The concept of an "oligometastatic state" is that there exists an early stage where metastases are few in number and are in some way different from metastases that develop later. It also means that there are no micrometastases in systemic circulation (in bone and lymph) and in reservoirs like bone, nerve cells, lymph nodes and other organs. If such a state exists, the cancer can be picked off, like dandelions in a lawn, and the person can be cured.
The alternative concept is that cancer spread is always polymetastatic. Thousands of cells are released from the primary tumor. They find their way to sites where they change the tissue they land in, making it amenable to future growth. This is called "seed and soil." A metaphor might be mushrooms growing at the base of an oak tree. The mycelium extends everywhere throughout the soil and into the roots of the tree. Occasionally, a mushroom crops up. You can pick all the mushrooms you want, but the fungus is never destroyed. There is no way to destroy the fungus short of destroying the roots of the oak tree and sterilizing the soil. This is what "systemic" means.
Is there an oligometastatic state that is part of the natural history of all cancers? It may be that there is an oligometastatic state for some cancers but not others. We previously learned that SBRT + SOC to oligometastases in breast cancer did not slow progression or increase survival over SOC alone.
I updated this article with some new data about lung cancer.
Iyengar et al. reported the results of the NRG Lu002 trial. There were 215 patients at 68 sites with oligometastatic (≤3 mets) lung cancer. All were given systemic therapy (90% had both immunotherapy + chemotherapy). 81 were treated with "consolidative therapy" radiation/surgery to the lung and all metastatic sites followed by systemic therapy. After 2 years of follow-up:
• Overall survival was the same in both groups.
• Progression-free survival was the same for both groups.
• Grade 3 toxicity (pneumonitis) was higher in the consolidative therapy group (10% vs 1%)
TA—You raise an interesting question concerning other cancers but as one whose prostate cancer has been characterized as oligometastatic, with metastases to the upper spine and right femur identified to date, I appreciate even more your clear explanation of the differentiation between oligometastatic and polymetastatic characterizations of the disease. Many thanks.
if there is no such state of enhanced vulnerability of cancer, between primary tumor before seeding, and widespread visible mets, then a whole lot of the videos from dr scholz and the PCRI are undermined because he mentions this state of diagnosis with attendant spot treatment, all the time ..
That is a pretty strong statement against some very well respected oncologists. It’s one thing to have a differing opinion. But to call the other opinion “internet garbage” TA, seems a bit aggressive. Especially since there are no definitive studies at this point to prove or disprove their hypothesis.
Keep in mind these people are not not buffoons or charlatans and there are many other well respected doctors who share their opinion on the subject.
"Especially since there are no definitive studies at this point to prove or disprove their hypothesis." That's exactly the point! When a doctor markets his opinions to patients as medical science, he does patients and science a disservice, and it becomes Internet garbage. A top doctor would be more circumspect in his pronouncements, knowing that many patients will accept what he says as the gospel truth. I know that I don't know, and I also know that no one knows. Why not say so?
The problem that I have with Dr. Scholz is that he states his opinion as fact. Very confidently so. While his opinion is probably better than many others, it's still opinion that is prone to errors. Some super strong opinions of his can easily be falsified by scientific studies that say otherwise so I don't understand why he risks his credibility by being so absolute.
