Unexpectedly had cell call while some 30ish miles down a rough rode at about 8,300' elevation in the River Of No Return Wilderness, ID. It was MO in Houston, TX.
Will have second opinion (std request of mine) confirmation of lesion on my liver, at uPSA 0.033.
Still awaiting result on GUARDANT360 CDx liquid blood biopsy, done concurrently.
This is all I know and who knows? Nonetheless , why I self-direct investigative efforts well ahead of 'common guidelines'. For past nine years unwilling to give this beast time and obscurity.
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By consulting with doc's that think and act ahead of 'common guidelines'. It's my third in three years at 0.03X range; Ga 68 and two Pylarify. First two were 'clear'. Covered by private insurance and Medicare. Given that the Ferrotran nanoparticle MRI I had over six years ago, at 0.11, identified five suspicious pelvic lymph nodes, with six confirmed by salvage ePLND, I believe firmly in <0.010 as best indicator post RP and values above likely indicating cancer remains.
- Performed using the frozen section pathology method. Cancer was confirmed in six pelvic nodes.
6. **Annual Investigations**
- **PSMA PET with mpMRI**
- **GUARDANT360 CDx Liquid Biopsy**
### Supplements and Diet (which may also have systemic effects)
- **Curcumin**
- **EGCG (Epigallocatechin gallate)**
- **Sulforaphane**
- **Resveratrol**
- **Genistein**
- **Bergamot**
- **Lycopene**
- **Boron**
- **Vitamin D**
### Diet Strategies
- Reduced methionine and choline intake.
- Minimal processed/industrialized foods.
- Regular consumption of organic cruciferous vegetables, onions, garlic, berries, with limited meat, fish, and refined sugars.
Additionally, they maintain ferritin levels below 50 ng/mL due to a recent diagnosis of hemochromatosis, adding another reason to monitor their ferritin closely.
That is what the AI know about you. I had to feed manually your profile and asked for the summary because ChatGPT could not see it through a link.
"I can't access external websites directly, including specific user profiles on platforms like HealthUnlocked. However, if you describe the treatments or medications mentioned, I can help you understand them or provide more information about them."
I generally agree with your thought and prefer to read original comments based on personal experiences. However, the information Seasid has posted IMO is general and not subject to too much debate, he is not diagnosing me, and is speaking from at least some relative experience. Also, he has saved me time which I appreciate.
First, further investigation. I declined STAMPEDE seven years ago and remain confident in that decision. I PSA test monthly/bi-monthly and imagine annually with concurrent liquid blood biopsy, knowing ADT may come.
What do you plan to do? Liver metastasis should be treated promptly otherwise it is too late.
From ChatGPT ( please check for relevance):
Certainly, here's a refined list of treatment options specific to managing liver metastasis in prostate cancer:
### 1. **Systemic Therapy**
- **Androgen Deprivation Therapy (ADT):** Initiating or intensifying ADT could help control the cancer’s spread by reducing androgen levels.
- **Next-Generation Anti-Androgens:** **Enzalutamide** or **Apalutamide** could be considered in combination with ADT, especially if the disease is progressing despite low PSA.
- **Chemotherapy:** **Docetaxel** or **Cabazitaxel** might be suitable, particularly if the liver metastasis suggests a more aggressive cancer behavior.
### 2. **Targeted Therapy**
- **Stereotactic Body Radiation Therapy (SBRT):** This highly precise form of radiation could be used to target and treat the liver metastasis directly, especially if it’s a solitary lesion.
### 3. **Clinical Trials**
- Participating in clinical trials investigating novel therapies for metastatic prostate cancer, such as advanced targeted treatments, might be an option. This could include trials for new systemic agents that specifically target liver metastases.
### 4. **Immunotherapy**
- **Pembrolizumab (Keytruda):** Could be considered if the tumor has specific genetic characteristics like microsatellite instability (MSI) or a high tumor mutational burden (TMB), although this is less common in prostate cancer.
### 5. **Liver-Directed Therapies**
- **Transarterial Chemoembolization (TACE):** A localized treatment that delivers chemotherapy directly to the liver metastasis, potentially reducing systemic exposure and side effects.
- **Radioembolization:** Involves delivering targeted radiation to the liver metastasis via the bloodstream, which can be particularly effective for controlling liver-specific disease.
- **Surgical Resection:** If the liver metastasis is isolated and surgically resectable, removing the lesion might be an option, though this depends on the patient’s overall health and other factors.
### 6. **Monitoring and Palliative Care**
- Continued monitoring with imaging (such as PSMA PET scans) is important to track the progression. Palliative care measures may also be considered to manage symptoms and maintain quality of life.
### Considerations
- **Focus on Liver-Specific Treatment:** The above options focus solely on addressing the liver metastasis, whether through systemic or liver-directed therapies.
- **Coordination with Specialists:** A hepatobiliary surgeon, medical oncologist, and radiation oncologist should collaborate to create a personalized treatment plan.
These options should be discussed with his healthcare team to determine the best course of action based on his overall health, disease progression, and personal preferences.
What do I plan to do? As always for me, consult with my medical team. As may be obvious, I am steps ahead getting imaging and liquid blood biopsy at 0.033 - purpose of my post. I appreciate the quick summary of strategies.
If I have in your situation I would also perform a liver fibroscan in order to monitor in real time your liver health. Fibroscan is a non invasive ad quick procedure you can perform as often as you want. I am doing it yearly. You could also ask for an abdominal ultrasound.
Thanks! well, in addition to PC and two melanomas, I have hemochromatosis, with recent liver MRI - no lesion noted on that. I am camping in woods in Idaho through early fall with medical team in Houston. Although Starlink provides excellent connectivity may have to rethink current plans.
I act quickly - again - my purpose for this post is that I self-direct imaging at 0.03X; third PSMA in three years. A few members speak against ultrasensitive PSA testing and the imaging I just did. Had I listened to them I would not have had this imaging nor been uPSA testing bi-monthly. There is always the possibility of a radiology reading error - but I am not counting on this.
