Apologies in advance if I posted something similar a few days ago, but I didn't receive any responses and thought the post probably did not get published.
Age 66 and on ADT for 12+ yrs. Did whack-a-mole to largest tumor 2+ yrs ago when it appeared on PSMA scan to be responsible for PSA rise from undetectable to low numbers (less than 1.0). PSA went back to undetectable again and lasted about 6 months before becoming detectable and rose over the last 18 months or so, and most recently almost doubled over an 11 week period from ,20 to .35. Last weeks PSMA showed some increase in one of my several (4-5) tumors. The tuor was 1 of 2 in my vertebra.
I am meeting with my MO tomorrow to discuss how we should proceed and am wondering if whack-a-mole (radiation) is an option for a vertebral tumor WHEN it is not presently causing me any pain. Of course, regardless of the answer to this question, my MO and I will be discussing adding and/or modifying my present treat of Lipitor and Abiraterone. ( I just read about some positive phase 2 results in a specific type of 177 Lu-PSMA-I&T study published in Onclive.com that I will raise with her
Thank you in advance for your responses.
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jfoesq
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In June 2017 SBRT was applied to two spinal vertebrae from which I had not experienced any pain. The treatment was considered successful and has not been repeated.
I'll be watching for responses and I hope you post what your MO says. Our situations are similar. 61 years old. 6.5 years of treatment. Eligard and abiraterone. PSA is slowly rising from undetectable. Current PSA is 0.03. Recent bone scan shows possible growth in one tumour. No pain. I see my MO in January.
I have mets to two vertebrae and have not had unusual pain in either place. I was not terribly worried about them as pain was greater elsewhere. I had radiation to a few other places to reduce cancer bulk. Not sure why they chose sites that they did.
Just recently I had a pathological fracture to C1 with no trauma. Jut broke while sleeping, (probably dreaming something exciting.) The doctors are now talking about radiation. I wish they had done so before. Breaks other places such as the major double break of my femur are really nasty but your spine can be even worse. So it makes sense to me to wack the spinal mets to lessen the chance of pathological fracture?
You’ve been through the wringer for certain, S2! I’m sorry.
How did you find out about C1 fracture? I simply dunno…I did get radiation to my C2 tumor and it still fractured post treatment. Since the site still glows under PSMA PET even after all these years (7), there is a rather extensive surgery plan in place between my RO and neurosurgeon once growth is confirmed and I consent…maybe through another fracture?
I woke up and tried to get out of bed. Any movement to head produced extreme pain about 12 out of 10. I had to support my head with my hands and move an inch at a time to get vertical then i could walk baby steps and some how made it to the ER without unstabilizing the fracture. they gave me pain meds and did a CT which the initial late night consult said was not fractured. i some how managed to get home along dirt road in the fog without splitting the C1 completely. I now know that i can never go to that ER. i have a list of things to avoid and to question but the admin policies are hidden from the patient and you have no way of knowing what might be next.
What a nightmare, brother! I hear you on the 12/10 pain - about 2 weeks into the radiation on C2 I could hardly move to vertical and had to put a handle on my bedpost to get up...like you said, holding my head, etc. Based on your story - I now think it was fractured at that time and wasn't picked up because the contrast was blowing it out on scans.
You are a true superman to drive to and from the ER. Best of luck, brother. - Joe M.
**Oligometastasis: Good News from the ORIOLE Study
--To the growing and hopeful list of strategies for attacking prostate cancer, let us add this approach: Whack-a-Mole.
--That’s how Johns Hopkins radiation oncologist Phuoc Tran, M.D., Ph.D., describes it to his patients. The actual scientific name for this highly sophisticated strategy is stereotactic ablative radiotherapy (SABR, highly focused, intense doses of radiation), for men with oligometastasis – up to three small bits of cancer that have broken away from the main prostate tumor and started to grow elsewhere.**
FYI- I am familiar with radiation in cases of oligometastasis. I was not DXd with many tumors but was NOT DXd as oligomet....perhaps because another met was removed during my prostate surgery from my lymph nodes in the abdomen. Fortunately, I haven't developed any known new mets since my DX 12+ yrs ago.
