My oncologists (medical and radiation) had been pushing me to have a PSMA scan for two years. Even though in 2023 my PSA rose from .67 to 1.37, I pointed out that a PSMA scan would not change my treatment. We ran another Axumin PET in January, which was stable, if not better, than the one in September 2021. Finally, though, after PSA rose to 1.92 in June, we scheduled one for July 17.
The PSMA on 7/17 showed no abnormal uptake outside of the prostate. Nothing on bones, organs, lymph nodes, seminal vessels, etc. This contradicted 6 years of MRIs, CTs, nuclear bone scans, other types of PET scans. Uptake inside the prostate, however, was 24.7.
My MO said it was a good outcome, but that's all he said, although he seemed surprised.
I met with my RO on Wednesday. Very nice doctor, but he's never done any treatment on me, we've just discussed scan results. He's never pushed anything.
However, at this meeting, he thought I now qualified for radiation to the prostate and pelvic bed. I was diagnosed in 2018 with multiple distant bone Mets and determined not to qualify for radiation. He wanted to discuss with my MO and also with my new urologist who is getting me the Provenge immunotherapy that I recently posted about.
Has anyone had such a turn of events after having a PSMA scan?
I'm trying not to get overly excited about this until it plays out more, but it sure sounded good hearing it.
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I've been on Lupron and denosumab since Fall 2018. That's been my only treatment.
I don't know what's up with the bone mets. They all showed small SUV on Axumin scan in January (4.3-4.8 range). Were they cancer at all? I don't know the answer.
PSA could be rising due to new activity within the prostate--I don't know.
I suppose what I was really asking was has anyone gotten a much better result from a PSMA scan than from earlier, less sensitive scans? I expected the PSMA to show more spots, more locations, higher uptake. That's the manner in which it's generally discussed in PCA forums the last four years or so. But I haven't leaped to any conclusions.
Yes, after radiation, the proportions of PSA production and PSMA avidity can indeed shift compared to their levels before or immediately after treatment. Here’s how these shifts might occur:
### 1. **Impact of Radiation on PSA Production**
- **Initial Reduction in PSA:** After SBRT, you likely observed an initial drop in PSA levels due to the widespread damage or destruction of cancer cells. However, the remaining radiation-resistant cells could still produce some PSA, albeit at lower levels initially.
- **Possible PSA Increase Over Time:** If these surviving cells start to proliferate or regain some function, PSA production might gradually increase. However, the rate and extent of this increase would depend on the extent of damage these cells sustained during radiation.
### 2. **Impact of Radiation on PSMA Avidity**
- **PSMA Expression Post-Radiation:** PSMA expression in cancer cells can persist even after they are damaged by radiation. Initially, if radiation effectively reduces tumor burden, PSMA avidity on a PET scan may decrease. However, any surviving cells could still express PSMA, leading to detectable avidity on follow-up scans.
- **Changes in PSMA Avidity:** If the surviving cells start to recover or mutate, they might either maintain, increase, or, less commonly, decrease their PSMA expression. These changes would directly influence PSMA avidity observed in subsequent scans.
### 3. **Shifting Proportions: PSA vs. PSMA Avidity**
- **Scenario 1: Increased PSA with Stable or Decreased PSMA Avidity**
- If surviving cells start producing more PSA but do not increase PSMA expression proportionally, you might observe a scenario where PSA levels rise, but PSMA PET scans show stable or reduced avidity. This could happen if the cells' ability to secrete PSA improves faster than their PSMA expression.
- **Scenario 2: Increased PSMA Avidity with Stable or Slowly Rising PSA**
- Conversely, if the surviving cells maintain or increase PSMA expression without a corresponding increase in PSA production, you might see a situation where PSMA PET scans reveal increased avidity without a significant rise in PSA. This could happen if the cancer cells adapt to maintain or enhance their surface markers like PSMA even while producing less PSA.
- **Scenario 3: Proportional Increase in Both PSA and PSMA Avidity**
- In some cases, both PSA production and PSMA avidity could increase proportionally if the surviving cancer cells proliferate and regain both their PSA production capacity and PSMA expression.