Could you just find out from your medical team and also ask for second opinion from a radiation oncologist specialising in proton beam radiation therapy? It supposed to be less toxic to the healthy liver tissue. I am not a doctor but it is my guess that they will recommend SBRT with MRI Linac because they maybe don't have proton therapy on their site.
Not a diagnosis yet - but a clear PSMA avid lesion compared to last year's Pylarify. Taking steps for 2nd opinion including comparison to 'clear' Ga 68 done in 2022. I recently had a MRI Abdomen w/o contrast for iron deposition - I have hemochromatosis. No indication of lesion - perhaps not surprising with no contrast.
Currently planning further investigative strategy. Of course I am hoping for the "false positive" which I do not see as a negative warranting "do not image at very low PSA". As I also have had two melanomas, I really like begin skin biopsies and hence I see a 'false positive' in this instance as a great outcome.
My focus is to stay ahead of this challenging beast and not give it time and obscurity.
Q. Would for the above patient with the newly diagnosed liver metastasis on the PSMA pet scan a proton radiation therapy he possible or give any better results than an SBRT radiation therapy with high precision MRI Linac machine?
A. For a patient with newly diagnosed liver metastasis from prostate cancer, both **Proton Radiation Therapy** and **Stereotactic Body Radiation Therapy (SBRT)** using a high-precision MRI Linac machine are advanced radiation options, each with unique advantages and considerations.
### Proton Radiation Therapy
- **Mechanism:** Proton therapy uses charged particles (protons) instead of photons (X-rays) to deliver radiation. The key advantage of proton therapy is the "Bragg peak" effect, where the radiation dose is concentrated at a specific depth (the tumor) with minimal exit dose, sparing surrounding healthy tissue.
- **Advantages:**
- **Precision:** Proton therapy can precisely target tumors with minimal damage to surrounding tissues, which is particularly beneficial in sensitive areas like the liver.
- **Reduced Side Effects:** Lower risk of radiation-induced damage to nearby organs, such as the stomach or intestines, which is crucial for liver metastasis treatment.
- **Challenges:**
- **Availability and Cost:** Proton therapy is not as widely available as other forms of radiation and is typically more expensive.
- **Clinical Evidence:** While promising, there is still limited evidence directly comparing proton therapy to SBRT specifically for liver metastases in prostate cancer.
### SBRT with High-Precision MRI Linac Machine
- **Mechanism:** SBRT delivers high doses of radiation in a few fractions with sub-millimeter precision. MRI-guided Linac machines provide real-time imaging, allowing for precise targeting and adaptation to tumor movement (e.g., due to breathing).
- **Advantages:**
- **Real-Time Imaging:** The use of MRI allows for continuous visualization of the tumor during treatment, ensuring the radiation is delivered precisely even if the tumor shifts slightly.
- **Proven Efficacy:** SBRT is well-established for treating liver metastases, with a strong track record of effectiveness in controlling small, localized tumors.
- **Accessibility:** More widely available than proton therapy, and generally less expensive.
- **Challenges:**
- **Radiation Exposure to Surrounding Tissue:** Although SBRT is highly precise, it still uses X-rays, which means some radiation exposure to surrounding tissues, though typically minimal with modern technology.
### Which is Better?
- **Clinical Outcomes:** The clinical outcomes between proton therapy and SBRT for liver metastases are generally comparable, with both showing high rates of local control for small, well-defined tumors.
- **Tumor Characteristics:** The choice may depend on the specific characteristics of the liver metastasis, such as its size, location, and proximity to critical structures. Proton therapy might be favored if the metastasis is near particularly sensitive areas that would benefit from reduced radiation exposure.
- **Patient Factors:** The decision might also depend on the patient’s overall health, ability to access a proton therapy center, and the potential for side effects.
### Conclusion
For this patient, **SBRT using a high-precision MRI Linac machine** is likely a very effective option, offering excellent precision and real-time imaging capabilities. **Proton therapy** could be considered if there are specific concerns about sparing adjacent healthy tissue, particularly if the liver metastasis is in a challenging location. However, in many cases, SBRT with an MRI Linac provides sufficient precision with the added benefit of being more accessible.
Ultimately, the decision should involve a discussion with a radiation oncologist who can assess the specific case details and determine which therapy would offer the best balance of efficacy, safety, and convenience.
Is your liver tumour in a sensitive location? I had a gallbladder polip 20 years ago it was a premalignant process picked up by abdominal ultrasound and an excellent operator resulting with a Laparoscopic cholecystectomy performed by professor Ross Smith in Royal north shore Hospital here in Sydney. Maybe you should check the imaging also with MRI and ultrasound to see better the extent of the spread.
Definitely use system therapy first this time because you don't want further spread of the cancer.
Gallbladder pre-maligmant for? Gallbladder cancer? Prostate cancer? Were they able to biopsy they polyps?
I have a few gallbladder polyps that I discovered about a year ago from upper right abdominal ache. They are small (3mm?) polyps that have not changed in size from two ultrasounds. But I have noticed a persistent ache start up since I went off of adt and abiraterone last month.
I will tell you honestly. The professor of gastroenterology at the royal north shore Hospital here in Sydney admitted that they have no experience with it but he said ( I was younger than 45 years old) that it was a good thing to remove it. It was growing and of course we didn't do any biopsy. I had also like you a little pain which wasn't there all the time plus indigestion plus my now ex wife was scared that she will lose me and pushed me into the operation. My polip was a fundal polip and on the dopler ultrasound they noticed vascularization of the polip. It was long time ago and has nothing to do with PC. I went to the second opinion to one Macedonian GP here iim Sydney who was working before in a military hospital in Belgrade Serbia and decided to move first to England and than to Australia. He said that a gallbladder malignancy is very aggressive and ones you diagnosed it the next day you are gone. Therefore that also contributed that I had the operation, otherwise I probably would not. I had a meeting with the gastroenterologist first in a st Vincent's Hospital and he didn't recommend anything but than I went to see a professor of gastroenterology in a Royal north shore Hospital and he referred me to the surgeon. I believe his name was Danlop but I can't recall exactly. The surgeon than referred me to professor Ross Smith.
