I have been on Lupron and Abiraterone for most of my 12 yrs since dx in 2012, including constantly for the last 7 years. PSA became measurable about 2 yrs ago. Largest tumor, which appeared to be the culprit for the rise was radiated and PSA became undetectable again. The last 16 months have seen my PSA measure: .05 .06 .06 .09 .14. .17 and then .20 a few days ago. MO has advised continuing same treatment and holding off on PSMA FOR NOW, since the PSA increases are so small. She feels the likelihood of PSMA revealing anything under these circumstances as quite low, and thus not worth doing presently. Assuming PSA continues to rise, she will likely recommend a PSMA when my next lab results are done in 3 months.
Any thoughts?
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Although my uPSA has held very low stable 0.03X range for over three years now, my current Pylarify PSMA PET identified a 2.3 x 2 cm hypodense lesion on my liver, findings concerning for metastatic disease of uncertain origin. Concurrent GUARDANT360 liquid blood biopsy has identified TP53 R248Q biomarker.
It is well recognized that sometimes, prostate cancer changes and reduces PSA production, sometimes completely. Thereby, serum PSA may no longer be a good marker of cancer growth. I also learned circulating tumor DNA can and does rise before PSA increases, sometimes by months; why I also use serial liquid biopsy testing.
Justfor- I appreciate your commenting on my post but would appreciate you putting more meat on the bone. My MO and I are both aware of the “doubling time” but is that ALWAYS the only issue?Do you know if her thoughts that a PSMA at present would likely be useful in any way? Do you believe I should be adding chemo or changing my treatment in any other way? Tall-Allen responded to my post before you- I was wondering if you read it because I think Tall-Allen is EXTREMELY well informed and he seems to thing the advice my MO gave me was “good advice”?
I am on vacation from doublet therapy. My psa is undetectable. My MO ( MSK) sent me for psma scans twice already January and July) this year. Hard to figure out the right approach.
You asked for thoughts, I quantified your detection probabilities. Ask your MO to quantify her "quite low" and then I may provide more "meat". Numbers were invented for people to be specific. Expressions like "quite low" are vague and context related. Do you think that 1% is "quite low" when discussing aviation accidents?
Just some "fine print" on the link posted by Optimistic49. It relates to earlier stages i.e. BCR after primary RP or RT. The bulk of them is not under ADT like the OP. Also, it is very well known that at low PSA values short PSADT are predominant in estimating detection rates. The 8 months DT of the OP is the "apparent" DT as it is maintained by medication. The "underlying" DT, that is absent of medication, (according to my personal data) can be 3+ more faster, bringing it down to 2 months. The latter is the decisive factor in the case of the OP.
Any thoughts? Would a clear liquid blood biopsy and clear PSMA provide you any comfort? And what if the "quite low" chances reveal findings? I choose to not give this beast time and obscurity and take actions well ahead of common practices.
My current liquid blood biopsy, done at 0.031, no ADT, revealed TP53 mutation; last years was clear. My current Palarify PSMA, also done at 0.031, revealed a lesion on my liver. Previous two years were clear. Further investigations are being schedule.
Part of the resistance of investigative methods is reluctance to spend monies on us men with this disease. And hard to believe, negative findings don't always seem to benefit a doctors or a medical center favorably. All the best!
You’ve got it, part of the resistance of investigative methods is the reluctance to spend monies on you men with this disease, especially here in the UK. Had to question and push for investigations and treatments all the time. Recently asked about further treatment, told by the Oncologist my husband’s life expectancy at diagnosis was 5 years and he has had it 16years. If it had been left to this UK hospital trust and Oncologist he would have only had the 5 years, we had to sort investigations & further treatment ourselves, through trials and paying privately at times. If you want to kill this beast you can’t wait and see.
Examples of reluctance to spend monies, why not use a shield to protect the bowel while giving Radiotherapy. We heard about this recently from a patient who had paid for this privately, my husband has suffered for 5 years since Radiotherapy with bowel frequency/urgency rectal bleeding, anemic and recently had to have blood transfusion and iron. We would have willing paid if we had known that the shield might of helped. Very short sighted of the medical profession as now needing Colorectal & Gastroenterology support and at what cost.
