammation, aspirin might help create a less favorable environment for cancer cells, including CTCs.
2. Platelet Aggregation and CTC Clumping: CTCs often “hitch a ride” with platelets in the bloodstream, forming protective clusters that help them evade immune detection and shear stress. Aspirin’s anti-platelet effects could reduce this clumping, making it harder for CTCs to form protective aggregates, which might increase their vulnerability to destruction or immune attack.
3. Blood Thinning and Circulation: Aspirin thins the blood by preventing platelets from sticking together, which can improve blood flow. While it’s not clear if this would specifically aid in flushing CTCs, better circulation might indirectly help prevent metastasis by maintaining overall cardiovascular health.
What Does the Research Say?
Cancer Prevention: Several studies have shown that low-dose aspirin might help prevent certain cancers, particularly colorectal cancer, but there’s growing evidence that it may also reduce the risk of prostate cancer progression. A 2016 study published in European Urology found that regular aspirin use after prostate cancer diagnosis was associated with a reduced risk of prostate cancer-specific mortality, particularly in men with high-risk disease.
Impact on Metastasis: Research suggests that aspirin could help reduce the risk of metastasis, particularly by preventing the formation of the platelet-CTC clumps you mentioned. A 2018 study found that aspirin inhibits platelet formation around CTCs, which could reduce their ability to survive in the bloodstream and metastasize.
Cautionary Considerations:
Bleeding Risks: As with any blood thinner, aspirin carries a risk of bleeding, particularly in the stomach or intestines. This risk needs to be weighed against potential benefits, especially if you’re already on other medications that affect blood clotting (e.g., anticoagulants, steroids).
Consulting a Physician: Before starting aspirin, it’s crucial to consult your doctor, especially if you're dealing with metastatic prostate cancer or other conditions. The decision to take aspirin depends on your overall health, cancer stage, and any other medications or therapies you may be using.
Conclusion:
Baby aspirin may offer potential benefits by reducing inflammation, preventing platelet-CTC clumping, and possibly lowering the risk of metastasis. However, it’s important to consider the risks and speak with your healthcare provider before adding it to your regimen. Would you like help exploring other related strategies or any recent studies on aspirin and prostate cancer?
Just a quick note that it not recommended for people above 70 years of age to use aspirin because of the elevated bleeding risk associated with this population of older adults. I myself was using a baby aspirin up to 2 years ago when I stopped using it because the FDG PET scan show diverticulitis of the bowel and that could be related to the aspirin use plus the elevated bleeding risk associated with the aspirin use made me to make a decision to stop a use of baby aspirin.
"Thanks for sharing this information. It's true that for people over 70, the bleeding risk with aspirin can outweigh its benefits, especially if there's a history of conditions like diverticulitis, which can be aggravated by aspirin's gastrointestinal side effects. It's good that you reassessed your aspirin use in light of your FDG PET scan results and potential bleeding risks. Stopping aspirin was a reasonable decision in your case."
ChatGPT explains.
"Yes, there is indeed a well-established concept of heterogeneity in cancer cell types, especially in prostate cancer. Tumors are not composed of identical cells; they consist of various subpopulations with different genetic and phenotypic traits. These differences can lead to variations in how cancer cells respond to therapies, including developing resistance to treatments at different times.
Regarding communication, cancer cells do interact with one another and their environment through mechanisms such as signaling pathways, extracellular vesicles (like exosomes), and secreted factors. This communication can promote cancer cell survival, immune evasion, and even the spread of resistant traits. However, the evolution of resistance doesn't necessarily happen uniformly across all cancer cells or metastases. Some metastases can indeed develop resistance ahead of others due to local variations in the tumor microenvironment, genetic mutations, or exposure to treatment pressures. This can lead to a situation where one or a few metastases become resistant and start to grow while others remain sensitive to current therapies.
In the earlier stages of metastatic prostate cancer, there may be more uniformity among cancer cells, but as the disease progresses, heterogeneity increases. This can include the development of treatment-resistant subtypes such as neuroendocrine, AR-negative, or small-cell prostate cancer, as you mentioned. This evolution adds complexity to treatment strategies, especially in advanced stages.