In Japan I believe 3 percent of the population has polips in the gallbladder. My growth bigger than yours but I was suspected that maybe first time they didn't measure correctly the size of the polips. The professor of gastroenterology requested a special operator and after that we know the correct size and a vascularization of the polips to the fundus of the gallbladder to the liver. My Laparoscopic cholecystectomy was 2 h 15 minutes long.
"It sounds like your case was carefully evaluated, especially given the concern about the growth and vascularization of the polyps. It's good that a specialized operator was involved to ensure the correct measurement and assessment, which is crucial in determining the best course of action. A laparoscopic cholecystectomy typically takes about 1 to 2 hours, so your surgery lasting 2 hours and 15 minutes suggests it might have been a complex procedure, possibly due to the size and location of the polyps.
If there's anything specific you'd like to discuss about the surgery or its aftermath, feel free to share."
"It’s great to hear that the surgery was successful and bloodless, especially considering the complexity of removing both the gallbladder polyps and the liver lump. The precision and care taken during the procedure must have contributed to a smooth operation. How are you feeling now in recovery?"
"It's impressive that you were able to get back to such an active routine the very next day after surgery. It sounds like you recovered remarkably well!"
Q. What is more important in an early stage of the liver metastasis treatment, a system treatment or a local control of the prostate cancer in the liver?
A. In the early stage of liver metastasis from prostate cancer, the decision between prioritizing systemic treatment versus local control depends on several factors, including the biology of the disease, the extent of metastasis, and the patient’s overall health and treatment goals. Here's a breakdown of the considerations:
### 1. **Systemic Treatment**
- **Purpose:** Systemic therapy addresses not only the visible metastasis but also potential micrometastatic disease that may not yet be detectable. This approach is important because metastatic prostate cancer is generally considered a systemic disease.
- **When It’s Prioritized:**
- **Widespread Disease:** If there is concern that the cancer has spread beyond the liver metastasis (even if not yet visible on imaging), systemic therapy is crucial to control the overall disease.
- **Aggressive Cancer:** If the liver metastasis reflects an aggressive form of prostate cancer, systemic treatment with ADT, chemotherapy, or next-generation anti-androgens might be more effective at controlling the disease and preventing further spread.
- **Preventing Further Metastasis:** Systemic treatment can potentially slow the progression and prevent new metastases from forming.
### 2. **Local Control**
- **Purpose:** Local control focuses on directly treating the liver metastasis to eliminate or shrink it. This can involve surgical resection, SBRT, or other liver-directed therapies.
- **When It’s Prioritized:**
- **Oligometastatic Disease:** If the metastasis is limited to the liver and is the only known site of spread (oligometastatic disease), local control can be very effective. Treating the liver metastasis directly may offer the possibility of longer remission or even cure in some cases.
- **Symptomatic Metastasis:** If the liver metastasis is causing symptoms (e.g., pain, liver function abnormalities), local control may be prioritized to alleviate these issues.
- **Limited Systemic Disease:** If systemic disease is minimal or well-controlled, focusing on the liver metastasis with local treatment could be a key strategy in prolonging survival and maintaining quality of life.
### Balancing Systemic and Local Control
- **Combined Approach:** Often, the best approach involves a combination of both systemic therapy and local control. Systemic therapy can address any microscopic disease, while local control can target the visible metastasis in the liver. For example, systemic therapy may be started first, followed by local treatment of the liver metastasis once the disease is better controlled.
- **Sequential or Simultaneous Treatment:** Some strategies involve starting systemic therapy and, if the liver metastasis remains stable or shrinks, proceeding with local treatment (such as SBRT or surgery). Alternatively, local treatment may be used first if the metastasis is solitary and well-defined, followed by systemic therapy to maintain control.
### Conclusion
In an early-stage liver metastasis from prostate cancer, **systemic treatment** is generally crucial to address the overall disease and prevent further spread. However, **local control** of the liver metastasis can be equally important, especially in cases of oligometastatic disease where aggressive treatment of the metastasis might offer significant benefits.
The optimal strategy is often a tailored approach that combines both systemic and local therapies, determined by factors such as the extent of the disease, the patient’s overall health, and specific treatment goals. Consultation with a multidisciplinary oncology team is essential to develop the best treatment plan.
If you are still not sure in the interpretation of your last PSMA pet scan I recommend you to send it to professor Emmett here in St. Vincent's Hospital in Darlinghurst, Sydney. She interpreted all six of my PSMA pet scans. I could recommend her as I trust her very much.
thank you very much Seasid for all your shares. I shall add Professor Emmett to my US and European list of additional radiology opinions. And of course one must be ready to process different medical opinions; which do we choose to rely on?
My standard advice: "Measure twice, cut once". In your case, confirm by a second radioligand that it isn't excreted through the urinary track. There is one FDA approved, although we have in Europe the 1007 which is bad mouthed over there as providing many false positives. These are the same people that say nothing will show up bellow PSA of 0.2 or 0.5 (pick your magic number of choice). How do they know that the purported "false positives" are not lesions attracting PSMA above the concentration achievable by Pylarify, is just another assertion of silly docs and their parrots.
Thanks! Just got the initial call yesterday. Having had two melanomas out of maybe eight skin biopsies of course I am hopeful for a 'false positive' or a benign biopsy.
However, given that my 'done in Europe' Ferrotran nanoparticle MRI successfully identified cancerous pelvic lymph nodes at 0.11, I will not be dismissive like some, and as I am clearly not a naysayer about imaging at these very low PSA levels, nor dismissive of ultrasensitive PSA testing, I will be seeking additional radiology opinions and certainly considering further investigations as this just might be cancer - the very reason I had the Pylarify and liquid blood biopsy.
As to which radioligand is 'best'', seems to me we just don't yet know. Why so far I have had Ga 68 and Pylarify, and do not dismiss others. sciencedirect.com/science/a...
The above treatment sounds good but I don't know how it compares to other types of treatment for liver mets. Thank you for keeping us informed of your approach. All information is useful. Good luck with your next treatment plan.
False positives can occur in PSMA PET scans for liver metastasis in prostate cancer. While PSMA (Prostate-Specific Membrane Antigen) PET scans are highly sensitive for detecting prostate cancer metastases, including in the liver, several factors can lead to false positives:
1. **Benign Liver Lesions:** Non-cancerous liver conditions like hemangiomas, focal nodular hyperplasia, or regenerative nodules can sometimes show PSMA uptake, leading to false positives.