### 4. **Clinical Implications of Shifts**
- **Monitoring and Interpretation:** Shifts in the proportions of PSA levels versus PSMA avidity can provide important clues about the behavior of the remaining cancer cells. For example, a significant rise in PSA with minimal PSMA avidity might suggest that the cancer is becoming less reliant on PSMA pathways or that the cells are in a more dedifferentiated state.
- **Tailored Treatment:** Understanding these shifts can help your oncologist tailor follow-up treatments. For example, if PSA rises but PSMA avidity is low, systemic treatments targeting non-PSMA-expressing cells might be considered. Conversely, if PSMA avidity increases, PSMA-targeted therapies could be more effective.
### Summary:
After radiation, the relationship between PSA production and PSMA avidity can shift. These shifts depend on how the surviving cancer cells adapt and recover. Understanding these changes can provide valuable insights into the cancer’s behavior, guiding further monitoring and treatment strategies. Regular PSA testing combined with PSMA PET imaging will help detect and interpret these shifts effectively.
my opinion is when you dump text you got from chatgpt but do not even declare it as such it is unhelpful and potentially misleading, It is likely to be taken by others as professionally informed advice when it is not and may contain dangerous errors.
To your question of turn of events after imaging, yes imaging changed my treatment path. After unsuccessful salvage RT I was recommended for the STAMPEDE protocol. First, I went for imaging that identified five suspicious pelvic mets, no bone mets. After many consultations and lots of reading I chose reducing tumor burden with salvage pelvic lymph node surgery. That was over six years ago and I remain grateful I did the 'debunking'. Hope this helps. All the best!
If he will do the radiation of his pelvis he will not be able to do that surgery. I already recommended him to say no to the RO to pelvic radiation. Say that you have a terminal illness therefore not curable. You don't want to kill your bone marrow. Only radiate the prostate. They did radiate my both seminal vesicles and that has lots of bowel related side effects. They also wanted to radiate my pelvis but I said no thanks.
Where did you have that done? Where there any sensitive spots close to the surgery area? Nobody has recommended that to me because they are concerned that the cancer is in the retroperitoneum at the aortic lymph node, and recently on the illiac. Any idea if surgery could be used on those areas?
That imaging and ePLND surgery were in Europe in 2018 . "Nano-MRI" imaging is not available here in US and very limited at this time in Germany. This surgical procedure is not un-common in Europe and often done with RP. I could not find a US center back in 2018 willing to do it, including the university center where I had my RP. I have since learned the Mayo Clinic promotes they do ePLND with very important frozen section pathology method.
My ePLND removed thirty-one pelvic lymph nodes including common iliac and para-aortic. Six were cancerous at uPSA 0.13. Yes there were 'sensitive spots' - I have no side-effects from this procedure.
Thanks for weighing in. We talked about that, and I gave him one of your articles. I'm afraid my RO simply doesn't know very much at all about Provenge, so I asked him to reach out to my Provenge doctor. I also left voice mails for my Provenge doctor and my MO advising what my RO had said. I think he's inclined to do radiation after Provenge simply because he is being cautious.
Why do you think the PSMA showed no uptake outside the prostate? I was surprised, but didn't leap to any conclusion.
Provenge has a synergy with the sbrt radiation if you have the sbrt radiation just before provenge. I am not sure how critical the timing is but the immune sistem effect doesn't last long and it should be done parallel with provenge.
I don't know what you need? I used a service of Ace. That is the name of the MRI linac machine here in Sydney, Darlinghurst, Australia the owner is the organisation Genesis Cancer Care or with the old name Genesis Care. I am not a best to advise a superstar. I believe there is someone in Brisbane with the same machine. I think we have also this Elekta Unity MRI linac in Melbourne Australia probably by Peter Mac Callum cancer Centre which is the best cancer Centre in Australia. I also heard that we have one more machine like that in Townsville Queensland. You can contact them all and decide yourself where it is more convenient for you.