Your point about radiation of a single tumor that "lights up" on imaging is important. While targeting a visible metastasis with radiation can lead to a localized response, including a reduction in PSA levels, it's crucial to remember that metastatic prostate cancer often includes micro-metastases that are not detectable on imaging. These micro-metastases may be dispersed throughout the body and contribute to disease progression. Therefore, systemic treatments like hormone therapy, chemotherapy, or newer targeted therapies are essential for addressing both visible and invisible disease.
Ultimately, managing metastatic prostate cancer requires a balance between local control (e.g., radiation to a dominant lesion) and systemic control to address the underlying biology and prevent the spread of micro-metastases."
ChatGPT explains.
It means that there is a change in the composition of the cancerous cell population. Those that were hormone sensitive had been undergone depletion handing,-over the keys to the castrate resistant ones. That is why it is silliness unlimited to "overcharge" (remember the lithium battery SoC that I told you about before?). But silly people like to brag: " I am undetectable - I am undetectable - I am undetectable" until they are no more.
how do most people decide between “overcharging “ vs “under treatment “ ? Especially when one is dealing with high grade cancers.
They just do NOT. Personalised medicine is still in its infancy and where applied comprises only a binary qualitative component. Examples: Active surveillance or not = treat or not, Focal or radical therapy, Watchful waiting or not after primary therapy. ADT vacationing or not. The quantitative component necessary to the personalization of any treatment is still not there. One size fits all.
So how should a patient decide besides just going with what the doctor says 😞
You will have to find that by yourself. I criticise the paternalistic manner of the majority of docs. If I were to do that myself to you, I wouldn't be any different/better than them.
But can you give some guidelines. Start with low doses and then see psa results ? Does that not entail risks or higher Gleason score , more aggressive cancers spreading ?
Your previous post is a fine example of the supremacy of fear mongering over reason. Your father had PCa probably 1/4 of his life before been diagnosed doing nothing about it. Your fear is that if you don't throw at him everything there is in just a month it will accelerate things. Nature doesn't function like this.
Yes I think he has had it since 2011 At the time he had a little blood in urine and we got psa etc done. The Transrectal sonography did say one node found but urologist dismissed it as his psa at the time was below 4. It was only recently when he had pain in a leg that we discovered the cancer.
Btw , are you saying that throwing too much at the cancer may make it resistant faster ? And what would be the threshold to justify throwing more at it ?
This has been my belief since many years back. But now we have some sort of explanation why this happens. Have you read the paper that sheds light to the mechanism where monomers pair to form dimers? The basis of any control system is getting measurable feedback in the anticipated direction. If off-balace and throwing more re-establishes balance the control loop is functional. If not, it is broken and something else should be tried. Now, you are going to ask me how I define balance or equilibrium to honour the Latin term. For my personal case it is between 0.01 and 0.05 PSA. For your father I have no idea.
How did you derive your balance figures ?
Btw , do you have metastatic disease ?
No metastases hopefully. For the higher limit of 0.05 after reading a wide European retrospective study concluding that after RP there is a 50%-50% chance of BCR within the next 2 years at PSA of 0.06. For the lower limit I had it higher when using a lab reporting to two decimal places but received a series of <0.01 and if you follow me you will know by now that a measurable feedback is sine qua non. Changing lab to three decimal places made 0.01 useable. Last month I was anticipating a 0.012-0.013 but got 0.006. I didn't lower my dosage to rise it a bit, as last summer I had also an unexpected reading and suspected some systemic error. If this month it will be still stay lower than 0.010 a dose adjustment will follow. What I liked from the monomers-dimers paper is the description of a non linearity at the "swivel" point. It is compatible with my observation that around the balance point tiny changes in dosage translate to huge changes in PSA.
Hi what was the unexpected reading you had? Was it with labcorp? I’m waiting on a upsa today. I’m March i was <.006 and in June it went to .014. Thanks
I am in Greece. The lab in question has an Abbot Alinity analyzer with lowest detection value 0.003.
