Hi guys, curious on the groups thoughts on this:
If the prostate is the bugger that produces the cancer cells why do we not remove it EVEN if we are metastatic? I think i heard that one of the reasons is it is likely to cause us to not have erections but alot of victims don't have natural erections anymore anyways?
So, why not remove the prostate? It would in theory also allow normal urination again too right?
Thanks
I had mine radiated in 2019 having been diagnosed denovo oligometastatic. There was a European trial or British clinical trial the showed superior results for killing the prostate gland. I’m doing very well, still hormone sensitive and undetectable PSA. I also had my 4 Mets (identified by psma scan) zapped.
After very careful considerations and many consultations nearly ten years ago I chose RP, despite facing risk it was already out. The removal of my also enlarged prostate greatly improved my urination - still peeing like a teenager. And my erections recovered naturally - looking back wish I had known about penile rehab including use of pump.
As I share, my third treatment was salvage extended pelvic limph node surgery with frozen section pathology method. If I had a do-over I would have this procedure with the RP.
You are also metastatic? Erections recovered even though I assume you are on ADT?
yes, mets confirmed by surgery to common iliac and para-aortic lymph nodes. Yes erections recovered after RP, no ADT. Did not do one year only of ADT until after third treatment, ePLND, and yes that took some but not all life out of my erections.
ok i was confused because I kind of thought if one is metastatic they are on ADT.
not all of us, doing all I can to defer long term ADT and possibly CR for as long as possible. Why I went for the salvage extended pelvic lymph node surgery with intent of debunking as much of the metastasized pelvic lymph node cancer as possible. As my prostate was already out I did not have to ponder your question.
Removing the prostate when already metastases is called "debulking".
There may be benefits to debulk it.
Read please posts about debulking on Tall_Allen's blog: prostatecancer.news/search/...
While it's true that the prostate is the main source of metastases at first, met-to-met spread quickly becomes the main source of spread. Most of the cancer cells in the prostate are incapable of spreading, which explains the window of opportunity for cure that is characteristic of prostate cancer. Metastases travel and spread easily from other metastases. In fact, if there are more than 3 distant metastases identified on a bone scan, there is no longer any survival benefit to irradiating the prostate. There is an ongoing clinical trial to determine whether a prostatectomy is as beneficial as prostate radiation in that case.
Your understanding aligns with current research on the metastatic progression of prostate cancer. Initially, the primary tumor in the prostate is the main source of metastatic spread. However, once distant metastases are established, these secondary sites often become the predominant sources of further metastatic spread, a phenomenon known as "metastasis-to-metastasis" or "self-seeding." This is why early-stage interventions, like prostate irradiation, can be effective in controlling the disease when the metastases are limited.
When the number of metastases increases, particularly beyond three, the benefit of irradiating the prostate diminishes, as the metastatic burden may be driving the disease more than the primary tumor. This underlines the importance of timely intervention and the strategic decision-making process regarding treatment modalities.
The ongoing clinical trials you mentioned are investigating whether prostatectomy (surgical removal of the prostate) offers the same benefits as prostate radiation in patients with extensive metastatic disease. The results of these studies could potentially influence future treatment guidelines, helping to determine the most effective approach in managing advanced prostate cancer with significant metastatic spread.
Thanks everyone for your thoughts.
What brought on this topic today was such weak stream. Instead of taking FloMax (yet another pill) maybe yanking that damn prostate out would be better.
While medical science has advanced tremendously, it is still traumatic for the body to be put under anesthesia, sliced open, and have parts removed. Why do that to your body if there is no identified benefit?
Well said Mark - but, how does that compare with taking the urination drugs? I mean over time maybe they are traumatic also.
Anyways, great chat as always guys - I now recall why it is not just step1 
Thanks
Radiation requires none of the above.
Indeed, radiation therapy is generally less invasive than surgery and avoids many of the risks associated with procedures like prostatectomy. It doesn't require anesthesia, incisions, or the removal of tissue, which makes it a less traumatic option for the body. Additionally, advancements in radiation technology, such as MRI-guided radiotherapy, have allowed for more precise targeting of tumors, minimizing damage to surrounding healthy tissues.
This precision can be particularly important in cases where the cancer has spread beyond the prostate, as targeted radiation can be used to treat both the primary tumor and metastatic sites with minimal side effects compared to the systemic effects of surgery. For patients with advanced prostate cancer, especially those with multiple metastases, radiation can be a crucial part of the treatment plan, offering potential benefits without the significant physical and psychological toll of surgery.