After stopping R223 because of progression read a research paper that said that they had found progression in some patients while undergoing R223. A PET Scan would identify who would benefit from this treatment. My husband got progression while undergoing R223, asked why a PET Scan was not done, the Oncologist said the hospital does not fund PET Scan. If they had would have save on the cost of the treatment and more importantly my husband’s deterioration since undergoing 4 treatments of R223, Hospice Homecare for pain management with opioids.
The medical profession in the UK don’t tell you about things they can’t fund, and what they can fund is just standard treatment, nothing outside NICE guidelines which are mainly based on funding.
It is sad you did not know about the shield, neither did I and I suffer from similar SEs to your husband. This is not an isolated incident. Same applies to using cold therapy to protect against peripheral neuropathy resulting from chemo - I suffer from that. It’s not in the script so the nhs don’t tell you about it. We’re all wiser now, thanks to sites like HU and the knowledgeable contributors.
Cold mitts and socks, plus a cold cap if you’re worried about hair loss (usually temporary). Best bring a cooler, you do not want them frozen as they can cause frost bite.
I lived in Surrey and owned a small business there, paying for my staff's private insurance. Many things are not funded in the US, generally not funded via denials. And US doctors are often guided by their preferences of their own practices, contracts and value-based concept that can be translated to mean something like, if the chances of given investigative method being positive are small, do not do them. I see multiple dermatologists because I learned they face pressures to not have too many benign skin biopsies. This year my other dermatologist did a biopsy on a site that concerned me (the other doc passed on it). Turned out, my second melanoma.
During my screening years of bouncing PSA and 'clear' DREs, my US urologist never mentioned MRI - it was a urologist in London that did. The London doc mentioned genomic testing to me but 'way back' in 2015 it was not yet approved for use in US for prostate cancer. I did self-pay only to see it being approved about a year later.
From my patient experiences in US, UK, Netherlands, Belgium and France, including imaging and two surgeries in Europe, I see our 'different systems' quite similar. All the best to all off us!
I think the other issue is that the wack a mole approach has not been found to prolong life. So they do the PMSA scan and find something. What do we do about it that makes a difference. What if radiating the lesion cause a horrible side effect and he loses some good quality life. I would agree that the jury is still out on this question, however.
Some say my salvage extended pelvic lymph node surgery with the frozen section pathology method was wack a mole treatment because six cancerous pelvic nodes were confirmed; if only say three would it have more support?.
IMO characterizations like wack a mole, 'undetectable' PSA, over-treatment, 0.1 and 0.2 as line in sand (our blood actually) for definition of 'recurrence' post RP are misleading at best, and dangerous to the well-being of us all.
Further thought - one reason I use liquid biopsies is that it is well documented circulating tumor DNA often rises before the PSA increases, sometimes by months. Also, prostate cancer changes and can stop producing PSA, sometimes completely, so serum PSA is no longer a good marker of cancer growth. This is why I do monthly-bi-monthly PSA testing and annual blood biopsy and imaging.
As I share my uPSA has been holding very low stable, 0.03X range for over three years, no ADT. And now this biomarker and Pylarify identified lesion; which of course I hope is benign, but...
If you look at the PSMA-detection statistics you will be able to quantify that this is very low chance of detection at this point — see link below. Although my personal experience may not be yours, I’ve had scans between your level and 1.6 with no detection and continuous recent rise. In the end, you need to keep with your usual treatment protocol because something is there, which is all you know at this point. Depending upon where you are living, my understanding is that doctors might not offer chemo until they are sure you are oligometastatic. I’m not a doc, just a member of our exclusive club and my personal view (and I haven’t read your full bio).
I would also agree though with NanoMri that if you have access to the test and want to do it, then it wouldn’t hurt and you might be in the low probability group that finds something and can address it. I too like to have as much info as possible before making decisions.
I had four PSMA pet scans each two weeks apart at the start of my prostate cancer treatment and I believe it is better to find something at 0.2 PSA and address it rather than to wait until the PSA rise to 1 especially because your PSA doubling time is rapid.
I made a mistake not to add Bicalutamide when my PSA was 0.25 after radiation therapy of my prostate. I was waiting until my PSA rocketed to 2.5 and now I can't suppress my PSA. It is 3 now.
My point is get the PSMA pet scan and act immediately. Have a clear plan what to do and act immediately. Don't wait like I was waiting.