2. **Inflammatory Conditions:** Liver inflammation or infections, such as hepatitis or abscesses, can also result in PSMA uptake, which might be mistaken for metastasis.
3. **Other Malignancies:** If the patient has other cancers that can express PSMA or uptake PSMA tracers (such as some types of liver cancers), this might lead to false positive results.
4. **Radiotracer Uptake Variability:** Variability in the uptake of the PSMA tracer can sometimes cause non-cancerous liver tissue to appear suspicious on imaging.
To reduce the likelihood of false positives, PSMA PET scan results are usually interpreted alongside other imaging modalities (like MRI or CT) and clinical information. If a suspicious lesion is identified, further testing or biopsy may be required to confirm whether it is a true metastasis or a false positive.
Seasid again thank you for all your shares. I am happy to have a "false positive" as I do not see these as negatives. My intent with investigative methods is to rule out advancing prostate cancer. As I share I learned to not give this beast time and obscurity.
And as shared in another comment last years Pylarify did not indicate this lesion, neither did my 2022 Ga 68. But given that my cancer spread to para-aoric node and my PSA has risen through 0.01, 0.02 and into 0.03 range, keeping a very close watch.
Liver metastasis as the first site of recurrence in prostate cancer is uncommon but not impossible. Prostate cancer typically metastasizes first to the bones, followed by lymph nodes, lungs, and, less frequently, the liver. However, certain factors could make liver metastasis appear as the first or an early sign of recurrent prostate cancer on a PSMA PET scan:
1. **Aggressive Tumor Biology:** Some prostate cancers are more aggressive and have a higher likelihood of spreading to visceral organs like the liver early in the disease course, especially if the cancer has developed a more aggressive phenotype over time.
2. **Prior Treatments:** Previous treatments, such as androgen deprivation therapy (ADT), chemotherapy, or radiotherapy, might suppress or eradicate metastases in more common sites (like bones), allowing liver metastasis to emerge as the detectable site of recurrence.
3. **Subtype of Prostate Cancer:** Rare variants of prostate cancer, like neuroendocrine or small cell prostate cancer, may have different patterns of spread and could involve the liver earlier.
4. **Diagnostic Sensitivity:** PSMA PET scans are highly sensitive, and in some cases, liver metastasis might be detected earlier on a PSMA PET scan before other more typical metastatic sites become evident.
While it is less common for liver metastasis to be the first sign of recurrent prostate cancer, it is a possibility, especially in cases of aggressive or atypical disease progression. Further clinical evaluation, including the patient's overall disease history and possibly a biopsy, would be important to confirm the nature of the liver lesion.
My third treatment, over six years ago, salvage extended pelvic lymph node surgery with frozen section pathology method confirmed six cancerous nodes, including common iliac and para-aortic, so this would not be first site of recurrence.
do not have yet - first call was just yesterday. I am camping in woods of Idaho USA, communicating with medical team in Houston, TX via Starlink satellite network.
I really hope that you are not so unlucky to develop liver metastasis. Can't you ask for such a basic information like the PSMA SUV Max value of the prostate cancer liver metastasis?
Yes this and additional information is forthcoming. When I got the call about 36 hours ago I was in the River Of No Return Wilderness looking for signs of wolves and Bighorns.
There has been a paper from Germany, small cohort though, claiming better detectability using Zirconium-89 isotope labelled radio ligand having far longer half life (78.4 hr), thus attaining higher tracer concentration with time.
"Pylarify vs PSMA 1007 sensitivity to liver prostate cancer metastases"
ChatGPT responce:
"When comparing the sensitivity of ^18F-DCFPyL (Pylarify) and ^18F-PSMA-1007 for detecting liver metastases in prostate cancer, several key factors should be considered:
Radioisotope and Ligand Characteristics
Both Pylarify and PSMA-1007 use the ^18F radioisotope, providing similar benefits regarding positron energy, image resolution, and half-life (~110 minutes). However, the chemical properties and biodistribution of these ligands can influence their effectiveness in detecting metastases in different organs.
Tumor-to-Background Ratio and Biodistribution
Pylarify (^18F-DCFPyL):
Advantages: Pylarify is known for its high sensitivity and excellent tumor-to-background ratio. It has been widely validated in clinical settings, demonstrating strong performance in detecting prostate cancer metastases, including in the liver. Pylarify’s uptake in soft tissues allows for clear visualization of metastatic lesions.
Clinical Performance: Pylarify generally shows high sensitivity and specificity for detecting prostate cancer lesions due to its favorable biodistribution.
PSMA-1007:
Advantages: PSMA-1007 is notable for its low urinary excretion, reducing bladder activity, which is particularly beneficial for pelvic imaging. This characteristic, however, also affects its biodistribution and uptake in organs such as the liver.
Liver Metastasis Detection: PSMA-1007 has shown promising results for detecting liver metastases, with potentially higher uptake in the liver compared to Pylarify. This can lead to improved sensitivity for liver lesions specifically.
Comparative Studies and Clinical Data
Sensitivity and Specificity: Comparative studies suggest that both Pylarify and PSMA-1007 offer high sensitivity and specificity for detecting prostate cancer metastases. However, PSMA-1007 may have a slight edge in detecting liver metastases due to its distinct biodistribution properties that favor higher liver uptake.
Clinical Preferences: While Pylarify is well-established and widely used, PSMA-1007’s reduced urinary excretion and potential for higher liver uptake might make it more suitable for detecting liver metastases in certain cases.
Conclusion
While both ^18F-DCFPyL (Pylarify) and ^18F-PSMA-1007 are effective for detecting prostate cancer metastases, including those in the liver, PSMA-1007 may offer a slight advantage in sensitivity for liver lesions due to its biodistribution profile that results in higher liver uptake. Pylarify remains highly sensitive and widely validated, making it a strong option in clinical practice. The choice between these ligands can depend on specific patient circumstances and clinical preferences."
Same for Posluma (FDA approved) vs Pylarify:
".....