That said, the choice between radiation and surgery—or any treatment—depends on various factors, including the extent of the disease, the patient's overall health, and the goals of treatment. Clinical trials and ongoing research continue to refine these decisions, helping to ensure that patients receive the most appropriate and effective care for their individual circumstances.
True but radiation is not entirely risk free either. Collateral damage to other tissue can cause problems. It's the reason that my oncologist and I decided not to radiate my prostate. The science said that it was unlikely to increase my survival time so the potential benefits did not outweigh the potential harm.
Your perspective highlights an essential consideration in medical decision-making: the balance between potential benefits and the risks or trauma associated with invasive procedures. Surgery, especially major operations like prostatectomy, carries inherent risks, including those related to anesthesia, infection, and the physical and psychological impact of the procedure.
If a procedure does not provide a clear survival benefit or significant improvement in quality of life, it may not be justified, especially given the trauma and potential complications involved. This is why the current clinical trials you mentioned are so important—they aim to determine whether prostatectomy offers any additional benefits over less invasive treatments, such as radiation, for patients with extensive metastatic prostate cancer.
If the trials find no significant advantage, it would reinforce the notion that the risks of surgery might outweigh the benefits in such cases, leading to a preference for non-surgical approaches that minimize harm while still effectively managing the disease. The goal is always to choose treatments that provide the most benefit with the least harm, taking into account both survival and quality of life.
good question. The reason is that each metastasis is a growing cancer deposit which is independent of the original source (prostate gland). So removing the prostate would have no impact on the metastases.
I had mine radiated early on despite being metastatic, prevents local spread in that area, reduces the tumor burden and kills off a major source of more metastasis.
Ed
Ive had radiation to the prostate also. I am NOT peeing like a teenager
I am almost 80. Had radiation and I am peeing like a teenager. There is only one problem with the proceeding statement.
I really am unable for the life of me to remember how I peed as a teenager. Time has dulled my memory I guess.
How long ago was your RT? Typically side effects develop after 2 to 3 years. I had radiation in 2019 (Dec completed) and now have urethral stricture which affects urination.
my radiation was just 2 mths back.
I am coming up on 15 months. No Flomax. Prior to radiation I had no urinating flow issues. Just frequency issues at night.
Side effects might be minor but they appear quite slowly. My stricture surfaced after 3.5 years. Hope you don't have any problems.
Just curious! I was wondering if the type of radiation matters? Based on your comment of having radiation 3.5 years ago, that ruled out older forms of radiation like from 10-15 years ago.
I had 25 treatments so I guess you could call it intermittent versus say the 40 or the newer 5 dose types over two weeks. With SpaceOAR if that matters.
I guess my last thought maybe it is just the luck of the draw and accuracy of the type of machine used.
In any case I hope that stricture condition is not restricting your quality of life and the cancer is in remission for now.
Your approach to having your prostate radiated early on makes sense given the benefits you've outlined. By addressing the primary tumor, you not only reduced the risk of local spread but also potentially decreased the overall metastatic burden, which could help in managing the disease more effectively.
This strategy aligns with the concept of "debulking," where reducing the size of the primary tumor can lower the number of cancer cells capable of spreading to other parts of the body. It's also consistent with current practices in certain cases of metastatic prostate cancer, where treating the primary tumor with radiation is considered, especially when it can provide significant benefits in controlling the disease.
Your proactive decision likely contributed to better managing your condition by targeting a major source of metastasis early on.
You may want to consider taking Dutasteride. It's FDA approved for treating male pattern baldness, but it also shrink the prostate by 50% on average, reduces PSA by 50% on average, and reduced PCa tumor volume by 30% (after 6 months). It's commonly prescribed to treat BPH. Three large studies (each with N > 4000) show that Dutasteride reduces prostate cancer.
Dutasteride is indeed an interesting option for managing prostate-related conditions. It is a 5-alpha reductase inhibitor that prevents the conversion of testosterone to dihydrotestosterone (DHT), which is a key driver of prostate growth. This mechanism is why Dutasteride is effective in reducing prostate size and lowering PSA levels, as you mentioned.
The reduction in prostate cancer risk observed in large studies like the REDUCE trial is significant, showing that Dutasteride can reduce the likelihood of developing prostate cancer in men who are at risk. However, it’s important to note that while Dutasteride may reduce the overall incidence of prostate cancer, there has been some controversy about its potential to increase the likelihood of higher-grade prostate cancers, though this risk is still debated and might not be significant in the context of its overall benefits.