If you start Bicalutamide at PSA 1 it is much better than to wait until it is 2.5. I was very naive. Plus ask ChatGPT about adding dexamethasone 0.5 mg per day instead of Prednisone to Abiraterone. I know that your MO didn't approve it but it is your life.
When Abiraterone combined with Prednisone starts to lose effectiveness, one strategy is to replace Prednisone with Dexamethasone at a lower dose, typically 0.5 mg per day. The potential advantages of this switch are:
1. **Different Mechanism of Action:** Dexamethasone is a more potent glucocorticoid than Prednisone. It has a stronger anti-inflammatory effect and may suppress the adrenal glands more effectively, which can further reduce androgen production that fuels prostate cancer growth.
2. **Lower Mineralocorticoid Activity:** Dexamethasone has lower mineralocorticoid activity compared to Prednisone, which may help in better managing side effects related to fluid retention, high blood pressure, and hypokalemia (low potassium levels) that are sometimes exacerbated by Abiraterone.
3. **Possible Enhanced Cancer Control:** Some studies have shown that prostate cancer cells can become resistant to Prednisone but remain sensitive to Dexamethasone. The change can sometimes restore or enhance the effectiveness of Abiraterone, possibly providing additional cancer control.
4. **Lower Dosing:** Since Dexamethasone is more potent, it is given in much lower doses than Prednisone (0.5 mg of Dexamethasone vs. 5 mg of Prednisone), which can reduce the risk of some side effects associated with higher doses of glucocorticoids.
It's important to monitor the patient closely when making this switch, as Dexamethasone's increased potency could also lead to a different side effect profile that needs careful management.
Good comments but also remember that the amount of cancer is not equally correlated with the psa number. Each person is different. Some have low psadt and highly visible tumors. Other men have a high higher or doubling time and no visible cancer.
Replacing Prednisone with Dexamethasone in the treatment of metastatic prostate cancer, particularly when using Abiraterone, can have several potential downsides:
1. **Increased Risk of Side Effects:**
- **Immunosuppression:** Dexamethasone is more potent than Prednisone, so even at lower doses, it can lead to greater immunosuppression. This increases the risk of infections.
- **Metabolic Effects:** Dexamethasone can cause more significant alterations in glucose metabolism, potentially leading to hyperglycemia or worsening existing diabetes.
- **Osteoporosis:** Prolonged use of Dexamethasone can increase the risk of osteoporosis and fractures due to its stronger effects on bone resorption compared to Prednisone.
2. **Adrenal Insufficiency:**
- Dexamethasone suppresses the hypothalamic-pituitary-adrenal (HPA) axis more strongly than Prednisone, which can lead to adrenal insufficiency if Dexamethasone is stopped abruptly or if the body's demand for corticosteroids suddenly increases (e.g., during stress or illness).
3. **Mood and Cognitive Changes:**
- Higher potency glucocorticoids like Dexamethasone are more likely to cause mood swings, anxiety, depression, or even steroid-induced psychosis, especially with long-term use.
4. **Fluid Retention and Hypertension:**
- Although Dexamethasone has lower mineralocorticoid activity than Prednisone, it can still cause significant fluid retention and hypertension, particularly when used long-term.
5. **Myopathy:**
- Glucocorticoids can cause muscle wasting or myopathy, and this effect may be more pronounced with Dexamethasone due to its greater potency.
6. **Long-term Toxicity:**
- The long-term use of Dexamethasone, even at low doses, can lead to cumulative toxicity, potentially affecting various systems in the body, including the cardiovascular system, skin (e.g., thinning), and eyes (e.g., cataracts, glaucoma).
Because of these potential downsides, the decision to switch from Prednisone to Dexamethasone should be carefully considered, weighing the benefits of possibly enhanced cancer control against the risks of increased side effects. Close monitoring and appropriate supportive care are essential to manage any adverse effects that arise.
The extent to which switching from Prednisone to Dexamethasone can extend the efficacy of Abiraterone varies between patients and is influenced by several factors, including the biology of the cancer, the patient's overall health, and prior treatments.
**Key Points to Consider:**
1. **Potential Extension of Efficacy:**
- Clinical studies and case reports suggest that switching to Dexamethasone can sometimes re-sensitize prostate cancer to Abiraterone, leading to a temporary reduction in PSA levels and a potential delay in disease progression. However, the exact duration of extended efficacy is highly variable. Some patients might experience several additional months of disease control, while others may see a shorter or longer benefit.