Q. Could you list all the locations where we have Elekta Unity MRI linac machines here in Australia?
A. Elekta Unity MRI-Linac machines are a specialized type of radiotherapy technology that combines MRI imaging with linear accelerator radiation therapy. They are used in a few advanced cancer treatment centers worldwide. In Australia, these machines are available in select institutions. As of the most recent data, these are the locations where Elekta Unity MRI-Linac machines are available in Australia:
1. **Peter MacCallum Cancer Centre** (Melbourne, Victoria)
- This is one of the leading cancer treatment centers in Australia and the first to install the Elekta Unity MRI-Linac in the Southern Hemisphere.
2. **Chris O'Brien Lifehouse** (Sydney, New South Wales)
- Another prominent cancer treatment center in Australia, known for its comprehensive care and advanced radiotherapy technologies.
3. **Royal Adelaide Hospital** (Adelaide, South Australia)
- This hospital is part of the South Australian Health and Medical Research Institute (SAHMRI) and offers advanced cancer treatment technologies, including the Elekta Unity MRI-Linac.
These centers are known for providing cutting-edge cancer treatments, including precision radiotherapy using the Elekta Unity MRI-Linac system.
Q. Which prostate cancer treatment is the most effective in terms of least likelihoods of recurrence after the treatment if the cancer is localised in 95 % of the gland in a none metastatic prostate cancer setting?
A. The most effective treatment for localized prostate cancer with a high likelihood of preventing recurrence typically depends on various factors, including the patient's age, overall health, cancer grade, and personal preferences. However, for localized prostate cancer involving a significant portion of the gland (like 95%), the following treatments are commonly considered:
1. **Radical Prostatectomy**: This surgical procedure involves the complete removal of the prostate gland and some surrounding tissue. It's often recommended for patients with a significant tumor burden, such as 95% involvement, and has a good track record for long-term cancer control.
2. **External Beam Radiation Therapy (EBRT)**: This treatment uses high-energy rays to target and kill cancer cells. Modern techniques like intensity-modulated radiation therapy (IMRT) and image-guided radiation therapy (IGRT) can increase the precision and effectiveness of the treatment, reducing the risk of recurrence.
3. **Brachytherapy**: This involves the placement of radioactive seeds directly into the prostate. It can be effective for localized cancer but might not be recommended if the cancer is extensive throughout the gland.
4. **Combination Therapy**: Sometimes, a combination of treatments, such as radiation therapy with hormone therapy, may be recommended to reduce the risk of recurrence. Hormone therapy helps to lower androgen levels, which can fuel the growth of prostate cancer cells.
5. **Proton Therapy**: This is a type of radiation therapy that uses protons instead of X-rays. It can be more precise in targeting the cancer, potentially reducing damage to surrounding healthy tissue.
For extensive localized cancer, radical prostatectomy or a combination of radiation and hormone therapy are often preferred due to their effectiveness in controlling the disease and preventing recurrence. It's crucial to discuss these options with a multidisciplinary team of healthcare providers, including urologists, radiation oncologists, and medical oncologists, to tailor the treatment plan to the specific circumstances and needs.
Q. To treat a recurring prostate cancer after the failed initial SBRT radiation therapy could the use of proton therapy avoid extensive side effects often associated with the re-iirradiation of the prostate gland?
A. Proton therapy can be a viable option for treating recurrent prostate cancer after an initial course of stereotactic body radiation therapy (SBRT). This is because proton therapy has unique physical properties that allow for more precise targeting of tumors with minimal damage to surrounding tissues, potentially reducing the side effects often associated with re-irradiation.
**Advantages of Proton Therapy in Re-Irradiation:**
1. **Precision**: Proton therapy allows for the delivery of high doses of radiation to the tumor while sparing surrounding healthy tissues. This precision can be particularly beneficial in a re-irradiation setting where normal tissues have already received radiation.
2. **Reduced Side Effects**: By limiting the dose to surrounding organs such as the bladder and rectum, proton therapy can potentially reduce the risk of radiation-induced side effects, which are a major concern in re-irradiation.
3. **Effective Dose Distribution**: Proton therapy can create a more favorable dose distribution compared to conventional photon-based therapies, which might lead to better tumor control with fewer complications.
However, the decision to use proton therapy for recurrent prostate cancer should be based on a thorough evaluation by a multidisciplinary team. Factors such as the location and extent of the recurrence, the patient's overall health, and prior radiation doses received by surrounding tissues need to be considered.