I understand your point but O wholeheartedly disagree. Based upon my own experience, i have a differing opinion. I prefer a doctor that is thinking out of the box. Scholz does so based upon his own knowledge and experience with literally over 3000 patients. Thats a big number. I am personally convinced that that type of thinking saved my life and my wife’s life when she had a very aggressive form of breast cancer 20 years ago. Let me explain
First me. When I was diagnosed with stage four metastatic PC some 7 years ago, Scholz advised me to do what is now known as the “triplet therapy” (chemo/Lupron/Zytega). Only thing is at the time the triplet therapy was not proven to extend lives. I got a second opinion from UCLA where they told me that this triplet therapy “made sense” and they’d like to see a study, but they could never recommend it without a study proving its efficacy. Scholz was clear that this was not yet proven but he’d been using it for years and he had seen how well it performed. It was my choice and I did it. Fast forward 2-3 years and the triplet therapy was proven to extend lives substantially. By the way, before that, Scholz was combining Zytega and lupron long before that double treatment was proven to extend lives by some 40%. The theory most oncologists were operating under for years was to use one treatment at a time until it stopped working saving treatments for the future. Scholz saw it very differently. Attack the cancer hard while it was weaker
Now my wife. When she was diagnosed with Her2 positive aggressive breast cancer we went to a Scholz clone in the breast cancer business. Dr. Link. He told us that a new drug being used against her2 at UCLA on very advanced patients (Herceptin) was working quite well. Although these patients were still dying, they were first improving. He thought it might work better at her early stage than the SOC. Again, we decided she would use it fully aware of the unknown risk/reward profile. 7 years later Herceptin was proven to reduce recurrence by over 60% and hers never recurred. It was such a game changing medicine that they made a movie about it in 2008. “Living Proof”.
My point is that the medical world is moving so fast right now that I prefer doctors willing to look forward and give me the opportunity to consider “out of the box” alternatives based upon logic and reason. I will then make the choices and live with the upside and downside. I am currently continuing to do this with Dr. Scholz as I use SBRT to attack individual mets despite no proof yet that it extends life and I tried Provenge even tho not approved for hormone sensitive men.
I know others would disagree but I see Scholz as brave and kind to present patients with options that are not SOC. What’s in it for him? It’s a liability risk. He does it to help his patients understand their options.
"Out-of-the-box" thinking is great for formulating hypotheses, and kudos to researchers who formulate testable hypotheses. A hypothesis is tested in a randomized clinical trial, not by treating all patients with it. Some actually conduct clinical trials, for which many men owe their lives. That's exactly what Tanya Dorff does when she has a hypothesis.
But treating patients only based on hypotheses is just confirmation bias at work. I remember Scholz criticizing Snuffy Myers for doing just what he is doing now. The researcher should have "equipoise" between the alternatives tested.
Let me share an anecdote with you... A patient of his initially had only pelvic lymph node mets for which he should have had whole pelvic radiation to possibly cure him. Instead, Schotz told him to get only those lymph nodes zapped. The patient soon had bone mets, in addition to some new LN metastases. Scholz recommended he play whack-a-mole with the new metastases. I argued that he now has systemic cancer and needs systemic therapy. The patient saw the logic and got Pluvicto in Germany and hormone therapy. Who was right? I don't know for sure yet, but playing whack-a-mole without systemic therapy is very risky.
I think every person should decide on his own therapy based on full information about potential benefits and risks. But hawking one kind of therapy on a youtube video is the opposite of full disclosure. If you have any influence on him, you might want to persuade him of that.
I stand by you every person should decide on his therapy based on information about potential benefits and risks. Let me give an example. My urologist didn’t know when to stop chemotherapy (8 fusions) until I told him stop the therapy as I was having serious side effects like edema and eczema.
That's a laugh. And our resident super-authority TA, with no medical degree, expresses his opinion as fact and decries a well respected medical doctor's advice as "just a lot of Internet garbage." Well done TA, you've just exposed your insufferable arrogance for all to see. You've really outdone yourself this time. BTW, I've read Dr Scholz' book "Invasion of the Prostate Snatchers" and I've seen plenty of his online videos. All excellent in my opinion.
I don't need research to defend Dr Scholz. His reputation will withstand the insults you gratuitously hurl at him. No, he's not a god, just a man who has dedicated his life to the treatment of men with prostate cancer and has the intellect and credentials to do so. He's the real deal and not a wannabe like you. You could have fooled me about not pretending to be a doctor. A little humility would go a long way.
No, just a medical degree and a history of successfully treating hundreds if not thousands of patients will do. I'm sure he's done plenty of research that you wouldn't even begin to understand but hey you are pretty good (almost said god) at being a keyboard research warrior.