2. **Limited Clinical Data:**
- While there is some evidence supporting this strategy, robust, large-scale clinical trials directly quantifying the average duration of benefit are limited. In smaller studies or retrospective analyses, some patients have experienced a median extension of several months before disease progression resumes.
3. **Personalized Response:**
- The response to Dexamethasone can be highly individualized. In some cases, switching to Dexamethasone might offer several months of additional control, while in other cases, the benefit might be less pronounced. It's also possible that some patients may not respond to the switch at all.
4. **Overall Survival Impact:**
- While the switch might delay disease progression, it is unclear how much it impacts overall survival. It is generally considered a strategy to extend the time on Abiraterone before moving to another line of therapy.
**Conclusion:**
Switching to Dexamethasone instead of Prednisone could potentially extend the efficacy of Abiraterone by several months, but the duration is unpredictable and varies between individuals. This approach may provide additional time before needing to transition to other treatments, but the benefit should be weighed against the possible side effects and overall treatment goals. Regular monitoring is essential to assess the effectiveness and manage any emerging side effects.
Your approach of considering an earlier switch from Prednisone to Dexamethasone, rather than waiting for substantial cancer progression, is indeed a strategy that some oncologists and patients prefer. There are several reasons why an earlier switch might be beneficial:
### Advantages of an Earlier Switch:
1. **Proactive Management:** Switching earlier may help to delay substantial disease progression by addressing the potential resistance to Abiraterone before it becomes more pronounced. This could maintain better overall control of the cancer.
2. **Potential for Longer Disease Control:** By switching to Dexamethasone before significant progression, you might extend the period during which Abiraterone remains effective. This could lead to longer overall survival and delay the need for more aggressive or toxic therapies.
3. **Avoiding Symptom Onset:** Switching earlier can potentially prevent the development of symptoms associated with disease progression, such as bone pain, which could negatively impact your quality of life.
4. **Maintaining Lower PSA Levels:** An earlier switch might help keep PSA levels lower for longer, which could be psychologically reassuring and indicate ongoing disease control.
### Considerations:
- **Monitoring:** Even with an earlier switch, close monitoring of PSA levels, symptoms, and imaging results remains essential to ensure that the treatment is still effective.
- **Side Effects:** Although Dexamethasone may be more effective in controlling PSA levels in some cases, it is also important to be mindful of the potential for increased side effects due to its potency. Regular assessments of overall health and side effect management will be crucial.
### Conclusion:
Switching to Dexamethasone earlier rather than waiting for substantial progression can be a reasonable and proactive approach. It may help to maintain better disease control and quality of life. However, this strategy should be personalized, considering your overall health and how your cancer has responded to treatment in the past. Discussing this approach with your oncologist will ensure that the decision aligns with your treatment goals and current clinical situation.
seeing multiple sequential PSA rises such as tho vindicates Biochemic Recurrence, BCR, so residual PC is growing somewhere. Very helpful to identify as early as possible exactly where (local, pelvic or remote metastasis) as this will guide the next treatment. PSMA scan with a PSA of 0.20 to 0.25 can be very effective at identifying sites of recurrence or metastasis. So I would not wait much longer.
The switch from Prednisone to Dexamethasone to see if this will enhance the efficacy with Abiraterone is worth trying. It is not dangerous as you would use an equivalent lower dose just for required replacement.
I totally agree with you he should get a PSMA pet scan now.
I had four almost "real time" PSMA pet scans every two weeks from my first Degarelix injections without any health issues until now six years later.
I took part in a study "ADT and me" for professor Emmett in order to see how the PSMA SUV Max value is changing. I had lots of bone metastasis everywhere even in my neck.
I just hope that they don't want him to wait in order to put him into one of their own clinical trials and for that they need a bit higher PSA? I can recommend from my own experience to do the scan now. If you find nothing it is great.
Wrong point! PSA is proportional to the number of PSA expressing cells. Imaging detection is proportional to the concentration or density (population/volume) of the PSMA expressing cells. Apples to oranges. Even if we assume that the PSA expressing cells are also doing PSMA, which is a very rough approximation, it is the spatial distribution of these cells that governs imaging detection. Too many of them squeezed into a small lesion will light up. The same amount and type of cells dispersed all over, will pass under the radar.