^18F-Posluma (Flotufolastat F-18)
Mechanism: ^18F-Posluma targets PSMA similarly to Pylarify but uses a different ligand with potentially unique binding and imaging properties.
Pharmacokinetics: Posluma has shown favorable characteristics in clinical studies, with a high tumor-to-background ratio that helps in detecting prostate cancer metastases. Its uptake patterns might provide different sensitivities compared to other PSMA ligands.
Clinical Studies: Early studies suggest that Posluma is effective for detecting prostate cancer metastases, including in the liver. However, specific comparative studies with Pylarify are still emerging.
.....
Comparative Sensitivity for Liver Metastases
^18F-Posluma: Emerging data suggests that Posluma has potential advantages in detecting liver metastases due to its unique pharmacokinetics and binding properties. Its effectiveness might be comparable to or exceed that of Pylarify in certain settings.^18F-DCFPyL (Pylarify): Pylarify is established as a highly effective agent for detecting prostate cancer metastases, including those in the liver, due to its excellent imaging characteristics and high sensitivity.
Summary
Both ^18F-Posluma (Flotufolastat F-18) and ^18F-DCFPyL (Pylarify) are effective for detecting liver metastases from prostate cancer, but the choice between them may depend on specific clinical needs and available data. ^18F-Posluma is promising and may offer advantages due to its distinct imaging properties, while Pylarify remains a well-established and highly effective option with robust clinical validation.
For the most up-to-date information, reviewing recent comparative studies and clinical trials would provide the best insights into their relative sensitivities and performance in detecting liver metastases".
Thanks again! Such a challenging disease and so many disparities.
I find it baffling that so many men and docs scuff at imaging at very low PSA levels. As if, the "win" is waiting until many mets can be found instead of finding first indication.
"And yet it moves" (in Latin, "E pur si muove") attributed to Galileo Galilei. According to legend, Galileo muttered this phrase after being forced to recant his support for the heliocentric model of the solar system, which posited that the Earth moves around the Sun.
imaging at these levels misses cancer. It is unfortunate that this is characterized as failure so let's not try. Takes focus off cancer is present, growing and spreading. If it 'works' for some men, as the Ferrotran nanoparticle MRI did for me over six years ago at 0.11, what a success for the men imaging works for.
sorry to hear Nani. Wishing you the best. Just curious. Is your cancer ductal prostrate cancer? I ask because I have ductal, and it became metastatic two years ago, with very low PSA readings. Been on ADT and zytiga since, and PSA was undetectable for two years. Most recent test has it at 0.06, which has me concerned. Ductal cancer is usually associated with low PSA results. Just curious
Thank you! I am hopeful this may be 'false positive' that is often used as reasons to not screen.
No, I do not have a diagnosis of ductal cancer. What I do have is strong indication that I have low PSA results. Many docs have been surprised by the volume of cancer my salvage ePLND identified - six pelvic nodes including common iliac and para-aortic, at uPSA 0.11.
This thread has been quite informative for me. Thanks to you and SeaSid, Justfor and others. I found the Chat GPT postings to conform to established evidence based guidelines and the usual caveats quite well. Yet not picking up any non SOC options that may be worthy of consideration with less mature evidence to support them and yet with possible utility and low risk for certain patients. Perhaps the emerging leading edge? Anyway, thanks for the discussion and best wishes for each or you. Paul / MB
P.S. I would be curious about a Chat GPT on preventing or slowing the progression of prostate cancer at stages such as BCR after primary treatment of the prostate, or of preventing progression of HSPC to CRPC and non metastatic to metastatic? These progressions are driven by the "Hallmarks of Cancer" and are underpinned primarily by inflammation and genetic instability. What would be optimal strategies to restrain progression?
Great question - what would be optimal strategies (plural) to restrain progression?
Removing tumor burden is key strategy of mine - main reason I chose RP for my primary treatment and salvage extend pelvic lymph node surgery after my unsuccessful salvage RT.
Imaging: Nearly ten years ago a urologist in the UK introduced me to multiparametic MRI - my US urologist had never mentioned this despite a rising PSA as my 50's progressed. Multiple docs concluded the mpMRI indicated my cancer had likely gotten out.
Discerning Ultrasensitive PSA testing, (dispite the naysayers), has been and is for me an optimal strategy. My post RP nadir was 0.050 - we accepted cancer remained. I tried salvage RT to prostate bed at 0.11, shooting blind (no Ferrotran nanoparticle MRI, no PSMA), which resulted in a nadir of 0.075. We immediately knew cancer had spread beyond the prostate bed.
Liquid blood biopsy testing is my 'latest' strategy.
The topic of this thread, PSMA and other imaging at very low PSA is another optimal strategy of mine. If the Ferrotran nanoparticle MRI was available I would be making plans to go to Europe for my second if this current Pylarify finding is confirmed to be concerning. Not for confirmation of this finding but more importantly what might the Pylarify have 'missed', for if I indeed have more than one lesion my treatment strategy might change.
I recognize ADT restrains progression but my focus since diagnosis has been and continues to be to defer this non-optimal strategy for as long as possible, and thereby, deferring the possibility (likelihood) of CR for as long as possible.
I do take supplements, phytochemicals listed in bio, that get acknowledgment as cancer stem cell fighters. IDK, and do not think of them as an optimal strategy, but a strategy none-the-leas.
Have you considered a very short ADT course (few weeks) that amplifies PSMA receptors on the cancer then do a scan? the amplification effect has been researched pretty extensively but is not yet standard.. The amplification can be 2-3x for non metastatic and higher for metastatic colonies. In theory that could bring the visibility up enough to see them.
Appreciate the thought - one it seems few docs would suggest. I am aware of this technique but have not yet given it much thought in this 0.03 range. My thinking could change if when PSA moves up into 0.04+ range; been holding 0.03X for over three years now. I do understand imaging identifying mets at my very low PSA is generally unlikely, however, over six years ago learned this is done in Europe beginning at 0.03 in hope of remaining cancer being in one or two sites and not dispersed in more smaller sites. (Time for a bit of luck).
Awaiting 2nd opinion of this Pylarify, including comparison to Ga 68 done three years ago. This current Pylarify has been compared to last years Pylarify.