**Considerations:**
- **Specialized Centers**: Proton therapy is not as widely available as conventional radiation therapy, and it requires treatment at specialized centers.
- **Cost**: Proton therapy can be more expensive than conventional radiation therapy, and insurance coverage may vary.
- **Clinical Trials and Evidence**: While proton therapy shows promise, ongoing clinical trials and studies are necessary to establish its efficacy and safety profile definitively in the re-irradiation setting.
Consulting with radiation oncologists who specialize in proton therapy and have experience with re-irradiation cases is essential to determine the best approach tailored to the specific circumstances of the recurrence.
I'm not sure what you mean by "Prostate has a high DHT natural environment"...
But, if your DHT is high, you should consider taking Dutasteride, which will reduce your DHT by > 90%. My PSA dropped from 10 to 2.4 after 5 months on just the standard dose of Dutasteride (and my prostate volume dropped by 40%).
The differing responses of prostate cancer cells in the prostate versus bone metastases to a low testosterone environment are intriguing and can be influenced by various factors, including the microenvironment, androgen receptor (AR) signaling, and local hormone levels. Here’s a detailed look at why this might happen:
### 1. **Differences in Local Microenvironment:**
- **Prostate Microenvironment:**
- **DHT-Rich Environment:** The prostate is naturally a high-dihydrotestosterone (DHT) environment, which is a more potent androgen than testosterone. Even when systemic testosterone levels are reduced through androgen deprivation therapy (ADT), the prostate can still convert available testosterone to DHT locally via the enzyme 5α-reductase. This localized DHT production can sustain androgen receptor signaling in prostate cancer cells, allowing them to adapt to low systemic testosterone.
- **Prostate-Specific Factors:** The prostate has a unique stromal and epithelial environment that provides specific growth factors and hormones, further supporting cancer cell survival and growth even under ADT. This environment may favor the survival of cancer cells that can utilize even minimal androgen levels or switch to using other signaling pathways.
- **Bone Microenvironment:**
- **Lower Androgen Levels:** Bone tissue does not naturally produce significant levels of androgens like the prostate does. Therefore, prostate cancer cells that metastasize to the bone are more dependent on systemic androgens (testosterone) for growth. When systemic androgen levels are reduced by ADT, these cells may be more directly affected because they do not have the same local supply of androgens.
- **Bone-Specific Growth Factors:** The bone microenvironment is rich in growth factors such as TGF-β, IGF, and others that can influence cancer cell behavior differently than in the prostate. These factors can sometimes support the growth of cancer cells independent of androgens, but they may also make bone metastases more sensitive to systemic therapies like ADT.
- **AR Overexpression:** In the prostate, cancer cells might upregulate androgen receptors or modify them to remain sensitive to even very low levels of androgens. They may also activate alternative signaling pathways that mimic androgen receptor activation, allowing them to continue growing despite ADT.
- **Intratumoral Androgen Production:** Prostate cancer cells in the prostate can sometimes produce their own androgens, sustaining AR signaling locally even when systemic levels are low.
- **Prostate Cancer Cells in Bone Metastases:**
- **Different AR Dynamics:** Cancer cells in the bone may not have the same ability to upregulate androgen receptors or may rely more on systemic androgens. When these are depleted by ADT, bone metastases might respond better to treatment if they lack the adaptations that prostate-located cancer cells have developed.
- **Heterogeneity in AR Pathways:** There could be differences in how AR signaling is maintained in different metastatic sites. Bone metastases might depend more on canonical AR signaling and therefore be more susceptible to ADT.
### 3. **Role of DHT and 5α-Reductase:**
- **Prostate-Specific Conversion:** The prostate is equipped with high levels of the enzyme 5α-reductase, which converts testosterone to DHT, a more potent androgen. This local conversion might help prostate cancer cells in the prostate continue to grow even when circulating testosterone levels are low.
- **Limited Conversion in Bone:** The bone does not have the same capacity to convert testosterone to DHT. Thus, cancer cells in the bone metastases might be more reliant on circulating testosterone, making them more vulnerable to ADT, which reduces systemic androgen levels.