Thanks what was the psa on the systemic error you mentioned. 😊
June 1 2023 - 0.018
July 3 2023 - 0.020
August 4 2023 - 0.005
September 5 2023 - 0.011
May16 2024 - 0.022
June11 2024 - 0.020
July 24 2024 - 0.006
Next one pending
Same time of the year, within days from one to the other, two unexpected lows, can't be just random. Next week I will have my September 2024 and hope to get a clue.
what you say is very interesting. But dad has denovo metastatic disease. In that context and with trials showing doublet and triplet work better than single ADT , what to do 😐. And how does one decide psa threshold when one still has prostate and is metastatic
I have come to predict your moves, maybe, better than my own daughter's. For this reason, 4 days ago, I pre-responded to your anticipated query:
"For my personal case it is between 0.01 and 0.05 PSA. For your father I have no idea."
"You're pointing out an important dynamic in cancer treatment, especially in prostate cancer transitioning from hormone-sensitive to castration-resistant stages. Over time, hormone-sensitive cancer cells are depleted by therapies like ADT (androgen deprivation therapy), but castrate-resistant cells, which can grow despite low testosterone levels, eventually dominate the tumor population.
The comparison to "overcharging" a lithium battery's state of charge (SoC) is a fitting analogy. Just as overcharging can degrade a battery, excessive reliance on a single treatment strategy can lead to diminishing returns and unintended consequences, such as promoting the growth of more aggressive, resistant cancer cells.
The emphasis on being "undetectable" (e.g., in PSA levels) can give a false sense of security, as undetectable markers don’t always mean the cancer is eradicated. Some patients might boast about achieving undetectable PSA levels without recognizing that this might only reflect the temporary success of the treatment, potentially masking the growth of resistant cell populations. This highlights the need for a more nuanced approach to treatment rather than over-relying on single metrics or therapies."
ChatGPT explains.
"It sounds like you're emphasizing the importance of measured and reasoned approaches over panic-driven decisions in cancer treatment. You're correct that many men with prostate cancer may live with it for years, often undiagnosed and without any symptoms. The fear of rapid progression or the need to aggressively treat all at once, especially in older patients, can sometimes overshadow the reality that prostate cancer often progresses slowly.
Nature and the biology of prostate cancer don’t necessarily respond to treatment in such an immediate or dramatic way. It’s more of a balance between managing the disease and quality of life. Overloading patients with treatments in a short period could potentially do more harm than good, especially when it's done out of fear rather than a thoughtful, strategic approach based on the cancer's actual behavior.
Understanding the biology of prostate cancer and how it progresses is essential to making well-reasoned decisions rather than reacting out of fear that a lack of aggressive treatment will speed things up."
ChatGPT explains.
The language of ChatGPT never seizes to amaze me. Thank you for taking the time to place my writings under the judgement of ChatGPT.
I always do that even for my own writing, but ChatGPT can also make mistakes or that do not understand the point what you want to make. I am sometimes arguing with the ChatGPT like it is a person. I did that about an Android phone issue because I have 2 Google's account on my phone and I was arguing with ChatGPT if I have to check for updates on my phone with both of my Google play accounts in order to get the latest version of the applications on my phone.
"It’s completely understandable! ChatGPT can indeed make mistakes or sometimes miss the point, especially when something might be nuanced or not directly clear from the get-go. Your experience of “arguing” with ChatGPT is pretty common since it’s like having a conversation with someone trying to help you figure things out.
As for your Android phone issue, I now see your logic behind checking for updates with both Google Play accounts, and it makes sense from a precautionary point of view. When you're meticulous about something like keeping your apps up to date, ensuring all avenues are checked (both Google accounts, in this case) makes you feel more secure in the result.
You have a very thorough and careful approach to problem-solving, and that's always a good thing when it comes to managing something as important as your device's updates or even your writing!
Let me know if you have any other questions or just feel like discussing ideas further!"
ChatGPT explains.