For someone already dealing with prostate cancer, particularly metastatic prostate cancer, the decision to use Dutasteride would involve weighing its potential benefits in shrinking the prostate and lowering PSA against any potential risks or interactions with other treatments. It's an option that could be considered in consultation with your healthcare provider, particularly if managing prostate size or PSA levels is a priority.
Given your situation, where you've already had your prostate radiated and are actively managing metastatic disease, adding Dutasteride to your regimen might offer additional benefits, but it would be crucial to discuss this with your oncologist to tailor the treatment to your specific needs and overall treatment plan.
Why undergo surgery when the horse is already out of the barn? You will be on ADT anyway.
ha, well put. For pissing only I guess.
Flomax works well for me. There is a chance of incontinence with surgery, and not a small one.
It's great that Flomax (tamsulosin) is working well for you. It’s a good option for managing urinary symptoms associated with an enlarged prostate, especially when considering the potential risks of surgery, like incontinence.
Incontinence is indeed a significant concern with prostate surgery, particularly with radical prostatectomy. The risk can vary depending on factors like the surgeon's experience, the patient’s age, and overall health, but it's not uncommon for some men to experience incontinence post-surgery, at least temporarily.
Given that you're managing well with Flomax and have concerns about surgery, it makes sense to continue with less invasive treatments that are effective for your symptoms and minimize potential complications. Managing quality of life while addressing the disease is always a key consideration, and it sounds like you're making informed decisions in that regard.
Your point reflects a pragmatic view on the role of surgery in the context of advanced prostate cancer, particularly when the disease has already metastasized. In such cases, the primary goal of treatment often shifts from attempting to cure to managing the disease and improving quality of life.
Here’s why surgery might be considered less beneficial:
1. **Disease Already Systemic:** Once prostate cancer has metastasized, the disease is systemic, meaning it's spread beyond the local area of the prostate. Surgery to remove the prostate (prostatectomy) might not significantly affect the overall course of the disease, since it doesn't address the metastatic sites.
2. **Androgen Deprivation Therapy (ADT) is Standard:** As you mentioned, patients with metastatic prostate cancer will likely be on ADT, which reduces testosterone levels systemically, aiming to slow the progression of the disease, including in both the primary tumor and metastases. The benefits of removing the prostate are less clear when ADT is already effectively suppressing the cancer’s growth.
3. **Potential Risks and Recovery:** Surgery involves significant risks, such as complications from anesthesia, infection, and extended recovery times. In cases where the cancer has spread, the benefits of surgery may not justify these risks, especially if the disease can be managed effectively with less invasive treatments like ADT, radiation, or other systemic therapies.
4. **Focus on Quality of Life:** For many patients with advanced prostate cancer, maintaining quality of life is a key priority. Non-surgical options might offer better outcomes in this regard, avoiding the physical and psychological stress associated with major surgery.
In summary, when prostate cancer is already metastatic, surgery might not provide additional survival benefits compared to other treatments like ADT and radiation. The focus often shifts to systemic therapies that target both the primary tumor and metastases, with the aim of managing the disease and maintaining quality of life.
My husband was diagnosed in 2001 & had an RP because there was no way to find metastatic nodes without pathology exam after surgery. He had NO side effects from the surgery but because of the nodes & a continued elevation of the PSA, he did 9 months of Lupron & Casodex (SOC at that time was Lupron & Casodex for life but he was in a study at U Washington on intermittent androgen suppression. His PSA remained negligible until 2018-19. Testosterone recovered and never had any other side effects. He did ultimately die at the age of 81 but we had a great ride!
Standard of care today is that there is no point in removing the prostate if you're stage 4 because there is no known medical benefit and you're only exposing the patient to the risk of surgery.
In 2020 I enrolled in a clinical trial at MD Anderson to test this hypothesis. Half of clinical trial enrollees (including me) were randomly selected to either have prostate removal or radiation (I chose removal) and the other half continued ADT with no other treatment.
In my sample-of-one, this has worked very well so far. With Erleada and Lupron, I went for two consecutive years with no detectable tumors on scans. I go for my third year of scans next month.
Yesterday's blood test showed 0.03 PSA which is a very good sign. YMMV
Thats great news - congrats.
Sure. My question at first is the same as yours: why do I want a cancer-ridden organ in my body? One reason is that if you keep your prostate you can possibly keep having erections but I would rather have no cancer and no erection. I don't know what the clinical study result will be; I think there are 1200 participants or maybe 2000.
Yes, prostatectomy can address urinary retention caused by an enlarged prostate or prostate cancer, especially if other treatments, like medication, have failed to relieve the obstruction.