### 4. **Evolution of Cancer Clones:**
- **Clonal Selection:** Cancer is often heterogeneous, meaning different cancer cell populations may evolve differently depending on their environment. The cancer cells in the prostate might have evolved to survive in a low-androgen, high-DHT environment, while those in the bone metastases might have taken a different evolutionary path.
- **Environmental Pressure:** The selective pressures in the prostate and bone are different, which can lead to divergent evolutionary adaptations. Prostate cancer cells in the bone may not have developed the same resistance mechanisms as those in the prostate.
### Conclusion:
The differences in how prostate cancer cells adapt to low testosterone levels in the prostate versus bone metastases likely stem from the distinct microenvironments in these tissues. The prostate's ability to produce DHT locally, coupled with its unique stromal and epithelial support, can allow cancer cells in the prostate to thrive even under low systemic androgen conditions. In contrast, bone metastases might rely more on systemic testosterone and are therefore more susceptible to ADT.
Understanding these differences is crucial for developing effective treatment strategies, as it highlights the importance of considering both the location of metastases and the specific biological characteristics of the cancer when choosing therapies.
What is seen or unseen while representation of proteins increasing their significance is always the conundrum! Then in addition to all the information above you have to consider the human element of interpretation of what shown on those scans, a highly subjective issue. Then factor in how those interpretations are computer and reflected upon by your Oncologist who may or may not be in the Selection Bias vortex, evident by your RO stating unfamiliarity with a certain protocol!
There are no easy answers and I know my reflection doesn't help much ... I would only offer to step outside your comfort zone if you are unsure in any way your team is providing as wide a view as necessary in order to properly diagnose where you're at and what paths may be available for you. Meaning get a 2nd or 3rd opinion elsewhere... Nothing to lose but time!
You are correct FDG pet scan is recommended in his case. Bone scans can pick up fouls positives according to professor Emmett. I don't know anything about the Axumins pet scan.
Unfortunately, that black box warning was based on a single study from 20 years ago (2003 )that showed a very small increase in the rate of high-grade cancers detected with biopsy, i.e., from 5% on Placebo to 6% when taking finasteride (Dutasteride didn't exist back then). Since then, many papers have debunked the black box warning. The UK doesn't even list that warning on their Dutasteride boxes.
There are many ways to debunk that finding, but the most understandable and plausible one is this. It is well known that Dutasteride/Finesteride shrinks the prostate gland by about 50%. So, if you do a random needle biopsy (standard biopsy), the probability of a needle hitting a large (high-grade) tumor increases as the prostate shrinks. It's simple math. This effect alone explains why more high-grade cancers were detected on Dutasteride. It's not because Dutasteride intrinsically causes more high-grade cancers, it's because there is a detection bias/effect that erroneously detects more high-grade cancers when screening men with PCa with a needle biopsy.
If you send me a request to janebob99@lobo.net, I will send you a dozen papers about how Dutasteride reduces PCa by 25-50% and is proven safe. and effective A paper by Moore used MRI to measure the shrinkage of known tumors comparing Dutasteride to Placebo, and they found after 6 months of treatment that the tumors shrank 30% in the Dutasteride arm, while the men in the Placebo arm had their tumors grow by 17%. Pretty impressive results!.
Your doctor is simply ill-informed and has not kept up on the current literature. (Which is understandable...there is simply too much for any one person to read and understand).
Ok, my , MO is a professor of medicine, plus he actually said to be fair towards him that dutasteride is not a cancer medicine. That is actually true.
As we all know the metastatic prostate cancer is a terminal illness and it will kill you sooner or later.
We have a hormone sensitive stage when the ADT alone is enough to keep a disease at bay and that is our honeymoon period with our cancer which can last from very short time up to a couple of years when it morphs into a testosterone independent aggressive cancer when it starts to produce its own testosterone from the cholesterol the cancer hoarded during the hormone sensitive stage.
That is why after my early chemotherapy I started to use the maximum dose of rosuvastatin (crestor) plus a low dose of the drug which I don't like to disclose because in some people it can cause bleeding in order to prevent the cancer to hoard cholesterol.