If findings confirm concern, I would like to get the Ferrotran nanoparticle MRI, especially if I add ADT amplification. Perhaps to some (maybe many) over the top crazy (and futile) investigations but I remain focused on doing all I can, if it comes to it, to defer ADT as long as possible.
Detecting liver metastasis at a uPSA level of 0.033 ng/mL using a PSMA PET scan is challenging and somewhat unlikely, but not impossible. Here are a few key points:
1. **PSMA Expression in Liver Metastases:** Liver metastases from prostate cancer do express PSMA, but the level of expression can vary. PSMA PET scans are highly sensitive, but their ability to detect very small or early metastatic lesions is generally better when PSA levels are higher.
2. **Detection at Low PSA Levels:** While PSMA PET scans can detect metastases at relatively low PSA levels, the probability of detecting liver metastasis at a PSA of 0.033 ng/mL is low. Most successful detections are reported at PSA levels above 0.2 ng/mL. However, if the metastatic lesion is large or highly active metabolically, it could still be detected.
3. **Risk of False Positives:** At such a low PSA level, the possibility of false positives increases. This could be due to non-specific uptake of the tracer in other tissues or benign liver lesions that may also express PSMA to a minor degree, leading to potential misinterpretation.
4. **Clinical Context:** If a liver lesion is detected at this PSA level, the clinical context and any prior imaging or clinical data would be crucial in interpreting the finding. A multi-disciplinary discussion involving the oncologist, radiologist, and potentially a nuclear medicine specialist would be important to determine whether a detected lesion is likely to be a true positive or a false positive.
Given the low uPSA level, if a PSMA PET scan does detect a liver lesion, further investigation would be warranted to confirm whether it is indeed a metastasis or a false positive. This might include additional imaging, biopsy, or follow-up scans as the uPSA level changes.
You should see at least if your PSA is still going up and how fast. I would probably repeat the PSA test to see if it is dropped, same as before or going up. We don't even know if on the PSMA pet scan is it possible to see anything at your current PSA level? Maybe it is fauls positive result but we don't even know what is the SUV Max value of your supposed liver metastasis which should not be even detected at such a low PSA. Sorry it is only my thinking. What your doctors think about this?
Maybe you are just unlucky to have a faulty PSA lab test in a same time when someone see something on the PSMA pet scan what we don't know anything about. I would reapet at least a PSA test.
Q. Could the PSMA pet scan pick up something at extremely low uPSA 0.033?
A. A PSMA PET scan is generally most effective at detecting prostate cancer metastases when PSA levels are higher. While it has high sensitivity, especially compared to traditional imaging techniques, its ability to detect cancer at extremely low uPSA levels, such as 0.033 ng/mL, is quite limited.
At such low levels, the chance of the PSMA PET scan detecting anything is relatively low. Studies suggest that the detection rates improve significantly as PSA levels rise, with better results typically seen at PSA levels above 0.2 ng/mL. However, the technology is constantly improving, and some centers may have advanced techniques that might increase the sensitivity at very low PSA levels.
If your PSA level is steadily rising, even at such low levels, your medical team might recommend close monitoring and possibly a repeat scan at a slightly higher PSA level to increase the likelihood of detecting any recurrence or metastasis.
I have had nearly 100 PSA tests over 10+ years, different labs, different US States, even different countries; never seen a faulty one.
As shared in bio my bi-monthly testing has been holding very low stable 0.03X range for over three years, no ADT. Tested just last week, 0.031.
Plan is for 2nd PSMA Pylarify opinion this week including comparison to Ga 68 three years ago. Also awaiting result GUARDANT 360 liquid blood biopsy.
Several next step opinions on table, including the suspicious site might be ruled out for concern. As has been my strategy for ten years will continue to do all I can to defer ADT and thereby possibility of CR for as long as possible.
I understand. I wish you luck to troubleshoot the possibility of the liver metastasis. If you start ADT then consider Degarelix injections because when you stop your testosterone will recover quickly.
"Your approach to managing your prostate cancer with close monitoring and regular testing shows a strong commitment to staying informed and proactive about your health. The consistency in your PSA levels over a long period, particularly in the 0.03X range, is encouraging, especially without androgen deprivation therapy (ADT).
Given that you are undergoing a second PSMA Pylarify PET scan for comparison with a previous Ga-68 scan, it sounds like you're taking all the necessary steps to ensure that any potential areas of concern are thoroughly investigated. The PSMA scan comparison will provide valuable insights, particularly if there have been any changes or developments in the suspicious area that was identified previously.
Your plan to delay ADT as long as possible, with the goal of avoiding or postponing castration resistance (CR), is understandable given the long-term side effects associated with ADT. By using advanced imaging and blood biopsy techniques like the GUARDANT 360, you're ensuring that any decisions regarding further treatment are made with the most comprehensive information available.
It's also wise that you're gathering multiple opinions on the next steps, as managing prostate cancer, particularly in the context of your history and current stability, can involve complex decision-making. By continuing to monitor closely and defer more aggressive treatments, you're aligning with a strategy that prioritizes quality of life while maintaining vigilance against progression.
If you have any specific questions about your test results, the implications of the second PSMA scan, or how to interpret the GUARDANT 360 results, feel free to ask."
It was not me. It was ChatGPT. I would just add that I am myself always concerned about the even remote possibility of fauls laboratory results.
trends are reliable - individual results are just singular. Why I test more frequently than the common 2-4 times a year. ChatGPT is interesting - thank you for introducing the process.
If you start using the AI app you will be presently surprised and they are getting better. My sister was angry at me why I didn't tell her earlier to start using it. I already learnt lots of new things by using the AI. Recognised that even doctors don't know everything because asking the AI I could get a better answer. Of course AI don't have the experience of the doctors and has lots of limitations but as a tool is perfect if you understand the limitations. It is to easy to dismiss AI as garbage in garbage out.
I was/am not on ADT. I stopped my 150mg daily bicalutamide back in April 2019. This current Pylarify was compared to the one done two years ago - which was clear and no ADT. I am getting 2nd radiology opinion with comparison to Ga 68 done in December 2021; that was 'clear' also and no ADT. I have read your posts - so much for us to consider with imaging given that the knowledge and experience base is new and IMO insufficient and dictated by intentions that are not necessarily in the best interest of us the patients.