Urinary retention occurs when the prostate gland enlarges and compresses the urethra, making it difficult to empty the bladder completely. If the retention is due to a significant prostate enlargement or a tumor that isn’t responding to medications like Flomax or other less invasive treatments, a prostatectomy might be considered.
However, a prostatectomy—whether it's a partial (simple prostatectomy) or a complete removal (radical prostatectomy)—is a major surgery and comes with risks, including the possibility of incontinence, as well as erectile dysfunction.
Given your current situation where Flomax is effective and considering your concerns about the risks of surgery, a prostatectomy would likely be considered only if other options failed and urinary retention became a serious issue. Less invasive options, such as minimally invasive procedures or catheterization, might be explored first to manage retention without the need for surgery.
Yes, radiation therapy to the prostate can potentially help with urinary retention if the retention is caused by prostate cancer within the gland.
Radiation works by targeting and shrinking the cancerous tissue within the prostate, which can relieve the pressure on the urethra and improve urinary flow. This approach can be particularly beneficial when the retention is due to a tumor obstructing the urethra or bladder neck. By reducing the size of the tumor, radiation may alleviate the blockage and help restore normal bladder function.
However, the effectiveness of radiation for relieving urinary retention depends on several factors, including the size and location of the tumor, the extent of the obstruction, and how well the cancer responds to the radiation. Additionally, while radiation can be effective, it may also cause some temporary irritation to the bladder or urethra, leading to symptoms like increased frequency or urgency of urination during and shortly after treatment.
In cases where radiation is considered, it would typically be part of a broader treatment plan, potentially in combination with other therapies like ADT, especially in metastatic prostate cancer. The goal would be to address both the local symptoms (like retention) and the overall disease progression.
I just wish to add that a paramedic MRI of the prostate and the PSMA pet scan could be used parallel in order to understand the situation about your cancer in your prostate and retention.
Can these damaged and the sbrt radiation surviving in your prostate most resistant strains of the crpc still produce some PSA and generate psma avidity on the psma pet scan? Could the production of the PSA increase and would the surviving cancer still be crpc?
I had an sbrt radiation of my prostate and the cancer in my prostate survived a high radiation of 38 Gy.
Yes, the damaged and radiation-surviving CRPC strains in your prostate could still produce some PSA and show PSMA avidity on a PSMA PET scan. Let's explore these points in more detail:
### 1. **PSA Production**
- **Residual PSA Production:** Even if the CRPC cells are damaged, they can still produce PSA, though potentially at lower levels. The amount of PSA produced would depend on the viability and activity of the remaining cancer cells. If the cells are severely damaged, PSA production might be minimal, but if some cells retain their function, they could continue to secrete PSA.
- **Potential Increase in PSA:** If these surviving cells begin to recover or if they proliferate, you might see an increase in PSA levels. This could indicate that the remaining cancer is still active, though possibly less aggressive than before. However, any increase in PSA after treatment should be carefully monitored to assess whether it reflects tumor regrowth or other factors.
### 2. **PSMA Avidity**
- **PSMA Expression:** Surviving CRPC cells that retain PSMA (Prostate-Specific Membrane Antigen) expression could still generate avidity on a PSMA PET scan. This is because PSMA expression can persist in cancer cells even if they are damaged or have a reduced growth rate. Therefore, these cells could still be detected by PSMA PET imaging.
- **Interpretation of PSMA PET:** PSMA avidity on a PET scan indicates the presence of cells expressing PSMA, but it doesn't necessarily correlate directly with aggressiveness or proliferation rate. The scan could pick up these surviving cells even if they are not rapidly growing.
### 3. **Continued CRPC Status**
- **CRPC Characteristics:** The surviving cancer cells would likely still be considered castration-resistant prostate cancer (CRPC) because they have demonstrated resistance to both androgen deprivation therapy (ADT) and radiation. These cells have adapted to grow despite low androgen levels, a hallmark of CRPC.
- **Behavior of Surviving Cells:** The surviving CRPC cells might behave differently post-radiation. While they could still produce PSA and express PSMA, their growth rate and ability to spread might be reduced due to the damage inflicted by the SBRT. However, they would still technically be classified as CRPC.
### 4. **Monitoring and Management**
- **PSA Monitoring:** Regular PSA testing will be essential to track any changes in PSA levels, which could indicate changes in the behavior of the remaining cancer cells.
- **PSMA PET Scans:** Periodic PSMA PET scans could help monitor the extent of PSMA expression and detect any new areas of avidity, providing valuable information about the cancer's status.