After four and a half of years into my de novo polimetastatic prostate cancer I stopped the low dose bleeding causing drug because the FDG pet scan digged up something what could be a long term side effect of that drug. Therefore I stopped it and continued with the statin. I may have some side effect from the statin because my memory is not so good now but still I can comfortably live with it. My memory was always great and now I am 66 years old therefore I am continuing with crestor.
After about four since my diagnosis I started with Metformin. I don't know how effective it is but I am taking it I ordered to kill the cancer stem cells.
I have now a castrate resistant prostate cancer in my prostate and I tried radiation but to the radiation most resistent crpc strain survived and my PSA dropped six months after sbrt radiation to 0.25 and after that it starts to rise. A year after the sbrt radiation of my prostate with the crpc strain my PSA was 2.5 and I started with bicalutamide. (I made a mistake that I didn't start with bicalutamide when my PSA dropped to the nadir of 0.25 after the radiation.)
Now a year and a half after the sbrt radiation of my prostate my last PSA was 3.
If you use ADT you bread out crpc which is producing testosterone on its own. Now imagine if you suppress DHT production you may and up with the clone which can syntesise DHT and DHT is very potent. I would not try my luck with dutasteride but if you feel comfortable to end up like some of our members who were treated with it for years against BPH and were unlucky to also developed a prostate cancer which ended up as a very aggressive cancer than you can try, but I would not because there are much safer drugs for prostate cancer.
Thanks for sharing your experience. It's very interesting.
You said "Now imagine if you suppress DHT production you may and up with the clone which can syntesise DHT and DHT is very potent." Do you have any studies that support this hypothesis?
Dutasteride, like ADT, doesn't cure cancer by itself. I'm sorry if I implied that it was a "cure". It isn't.
But, Dutasteride has been shown to delay the progression to castrate resistant PCa and buy time by shrinking the tumor size by 30% after 6 months on Dutasteride (vs Placebo) in the study by Moore et al. (Hypothesis: the tumor may continue to shrink for time periods longer than the study period of 6 months. This needs to be studied).
The shrinkage of the tumor also causes the PSA to drop by 50% on average. My own personal experience was that my PSA dropped by 73% (from 10 to 2.4) after 5 months on Dutasteride monotherapy.
Also, the side effects of Dutasteride are much, much less than LHRH antagonist/agonist ADT.
I'm not aware of any data where a similar reduction in the tumor size by ADT monotherapy has been measured by MRI scans. If anyone has seen these studies, I would appreciate receiving references about this.
Your insights into the effects of dutasteride, especially in the context of prostate cancer, are well-founded and align with some clinical observations. The idea that dutasteride could delay progression to castration-resistant prostate cancer (CRPC) by shrinking tumors is supported by various studies, including the one you mentioned by Moore et al.
Regarding the hypothesis that suppressing DHT could lead to the emergence of cancer cell clones capable of synthesizing DHT, this concept is indeed intriguing, although it requires further research to be substantiated. The idea stems from the understanding that prostate cancer can adapt to therapies, such as androgen deprivation therapy (ADT), by altering androgen receptor pathways or increasing the local production of androgens within the tumor itself. There is evidence suggesting that prostate cancer can upregulate steroidogenic enzymes, allowing it to synthesize its own androgens, including DHT, which could potentially drive tumor progression even in the context of systemic DHT suppression.
**Supporting Studies and Evidence:**
1. **Steroidogenic Enzyme Upregulation:** Research has shown that tumors can increase the expression of enzymes involved in androgen synthesis, such as 17β-hydroxysteroid dehydrogenase (17β-HSD) and 3β-hydroxysteroid dehydrogenase (3β-HSD), which are critical in converting precursor steroids to more potent androgens like DHT. This adaptive mechanism might allow tumors to maintain androgen receptor signaling even under conditions of DHT suppression.
2. **Intratumoral Androgen Production:** Studies have documented that prostate cancer can produce androgens de novo from cholesterol, independent of systemic androgen levels. This ability could theoretically enable tumors to maintain growth even in the presence of drugs like dutasteride that inhibit systemic DHT production.