I must be missing something after reading this lengthy thread. PSMA PET sensitivity is 30-50% at PSA 0.2 - 0.5 and 20-30% at less than 0.2 ng/ml. Extrapolating that out a bit, I'd venture to guess less than 0.05 PSA is in the 5-10% sensitivity range. Is the theory that a lesion say, => 2mm is detectable due to lesion producing little PSA but high PSMA? 0.03x PSA seems the chances of a false positive are higher than a reliable positive?
I started to scan more in the later half of the discussion. Did I miss where there was some sort of definitive confirmation or are we all still just guessing?
The (PSMA) PET CT finding I share about in this posting identified a concerning liver lesion (not a false positive) that biopsied as metastatic melanoma. I have already completed two of four doublet immunotherapy treatments.
As to the often cited PSMA sensitivity stats; back in 2017 I became aware that PSMA imaging was established in much of Europe and other countries, and learned they begin imaging at uPSA 0.03 post RP in hope of finding a few treatable mets (yes, they need to be 'big enough').
With this knowledge I traveled to Netherlands with uPSA of 0.13 for a GA68 PSMA PET CT and other imaging including Ferrotran nanoparticle MRI. (Note, US was in 'trials' with PSMA PET CTs). Although the Ga68 PSMA was clear the concurrent Ferrotran nanoparticle MRI successfully identified multiple cancerous pelvic lymph nodes; six total confirmed by salvage ePLND using frozen section pathology method. Again at 0.13 and back in January 2018.
Based on my patient experiences 'false positives' reflect inexperience and I believe are a mantra for those who want to treat this disease as a chronic illness with ADT.
Thanks for the information. I most likely will be needing salvage radiotherapy. Prior to your post I was highly skeptical of even bothering with a PSMA PET at =< 0.1 PSA. Although to get SBRT in the salvage setting I believe it's only currently available through a clinical trial which if I recall actually requires a PSMA PET regardless of your PSA level. I will definitely look into the Farrotran nonparticle MRI. I suppose another way to look at it is even if imaging isn't 90%+ sensitive, more data is better to better inform decision making.
Yes, I agree more data is better. Sharing a perspective on your comment "I most likely will be needing salvage radiotherapy". If you (will) need it, based on my experiences, you need it today. But is all the remaining cancer still within the treatment field?
In 2015/16 when I was investigating salvation RT to prostate bed and pelvic region, I pondered self-paying for the fluciclovine and Choline PET CTs; but I allowed doc's to talk me out of both (I was insurance denied). I was also denied acceptance into PSMA trials. I regret not self-paying for the imaging, for if by chance even one little met was identified outside of the prostate bed I would not have had salvage RT. I wish liquid blood biopsies were available then.
I've been meaning to ask this and have forgotten....Regarding the benefit of liquid blood biopsies, if someone has findings of cancer markers on the blood biopsy, but, say you have a PSA <0.006 like mine, what would you do? Seems like that may offer no benefit other than it gives you a start on knowing where you are headed wayyy down the road (assuming that prostate cancer is the cause of the positive liquid blood biopsy). I know some (many) here already say the uPSA isn't useful (and are wrong IMO), but the liquid blood biopsy might take that to an entirely new level of absurdity in their minds.
To your question what would I do if I had a cancer marker on the blood biopsy at PSA <0.006, based on my current experience with the surprise finding of metastatic melanoma on my recent Pylarify PSMA PET and liquid blood biopsy, I would immediately begin further investigative methods.
To whether 'clear' LBB offer benefits and as to whether they are absurd at very low PSA levels, here is why I find them a valuable additional data point that my (likely) remaining cancer is not getting ahead of my PSA.
In June 2022 I had a Pylarify PSMA PET CT, done at (absurd uPSA 0.031; no surprise, it was clear. But, we know these clear findings are not unequivocal for no cancer and I have reason to question if my prostate cancer is PSMA avid. In March 2023 I had my first liquid blood biopsy - it was clear.
With those Three investigative findings (my uPSA holding very low stable 0.03X range; my clear Pylarify PSMA done nine months prior at same uPSA; clear LBB ), I was confident my (likely) remaining prostate cancer was not advancing.
With my uPSA still holding 0.03X range, and with Pylarify PSMA and LBB done this past July being NED for prostate cancer, I remain confident my prostate cancer is not advancing. (How fortunate am I these investigations have given me a better chance with this surprising melanoma cancer).
Having had cancer at my para-aortic lymph nodes at 0.13, my choice is to do these investigative methods rather than rely on say a PSA of <0.2 as undetectable, no reason for concern.
I came across this over the weekend. It is a 10min presentation from about 5 years ago that talks about many aspects of BCR. It is a good summary from UCSF. What I found most interesting (and concerning) is that the probabilities he states in the video regarding recurrence being in the prostate bed is much lower than I assumed it was. This video cites only about 15% of recurrences are in that prostate bed location, whereas many more occur in the lymph nodes and other distant areas (about 2x the number of prostate bed recurrence).
It seems like if one has positive margins that these odds may be a little different and are more skewed toward a prostate bed recurrence. However, if you don’t have a positive margin, then it seems to me it is much more likely to have a recurrence out of the bed—like almost two fold more likely to have pelvic lymph nodes or disease outside the pelvic area.
Pete is one of the several doctors around the West Coast I consulted with a little over 3 years ago. One thing I would wonder is that for those that had extended lymph node dissection at time of prostatectomy ( I think that's at least 12 if not more lymph nodes removed), and the pathology was negative for all of them, how does that effect the chances of recurrence in the prostate bed versus extended pelvic area?
I have seen one video where the doctor claimed they don't see recurrence in any areas that were radiated in salvage therapy. This combined with the video you are sharing indicates to me, virtually all salvage RT should be whole pelvic whether imaging shows lesions outside the prostate bed or not. I'm not sure if it's not pretty much always done because patients want to avoid seemingly unnecessary side effects, or if it's not approved by insurance. I doubt insurance would deny it in intermediate to high risk patients with no positive imaging results though.