Monitoring prostate cancer when PSA levels and imaging alone aren't sufficient requires a multifaceted approach that combines various diagnostic tools and clinical assessments. Here's how such a strategy might look:
### 1. **Regular Imaging with Multiple Modalities**:
- **PSMA PET/CT or MRI**: Even if PSA levels are low, regular scans using PSMA PET/CT, MRI, or FDG PET/CT (especially for neuroendocrine variants) can help detect changes that might not be reflected in PSA levels.
- **Bone Scans**: If bone metastasis is a concern, bone scans might be used regularly to check for any new or progressing lesions.
- **Multiparametric MRI (mpMRI)**: This can be particularly useful for assessing local recurrences in the prostate bed or detecting small, indolent lesions.
### 2. **Blood and Tissue Biomarkers**:
- **Circulating Tumor Cells (CTCs)**: These cells can be detected in the blood and may provide information about the presence and type of metastasis, even when PSA is low.
- **Circulating Tumor DNA (ctDNA)**: Analysis of ctDNA can help detect specific genetic mutations or alterations associated with prostate cancer progression.
- **Neuroendocrine Markers**: If there's concern about a neuroendocrine phenotype, markers like Chromogranin A, Neuron-Specific Enolase (NSE), and Progastrin-Releasing Peptide (ProGRP) can be useful.
### 3. **Clinical and Symptomatic Monitoring**:
- **Physical Examinations**: Regular digital rectal exams (DRE) and other physical assessments by a urologist or oncologist can help identify any palpable changes in the prostate or surrounding tissues.
- **Symptom Tracking**: Monitoring for new or worsening symptoms, such as bone pain, urinary issues, or unexplained weight loss, can provide clues about cancer progression.
- **Quality of Life Assessments**: Tools like the EPIC (Expanded Prostate Cancer Index Composite) questionnaire can help track changes in symptoms and quality of life, which may indirectly suggest disease progression.
### 4. **Advanced Genomic Testing**:
- **Genetic Profiling**: In certain cases, genomic profiling of the tumor or blood can identify specific mutations (e.g., BRCA1/2, ATM) that may guide treatment choices and suggest a more aggressive monitoring approach.
- **Liquid Biopsy**: This non-invasive test analyzes DNA fragments from tumors circulating in the blood, helping to detect mutations and guide therapy, especially when traditional biopsies are difficult.
### 5. **Therapeutic Monitoring**:
- **Response to Therapy**: Observing how the cancer responds to current treatments (e.g., hormone therapy, chemotherapy) can provide insights into the cancer’s behavior. For example, a lack of response may suggest the need for more frequent monitoring or a change in treatment.
- **Adjusting Treatment Based on Monitoring**: The treatment plan may be adjusted based on the results of these comprehensive monitoring strategies, with the goal of staying ahead of any potential progression.
### 6. **Patient-Reported Outcomes**:
- **Regular Communication**: Frequent communication between the patient and healthcare team ensures that subtle changes in health are addressed quickly.
- **Health Apps and Wearables**: Some patients use health apps or wearable technology to track vital signs, activity levels, and symptoms, which can provide additional data points for monitoring.
### Summary:
Monitoring prostate cancer in situations where PSA and imaging aren't fully reliable requires a comprehensive and personalized approach. Combining advanced imaging techniques, biomarker analysis, genomic testing, and regular clinical assessments ensures that changes in the cancer's status are detected early, allowing for timely and effective intervention. Regular follow-ups with a multidisciplinary team are essential for integrating all these data points into a cohesive monitoring and treatment strategy.
Reasonable plan, I’m in the same boat but usually when I hit 0.2 it’s time to get scanned. I’ve done this twice in the last couple of years and each time treated the tumor with SBRT and PSA fell back to nearly undetectable. My oncologist, Dr. Sartor said that I can do this indefinitely as long as location and tumor burden allows. I’m on 10+ years after stage 4 dx. Hoping to continue this route for many more. SBRT is a very easy form of treatment.
I am 66 yrs old and other than PC and my orthopedic surgeries, I have no other known health issues. I play an aggressive game of Pickleball almost daily for about 6-7 months of the year and am a couch potato for the winter and colder months. My diet isn’t the best but it’s much better than it was before I was dx.