Radiating those who are oligomet has been around for a few years. But, it seems as though MO's and the Radiation Oncs are expanding the use of 'whack-a-mole" beyond those who are oligomet and radiating some of us who have 1 or more mets that oligomet. My MO radiated my acetabulum 2+ yrs ago because she felt the Pet?CT identified that particular tumor as growing and causing the PSA rise. Now, she thinks, perhaps my vertebra tumor is responsible for the latest rise. I don't believe there are any quality studies indicating whack-a-mole increases life expectancy for non-oligmet PC but hopefully it will.
I played whack-a-mole this past summer. PSA was creeping up. PSMA scan showed 3 METs on pelvic lymph nodes. Received 5 treatments of radiation. Don’t know how many GYs. PSA has dropped from .51 to .2. Will continue to monitor PSA. If - when - it goes up, will undergo another scan.
Whack-a-mole refers to handling an infestation of moles in the yard by hitting them one at a time whenever one pops up out of a hole. It is descriptive of radiation to bone mets whenever one appears on a scan.
Whack-a-mole has a connotation of dealing with matters in a piecemeal manner without achieving a complete solution. I suppose that describes radiation of bone mets, because it is palliative and not curative.
Vintage- Of course, for many of us, it is not curative. But- it can be more than just palliative if it lengthens one's years of living That's what I was asking about when I indicated that my met is not causing me pain.
There are very experienced, knowledgeable MOs (and probably ROs) that believe oligo metastatic disease is potentially curable. Part of that aggressive initial therapy to treat newly diagnosed oligo disease involves MDT (RT). There are some MOs that are treating newly diagnosed Oligo disease with triple therapy, RT or RP of primary tumor (prostate), RT to any disease out side the pelvis and whole pelvic radiation following the triple therapy.
Of course, it depends on your definition of cure. MO have used that word in patients who have 5 years post treatment (for certain cancers) with no imaging, labtest or clinical evidence of cancer. If a prostate cancer patient has X years of undetectable PSA, clear PSMA PET, off all meds and T returned to a normal range-are they "cured". Only additional time in given studies will tell.
I find a water hose will keep them critters on the run. I also believe in the Jack Daniels Therapy for bone mets. Seems to be working well for me. I don't think there are any clinical trials right now.
I'm not into Whacking much. I hear Chicago is now Whacking More Rats than NYC. Wow. And what are these huge 30 acre wildfires John Muir is talking about? What is that? The size of a golf course?
Do you know why the MO elected to radiate them? Were they displaying "uptake" when a Pet/CT took place, indicating that they were PERHAPS responsible for a rise in PSA? Or, was there some other reason for radiating them? And- does he have mets elsewhere or are they all in the spine?
There was a slight uptake in them- they were previously stable. He was diagnosed with mets in his hip, pelvic bone and spine. All stable for a few years. He has annual scans. PSA did not go up significantly.
It is becoming commonplace to radiate isolated metastasis, whether bone or nodal. After RP for a G9 in 2021, I had a solitary T8 met appear detected on PSMA PET after my PSA started creeping up from undetectable to 0.37. It was successfully radiated with 3 separate high dose treatments (M,W,F with total of 30 Gy). It was killed on followup imaging.
I am currently undetectable 2 years post triple therapy. Last Lupron shot was 7/23. My JH MO said if I develop any future mets they will treat with radiation. His goal is to kill any visible tumor, not palliate pain.
My situation is very similar, my MO, Dr. Sartor, said that I can continue using SBRT indefinitely depending on location and number of tumors. The radiology oncologist will make the call on your location and his ability to treat. For me, I’m going to continue playing whack a mole as long as possible before moving on to other treatments. I’m trying to keep those bullets in the holster as long as possible.
I’m with you Ed. As long as I can get any cancer location identified, it will be guided SBRT to potentially kill it all, or at least greatly reduce/debulk that particular offender!
Had two abdominal mets found on PSMA last Fall, and treated both with a week each of SBRT. PSA (so far) has dropped down to .12! Staying with the Whack-a-Mole treatment unless simply too dangerous.
Trying to stay ahead of needing future debilitating drugs! I am avoiding hormonal, PARP, or chemo treatments as long as possible. Whack dem Moles!
I have been on Lupron for 12+ years except for 3 “vacations “ in my first 5 yrs. And, I have been on abiraterone for most of the time I was on the Lupron.
Well, TA and others would counsel ADT now, but my MO at Dana Farber said that MY cancer has been so slow-growing that waiting as long as medically safe to employ other treatments would be safe at this point. I concur. I know that ADT, and probably more radiation, is lurking in my future at some time. I’m 77, and trying get a bunch of ‘buffering years’ before accepting ADT and all that portends. My parents both died from cancers by 85. Trying to beat that record!