If most recurrences are due to micro metastatic PCa cells circulating in the blood in a certain population of patients, SRT amounts to simply a delay tactic like ADT as opposed to a secondary treatment that is curative.
Thank you for this. If having SRT I was seriously considering WPRT with MRI Guided SBRT Boost to the Prostate Bed regardless if my imaging came back positive or negative. My post surgical pathology was good but I had iPSA of 31 and Cribriform pattern in my Gleason 3+4 (20% 4). With no adverse pathology (including clean lymph nodes) other than Perineal Invasion, if my PSA continues to rise, there may be a high chance I fall into the majority of patients where recurrence is outside the prostate bed. Enduring the increased side effect of WPRT could potentially be the difference between dying earlier of Prostate Cancer versus something else later.
Factors involved in decision making can be much different when you have recurrence in your mid 50's as opposed to your 70's. Being at a younger age may warrant a more aggressive strategy being better suited to tolerate the adverse effects when younger and with a potentially much longer remaining lifespan.
Excellent presentation by Carrol and jazj your summary is excellent for those pondering salvage RT to prostate bed.
As I share, if I had a do-over, I would not have salvage RT to the bed only; not saying I would have it to whole pelvic region. My RadOnc said to me, as we discussed my post salvage RT to bed nadir of 0.075, "you were supposed to be easy".
I can’t say I necessarily agree with everything in the following link, but it does present reason for optimism with respect to the slow nature of the disease and deciding on salvage therapies. They left one thing out: “It’s slow—until it isn’t.” In any event, here is the study. The PCSM numbers are starkly low—even if you do nothing.
Thanks for sharing as this post and accompanying video has made me rethink how I will proceed when salvage RT is considered. My pathology following RALP is nearly identical to “jazj” and I echo his insights and concerns. With a post-RALP pathology of 3+4 with clear margins, nodes & vesicles, the statistical data from UCSF suggests BCR is beyond the prostate bed. I’ve been undetectable for 4 years but my last 3 PSA labs over a 9 month period are in the .02 - .03 range. Hopefully I can have them remain in this range for years to come. I, too, wonder if the very slight rise in PSA could be connected to benign tissue as discussed on this forum…
I pondered this question of benign tissue post RP - my nadir was 0.051. My surgeon reviewed video of the operation and was confident as possible in his work. I studied up on whether a few left behind healthy prostate cancer cells could continue to survive and thrive, 'forever'. My patient conclusion, no. Today, nearly nine years post RP, eight years post salvage RT to bed and seven years post salvage ePLND, I do not think my very low stable uPSA of 0.030 can in anyway be healthy prostate cells. Just as I felt with a rising uPSA post RP.
I did several reads of both links you shared. They are similar to others I read over years. I don't question whether some small amount of benign tissue can be left behind, although neither article IMO provides convincing evidence such as biopsied tissue. What I do not find in these studies is even minimal irrefutable evidence that benign tissues thrive resulting in rising PSA levels that might suggest cancer remains (recurrence) when in fact no cancer remains.
I’m not advocating a belief in the links shared, I just thought it was an interesting postulate. Moreover, you’ve undergone some of the latest and best scanning techniques available; including the Farrotran nanoparticle MRI, and benign tissue hasn’t been identified. That’s enough evidence to confirm that benign tissue isn’t involved. Your excellent book, “Prostate Cancer: Sheep or Wolf”, has also given me insights I never would have otherwise considered. Thankfully we may no longer have to travel to Europe to obtain the Farrotran MRI as I believe it’s now available at the Mayo Clinic in Rochester? I may be making an appointment if my uPSA rises above the .02/.03 range. Best regards!
If you're not doing any sort of therapy post salvage ePLND all this time and your uPSA isn't rising, then I've never seen a stronger case for it being a little tissue left in the prostate bed? To the counterpoint though, most recent studies say two successive reading of 0.03 or higher is very high confirmation of BCR without mentioning possibility of remaining healthy prostatic tissue. Yet you are a case in point that it's not unheard of to hear reports of people being "stuck" in the 0.02X-0.03X range! (But for how long?) Statistically though those could be very rare exceptions to what the studies have born out.
I am happy to be "stuck'. A good discussion and I am always willing to revisit my thinking and my decisions. I have not done ADT at any time. I did one year of bicalutamide post salvage ePLND, but that is a blocker and it has been nearly six years.
If the source of my very low stable PSA is healthy left behind prostate cells, how have they survived and reproduced over the past nine years? How did they survive salvage RT? How were they missed by my salvage ePLND surgeon? Why have they not shown up as a mass on any of my imaging including Ferrotran nanoparticle MRI that identified multiple cancerous pelvic lymph nodes, any of my four PSMA PETs, multiple pelvic MRIs, current full-body imaging concerning my metastatic melanoma?
How does one exclude the possibility of the PSA source being lingering, hanging-on cancer stem cells, micro mets, senescent cells including senescent fibroblasts and macrophages, etc, (very limited patient knowledge here)? Perhaps cancer cells suppressed by having their asses kicked by four treatments, my ever improving diet and intense physical fitness, just maybe some success from my supplement regime?
There is a view that just too few cells remain to grow and spread, that they are barely hanging one. But then, they can morph. When I think of the number of men whose prostate cancer comes back after ten, fifteen, even twenty years, I do not have the answers, which is why remain on regular guard.
Studies – I have read/studied a many and often am a skeptic of the findings, for many reasons, including IMO insufficient numbers of involved men, broad categories for acceptance, etc. Years back, I looked for data from autopsies indicating the presence of a mass of healthy prostate cells in men who had prostatectomies, but I did not find even a one.
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uPSA 0.031; no surprise, it was clear. But, we know these clear findings are not unequivocal for no cancer and I have reason to question if my prostate cancer is PSMA avid. In March 2023 I had my first liquid blood biopsy - it was clear. 
What about Pylarify DCFPyL, 18F-PSMA-PET-1007 and 68Ga-PSMA-PET
PSMA PET Scan result - false positive bone lesion?
PSMA PET scan 
PSMA pet scan