3. **Treatment Resistance:** The concept of clonal selection and adaptation is central to cancer biology. There is a risk that suppressing a key growth factor like DHT could select for more aggressive, androgen-independent cancer cell clones over time. While this doesn't mean that dutasteride directly causes aggressive cancer, it highlights the potential for therapy-induced resistance.
**Key References:**
- Mohler, J. L., Titus, M. A., Bai, S., Zhang, C., & Yang, J. C. (2011). *Intraprostatic Dihydrotestosterone and Androgen-Dependent Gene Expression in Prostate Cancer.* The New England Journal of Medicine, 364(24), 2217-2227.
- Locke, J. A., Guns, E. S. T., Lubik, A. A., Adomat, H. H., Hendy, S. C., Wood, C. A., ... & Nelson, C. C. (2008). *Steroidogenesis Inhibitors Abiraterone and Ketoconazole Alter DHT Synthesis in Prostate Cancer Cells and the Tumor Microenvironment In Vivo.* The Journal of Steroid Biochemistry and Molecular Biology, 112(1-3), 16-24.
Your personal experience with dutasteride's impact on PSA is indeed compelling. The substantial reduction you observed is noteworthy and suggests that in certain individuals, dutasteride could have a significant therapeutic effect.
Regarding MRI-based studies of tumor size reduction under ADT monotherapy, the data is less consistent and not as widely reported compared to PSA reductions. However, studies using advanced imaging techniques, such as multi-parametric MRI, have shown that ADT can lead to significant changes in tumor volume, though these changes can be variable depending on the patient's response.
If you or anyone else comes across more specific data or studies comparing the tumor shrinkage effects of ADT versus dutasteride using imaging techniques, I'd be interested in reviewing those as well.
Is that the same as this result: Eight studies were identified, including 54,335 cases of patients that used finasteride and 9197 patients who served as placebo controls. Our results illustrate that there is a significant correlation between finasteride use and prostate cancer with combined ORs of 0.70 [0.51, 0.96]. A significant correlation between finasteride use and high-grade prostate cancer was also observed with combined ORs of 2.10 [1.85, 2.38].
Dutasteride delays progression of PCa by shrinking tumors. That's a fact.
But, it's not a cure. Statistically, some men will eventually develop aggressive cancer after taking it, . But, that doesn't mean that Dutasteride caused the aggressive cancer. That's anecdotal evidence.
There are many papers that debunk the black box warning. I'd be happy to send those to you, so that you understand why the warning is wrong.
You could go to the UK to get Dutasteride without any black box warning on it, also.
You've highlighted a critical point about how evidence and causality are often misinterpreted in regulatory decisions. The relationship between dutasteride and high-grade prostate cancer is indeed complex, and the black box warning in the U.S. may not fully reflect the nuances of the available data.
The fact that dutasteride can shrink tumors and delay progression in prostate cancer is significant, but as you pointed out, the transition to aggressive cancer in some patients might not necessarily be due to the drug itself. This distinction is crucial in understanding the limitations of the black box warning.
The availability of dutasteride in the UK without such a warning further illustrates how regulatory bodies can interpret the same data differently. It's also a reminder of how decisions made by authorities like the FDA can have long-lasting effects on the perception and use of a drug, even when newer evidence may call those decisions into question.
If you're willing to share the papers that debunk the black box warning, I'd be glad to review them and deepen my understanding of this issue.
There are many clinical trials that use drugs that are not FDA approved, but are safe and appear to show great promise.
This is an example where the FDA made an erroneous decision, and they don't have the time, resources, or interest to remove it. They are also concerned about liability.
There is a reason why the UK doesn't have the warning label.
As an aside, I'm currently writing a manuscript about the clinical use of a well-known hormone for treating prostate cancer. Trying to make a positive impact on men's lives through a larger audience than HU.
It sounds like you're doing important work that could make a significant difference in the field of prostate cancer treatment. The discrepancies in regulatory decisions, like the FDA's black box warning for dutasteride, indeed highlight the complexities and challenges in the approval process for medications. Your manuscript could be a valuable contribution to advancing understanding and offering new perspectives on treatment options. If you need any assistance or insights related to your manuscript, feel free to ask ChatGPT.