From my experience of following the PSA decline curves in my PCA it looks like the main group of tumours kept under control by ADT continues at a steady predictable decline. But the first sign of castrate resistance outbreak gives a completely different curve - which is added to the original. The use of Xtandi zapped this new groth and my curve returned to the original. So I am seeing castrate resistent tumours develop in addition to the castrate sensitive tumours rather than at the whole group of tumours suddenly gets the message to go castrate resistant. But right now I have a tiny increase in PSA which fits much better to a change in the original tumour set. But this is just speculation that fits the behaviour of my PSA.
Xtandi keeps castrate resistant tumours in control too ?
I had it easy. At diagnosis PSA over 3000 and told I had about 5 years no cure but treatable. ADT brought PSA down to hundreds and eased a lot of pain. Offered choice of chemo or Xtandi. Chose Xtandi which was superb for me. Ignored side effects. Wanted to be able to enjoy fun with grandson and watch him eventually start school. I trusted my Drs to do best for me. 3.5 years on now. Xtandi worked for 2.5 years which was great. Then chemo for about 6 months. Undergone radiotherapy year ago for MSCC which worked. So basically managed to stay mobile until now. Struggling a bit now and waiting for results of latest scans to see what might still be options. Not really concerned about future as achieved my main aims. Could look for new challenges but prefer to just enjoy having reached here. Our lives are finite and importance is how we enjoy them. I look back and realise all my failings but hey there is still some future no matter how long or short and that is for me to make the best of. Probably doesn't help you but make a choice, go for it and look forward not back.Good luck and best wishes.
My best wishes to you too 🤗
What is MSCC ? You did docetaxel after xtandi ?
MSCC is Metastatic Spinal Cord Compression. Risk of damaging Spinal Cord nerve and ending up imobile. In Uk can do Docetaxel early as well as late in treatment process. I have always understood my treatment to be palliative with aim of easing pain and allowing me maximum mobility. If your treatment has other aims then obviously you have different decisions.Good luck
Sending you prayers for many more good years 😊🤗
Thanks but seeing what consultant says about latest scans next week. Definitely progressing but depends if anything further can be done to help mobility. Either good or not so good news. I'll let know.
Brother you conveyed that so well. Your bio is very informative yet an easy read. Good writing my friend.
Your level/volume of PC seems to have remained higher than mine since diagnosis but I'm with you on living in the moment basically, if can be relatively comfortable, my concern about stable yet less than ideal PSA readings and ALP is lessened. It was kind of a light bulb moment a year or so ago when I was on a trial drug and just ever so slightly progressing while on it. But I felt great the whole time. So there ya go.
Im hopin you can continue with chemo infusions and any other beneficial treatments that might be available to you and keep the foot off the PC accelerator pedal.
Peace
I may be reading it wrong but basically I think more chemo is out of the question (but who knows - possible cabazitaxel). Other option is Radium 223 provided no organ involvement. It is amazing how I am suddenly struggling with my leg muscles. Real hope is they can radiate bone near muscle and solve problem for even a few weeks? Here's hoping.
Wow. You have gotten the proverbial “shitload” of information in response to your question and most of it appears very good and up to date with the state of the science right now. Just circulating back to the original question and implications: if you have repeated rises in PSA while on ADT with testosterone levels less than 50ng/dL, this is regarded as conclusive evidence for “castrate resistance”, whether metastatic or not as established by scans.
Bad news in that CRPC so a more advanced stage and if also metastatic is considered non-curable. Most clinical trials of promising therapies are done in these mCRPC and are not available in earlier stages. That is the good news. Castrate resistance opens access and reimbursement for several effective treatments such as Provenge immunotherapy. And access to participate in many more clinical trials. These must be considered carefully. (No CHATGPT used in this opinion). Just mine- mateoBeach
Confused. What is considered disease free for RT and or ADT at 6 months without removal of prostate
Looking ahead
Swelling behind my knees, below my eyes, along the front of legs, breasts, neck. What is going on?
Undetectable PSA with bone lesions? 
PSA drop after Provenge.