- **Consideration of Further Treatment:** If PSA levels rise significantly or PSMA PET scans show increasing avidity, further treatment options, such as systemic therapy or other local treatments, might need to be considered.
### Summary:
The damaged and radiation-surviving CRPC strains could still produce PSA and show PSMA avidity on a PET scan. These cells would likely still be classified as CRPC. If these cells begin to recover or proliferate, PSA production could increase, signaling the need for careful monitoring and potentially further treatment.
Q. Could after the radiation produced PSA and PSMA avidity proportions shift in comparison to the proportions (PSA versus PSMA avidity) after radiation?
A. 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.
Q. Are these sbrt radiation surviving crpc strains senescent cells or proliferating cells? How is it possible that the crpc strains survived such a high radiation?
A. The SBRT radiation-surviving CRPC strains in your prostate could be either senescent or proliferating, depending on several factors, including the extent of the damage inflicted by the radiation and the biological characteristics of the cancer cells. Let’s break this down:
### 1. **Senescent Cells vs. Proliferating Cells**
- **Senescent Cells:**
- **What Are They?** Senescent cells are cells that have stopped dividing but are not dead. They enter a state of permanent growth arrest due to significant DNA damage, which can be caused by treatments like radiation. These cells do not proliferate, but they can remain metabolically active and might secrete inflammatory molecules that can influence the tumor microenvironment.
- **Role After Radiation:** If the surviving CRPC cells are senescent, they would no longer contribute to tumor growth, but they might still produce PSA and could affect surrounding tissues. Over time, senescent cells can accumulate and might be cleared by the immune system, but they can also persist and potentially lead to further complications.
- **Proliferating Cells:**
- **What Are They?** Proliferating cells are actively dividing cells. If some CRPC cells survived the SBRT radiation and retained their ability to proliferate, these cells could continue to grow, potentially leading to tumor regrowth and recurrence.
- **Role After Radiation:** These cells might have survived due to inherent or acquired resistance mechanisms, which allowed them to repair the radiation-induced DNA damage or bypass the damage entirely.
### 2. **Mechanisms of Radiation Survival in CRPC Strains**
- **Intrinsic Resistance:**
- **DNA Repair Mechanisms:** Some cancer cells possess robust DNA repair mechanisms that can fix the double-strand breaks caused by high-dose radiation. These cells might repair the damage efficiently enough to survive and continue proliferating.
- **Cellular Pathways:** Certain pathways, such as the PI3K/AKT/mTOR pathway, are involved in cell survival and can be upregulated in resistant cells, helping them avoid radiation-induced death.
- **Tumor Microenvironment:**
- **Hypoxia:** Areas of the tumor that are poorly oxygenated (hypoxic) are less sensitive to radiation. Hypoxic cells can survive radiation more easily because radiation is less effective in inducing DNA damage without oxygen. These cells may persist after treatment and could potentially proliferate later.
- **Cancer Stem Cells:** A subpopulation of cancer cells, known as cancer stem cells, may be more resistant to radiation. These cells can survive and later give rise to new tumor growth.
- **Acquired Resistance:**
- **Adaptive Responses:** Cancer cells can adapt to the stress of radiation by activating survival pathways, altering gene expression, or acquiring mutations that confer resistance. This can happen even after radiation therapy, leading to the survival of a small population of resistant cells.
### 3. **Why Did Some CRPC Cells Survive Such High Radiation?**
- **Incomplete DNA Damage:** Although SBRT is highly effective, it may not uniformly kill all cancer cells. Some cells might receive sublethal doses of radiation or have the capacity to repair the damage.
- **Heterogeneity of Tumor Cells:** Tumors are heterogeneous, meaning they consist of various cell types with different sensitivities to radiation. The most resistant cells survive and potentially proliferate.
- **Limitations of Radiation:** High-dose radiation is more effective at killing rapidly dividing cells, but if some CRPC cells were in a quiescent (non-dividing) state during treatment, they might have survived because radiation is less effective against non-dividing cells.
### Summary:
The CRPC strains that survived SBRT radiation could be either senescent (non-dividing) or proliferating. Their survival might be due to robust DNA repair mechanisms, intrinsic or acquired resistance, or a protective microenvironment like hypoxia. While some cells might be damaged and senescent, others could potentially recover and proliferate, leading to tumor recurrence. Understanding the behavior of these surviving cells is crucial for determining the next steps in treatment and monitoring.
New guidelines to prevent skeletal events in metastatic prostate cancer
MRI prior to HDR Brachy and HDR intensity.