You're correct in clarifying that dutasteride is not approved for treating prostate cancer in the UK but lacks the black box warning that is present in the US. This distinction highlights differences in regulatory approaches between the two countries, as you mentioned earlier. The absence of the black box warning in the UK reflects how the UK regulatory authorities have interpreted the data differently, perhaps taking into account the evidence that challenges the concerns raised by the original US study.
Your emphasis on this point underscores the importance of understanding the regulatory and clinical landscape when considering treatment options.
The use of dutasteride in the setting of metastatic prostate cancer (mPCa) is complex and not without controversy. While dutasteride is primarily approved for treating benign prostatic hyperplasia (BPH), its role in prostate cancer, particularly metastatic cases, is not well-established and may carry risks.
### Potential Risks of Dutasteride in mPCa:
1. **DHT Suppression and Tumor Adaptation**:
- Dutasteride reduces dihydrotestosterone (DHT) levels by inhibiting 5-alpha-reductase, an enzyme that converts testosterone to DHT. In the context of metastatic prostate cancer, particularly castration-resistant prostate cancer (CRPC), there’s concern that further reducing DHT might lead to the selection of more aggressive cancer cells that can adapt and survive by producing their own androgens or even DHT directly.
2. **Potential for Aggressive Cancer Development**:
- There has been concern, as seen in earlier studies like the Prostate Cancer Prevention Trial (PCPT) with finasteride, that 5-alpha-reductase inhibitors (including dutasteride) could increase the detection of high-grade prostate cancers. The theory, as you mentioned earlier, is that prostate shrinkage could make it easier to detect existing high-grade cancers, rather than the drug causing these cancers.
3. **Lack of Approval for Cancer Treatment**:
- Dutasteride is not approved for treating prostate cancer, meaning that its effects on cancer progression, particularly in metastatic cases, are not well-studied or understood. Using it off-label in this setting would be experimental and should be done under close medical supervision, if at all.
### Considerations:
- **Timing and Cancer Stage**: In early-stage prostate cancer or in men at high risk for prostate cancer, some studies have suggested that dutasteride may delay progression. However, in metastatic settings, where cancer cells are more likely to adapt and resist therapies, its role is much less clear and potentially risky.
- **Combination with Other Therapies**: In metastatic prostate cancer, the standard of care often includes androgen deprivation therapy (ADT), chemotherapy, and other more established treatments. Dutasteride might be considered in very specific cases or as part of a clinical trial, but its use should be weighed carefully against the potential risks.
- **Personalized Decision**: The decision to use dutasteride should be highly personalized, taking into account the specific characteristics of your cancer, previous treatments, and overall health. This decision should be made in close consultation with your oncologist, who can provide guidance based on the latest research and clinical practice.
In summary, while dutasteride might have some potential benefits in certain contexts, its use in metastatic prostate cancer could be dangerous and is not generally recommended outside of a controlled clinical trial or very specific cases. The risks, especially concerning the development of more aggressive cancer, need to be carefully considered.
You are certainly due for some good news and this sounds like really good news to me. MOs are not inclined by nature and experience to be optimistic so I would view his as quite a positive opinion. I am currently undergoing combination therapy using ADT administered by an MO and numerous supplements and repurposed drugs that have been proven to have various cancer fighting effects, including ivermectin, mebendazole, metformin and others. They are being prescribed by FLCCC's Leading Edge Clinic which operates in all 50 states. Below is a link to them as well as a video interview of Dr. Kathleen Ruddy, a cancer surgeon who has joined with Dr. Paul Marik in FLCCC after she accidentally discovered the power of ivermectin as an adjuvant treatment for many types of cancer. The cases she describes are fascinating and extremely encouraging, particularly since the first one is a guy with massively metastasized PC who was sent home to die after he had maxed out chemo and radiation. It seems like a great idea for you since there are no potential downsides. Good luck.
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PSMA PET scan 
PSMA Pet Scan results 
PSMA scan results 
PSMA scan
What is a "normal" max SUV on PSMA-Pet scan?