Update: My MO suggested we proceed with what-a-mole to the vertebra apparently responsible for the PSA increase and continue with Lupron and Abiraterone. The “uptake “ for the vertebra was not highly avid, so she didn’t think a shift in my treatment meds was warranted, at present. She thought. She thought DOCETAXEL should not be used currently because I will be more valuable later and also thought the side effects were not worth enduring presently. She also said XOFIGO works by attacking the “environment “ where the cancer cells are and also thought that wasn’t the best choice at this point. So, we will proceed with the radiation and monitor PSA and possible do more scans, if called for, following the radiation.
Xofigo is recommended when you have multiple visible bone Mets. Plus because you are on Abirateron plus Prednisone it could have consequences like bone fracture. Therefore it is too risky and to early to use xofigo for only one visible metastasis. Could you ask for an FDG scan later if your PSA goes up considerably?
To be clear, my Pet/CT showed only the veterbral tumor with increased sclerosis and “uptake”was 1 of my 2 veterbral Mets. I do have at least, 3 other bone Mets including my largest one in my left acetabulum (hip) which was radiated in 2014 and again about 2-3 yrs ago. The others are in my rib, right hip and another vertebrae.
Combining PARP inhibitors with SBRT radiation is an emerging area of interest in cancer therapy, particularly for prostate cancer and other cancers with DNA repair deficiencies. Here's an overview of how this combination could work and what to consider:
Rationale for Combining PARP Inhibitors with SBRT
1. Mechanism of Action Synergy:
SBRT delivers high doses of radiation to a precise area, causing double-strand DNA breaks in cancer cells.
PARP inhibitors (like olaparib or rucaparib) block the repair of single-strand DNA breaks. When these single-strand breaks accumulate, they can evolve into double-strand breaks, which are lethal to cells, especially those with DNA repair defects (e.g., BRCA1/2 mutations).
2. Enhanced Tumor Kill:
By using PARP inhibitors, cancer cells are less able to repair radiation-induced DNA damage, increasing the likelihood of cell death.
This combination can be particularly effective in tumors with homologous recombination repair (HRR) deficiencies.
3. Potential to Sensitize Tumors:
PARP inhibitors may sensitize tumors to radiation, potentially allowing for better control of the disease even in difficult-to-treat sites.
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Timing and Short-Term Use During SBRT
During SBRT: Using PARP inhibitors during the course of radiation could amplify the DNA damage caused by SBRT. This timing leverages the radiosensitization properties of PARP inhibitors.
Short-Term Use: Short courses of PARP inhibitors (initiated shortly before and continued during SBRT) could provide the synergistic benefit without prolonged exposure to the drugs, thereby reducing the risk of side effects like fatigue, anemia, or nausea.
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Clinical Considerations
1. Eligibility:
Best suited for patients with BRCA1/2 or other HRR gene mutations, as these patients derive the most benefit from PARP inhibitors.
For non-HRR-mutated cancers, the benefit might be less pronounced but is still being investigated.
2. Toxicity:
Combining PARP inhibitors and SBRT may increase side effects like gastrointestinal or hematologic toxicity. However, short-term use can mitigate these risks.
Close monitoring by your medical team is essential.
3. Evidence:
While preclinical studies and some early-phase clinical trials show promise, larger randomized trials are still needed to establish the safety and efficacy of this combination definitively.
4. Availability:
Discuss with your oncologist if this combination is feasible and whether any clinical trials are available that align with your case.
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Conclusion
Combining PARP inhibitors with SBRT radiation during treatment could be a highly effective, innovative strategy, especially for cancers with HRR deficiencies. Short-term use might optimize benefits while minimizing risks. However, this approach should be carefully tailored to your specific cancer type, genetic profile, and overall treatment goals. Collaboration between your radiation oncologist and medical oncologist is crucial to ensure the best outcome.
Would you like details about specific trials or examples of cases where this combination has been successful?
Timing- Wow. My MO mentioned this to me when I inquired about a particular PARP inhibitor and as I recall, she said pretty much what you just posted. But- she emphasized to me, as you stated that the PARPs seem to only be effective IF the patient has a DNA repair DEFICIENCY. Because I do not have such a deficiency, she recommended agst me getting treated with a PARP.
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