As for those suggesting a switch to DEX, I discussed this with my MO several months ago and she was well-informed about DEC but was not prepared to recommend it.
Determining when Abiraterone plus Prednisolone has failed is a critical decision point in managing metastatic prostate cancer. The decision typically involves assessing multiple factors to ensure that the treatment is no longer providing benefit before moving on to alternative therapies. Here’s how this decision is usually made:
### 1. **Rising PSA Levels**
- **PSA Progression:** A key indicator of treatment failure is a consistent rise in PSA levels, despite being on Abiraterone plus Prednisolone. The Prostate Cancer Working Group 3 (PCWG3) criteria define PSA progression as:
- A rise in PSA of 25% or more and an absolute increase of at least 2 ng/mL above the nadir (lowest level reached) on at least two consecutive measurements taken at least one week apart.
- **PSA Doubling Time:** Rapid PSA doubling time (the time it takes for PSA to double) can also suggest that the cancer is progressing despite treatment.
### 2. **Radiographic Progression**
- **Imaging Results:** Progression can also be determined by radiographic evidence, such as the appearance of new lesions or growth of existing lesions on imaging studies (e.g., bone scans, CT scans, or PSMA PET scans). If new metastatic sites appear or existing ones grow, this indicates that the cancer is progressing.
- **Bone Scan or PSMA PET Scan:** The appearance of new bone metastases or visceral metastases on these scans, even if PSA is stable or rising slowly, can indicate treatment failure.
### 3. **Clinical Symptoms**
- **Worsening Symptoms:** The emergence or worsening of symptoms, such as increased bone pain, fatigue, or other signs that the cancer is progressing, can indicate that Abiraterone is no longer effective.
- **Performance Status:** A decline in your overall physical condition or quality of life, particularly if it's related to cancer progression, may also suggest that it's time to switch therapies.
### 4. **Treatment Duration and Expectations**
- **Expected Duration of Response:** On average, patients respond to Abiraterone for about 12-24 months, though this can vary. If the treatment has been effective for a while but starts to lose its impact, it may be time to consider alternative options.
- **Clinical Judgment:** Oncologists will also use their clinical judgment, considering factors like how long you’ve been on the treatment, how rapidly the disease is progressing, and your overall health.
### 5. **Decision Process**
- **Regular Monitoring:** During Abiraterone therapy, you will typically have regular PSA tests, imaging scans, and assessments of symptoms to monitor the effectiveness of the treatment.
- **Consultation with Oncologist:** Your oncologist will evaluate all the data—PSA trends, imaging results, and symptoms—to determine whether Abiraterone is still effective or if it’s time to switch to another treatment.
- **Consideration of Next Steps:** If Abiraterone is deemed to have failed, your oncologist will discuss alternative treatment options, which may include switching to another androgen receptor pathway inhibitor (like Enzalutamide), starting chemotherapy again, considering radionuclide therapy (like Lutetium-177 PSMA), or enrolling in a clinical trial.
### Summary:
Abiraterone plus Prednisolone is considered to have failed when there is clear evidence of disease progression, as indicated by rising PSA levels, worsening symptoms, and/or radiographic progression. This decision is made based on a combination of these factors, guided by regular monitoring and close consultation with your oncologist. If progression is confirmed, the next step is to explore other treatment options that may be more effective in managing your disease at that stage.
Good question. Maybe. I have to look into it. We have to look always as is. Even when my MO say something to me I never asked for reference. Usually I just try to dig it up myself. When I do that I learn much more.
What would you like to know? I will try to dig it up for you and by that I will learn myself a lot. Please ask for a specific information.
When I see numbers I question the age because a person that is 78, 88 to 98 and you at 66 makes more sense to me for your numbers.
I’ve been told that if a man lived to 100 most likely he will have had PC or will get it.
Age, diet and exercise becomes lacking, the more the average male ages. Opening to higher numbers on that individual.
So if you were 78-88 and showing the numbers you have would be extremely good. For you and your life style you are very fortunate and not very alarming. Watchful eye is key to a better outcome in the years ahead. Full steam ahead warrior 👍
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Scans other than PSMA for PC
Risk vs rewards of allowing psa to rise high enough for a PSMA PET CT
Why do Bone Scans and CT Scans if PSMA-Pet are available?