Actually, he's done very little research. Compare the quantity and quality of published trials on prostate cancer to a true top GU Oncologist like Howard Scher at MSKCC:
As you can see for yourself, Howard Scher has published 441, while Scholz has just 27 under his belt. You can go through them yourself to see what influence each has had on the field.
So why haven't you even heard of Howard Scher, while you worship Mark Scholz? It's easy to see the reason: Scholz markets his private practice to patients with patient conferences and youtube videos, while Scher doesn't. Scher is famous among his peers, while Scholz is only famous among patients who don't know any better.
That is not to say Scholz is bad. I've met with him and found him to be as competent as most. I only object to his making unsupported claims to patients at conferences and on youtube. Patients deserve better.
And you've done no research at all. Patients deserve better than listening to your name dropping and so-called advice. I respect Dr Scholz. I don't worship him and I take offence at a rank layman disparaging him or his contributions.You've done a great job taking over this forum but not all of us worship you. Lighten up dude.
All I've ever done is report what researchers (like Scher) have found. If you didn't worship him, you wouldn't take offence at my very reasonable and limited criticism. Your ego, and lack of skepticism toward anything your god says, is getting in the way of acknowledging the truth, and may be ultimately detrimental to your health.
Listening to you condemning HIFU would have been detrimental to my health. Luckily I got that treatment before you showed up on this forum and I am doing just fine. I also take plenty of supplements ... just to annoy you. 😜
Your uninformed choices are your business, and don't annoy me. It only causes reaction when patients (or doctors) try to influence others with pseudoscience.
I would definitely try with the system therapy first and if I still see some Mets on the psma pet ct scan with contrast I would SBRT the visible Mets if it is safe to do so.
Bravo the logic here! And highlighting again the concept of "seed and soil". And the concepts of micrometastases and polymetastasis. And that oligometastasis as a state of PCa, with helpful implications for treatment, is only a hypothesis! Unproven and quite possibly wrong.
One implication is that one should always have a medical oncologist. Because "system-wide micrometastases" is a good description of prostate cancer after metastasis.
And it bothers me that the preponderance of expert presentations I see, on PCa groups I attend, so often concern ever-fancier surgeries and radiation treatments. And not so much on the topic of this post.
I think Dr Aggarwal said that he will not treat PSA if the imaging is not showing anything. Sorry, I am not a doctor just what I picked up on this forum.
It looks that the PSA alone is not enough to put you on more toxic medication.
You said to Brian that Abiraterone will not kill the cancer if it is administered later after the chemotherapy. His PSA dropped to very low (0.008) after the chemotherapy and he stayed on Degarelix alone (like myself).
I never thought that Abiraterone or ADT alone or in combination could kill the cancer. Maybe only after the chemotherapy?
Brian's PSA is now around 1-2 and has to decide what to do.
Even just only early chemotherapy 6 cycles what I also received on the recommendation of professor Izard (radiation oncologist) and the board of urologists at my hospital. My MO of the time thought that some people live long on ADT alone. When I realised that my median life expectancy is only 2 years after the diagnosis as polymetastatic with distant Mets in my neck it took me not long to decide to except the early chemotherapy as I believed that that would extend my life expectancy to 3 years median with my diagnosis. Now six years later people think that I just made up all of this (that I have a terminal illness).
I don't have visible Mets on any scan. The visible cancer is only in my prostate and it is a recurrent strain emerged after the failed sbrt radiation of my prostate a year and a half ago now. I am on bicalutamide 100 mg now because my MO thinks that I am not eligible for nubeqa while my RO said that if I get Enzalutamide than I have to pay myself for it because I don't have any visible metastasis at present and the Australian PBS would refuse to pay for Enzalutamide. My oncologist wish to solve this issue by putting me on the Astra Zeneca phase I/ii clinical trial to test for toxicity of the latest advanced Astra Zeneca parp inhibitor. That is why I am now stuck with the bicalutamide.
I don't really know how will they put me on the Astra Zeneca clinical trial if I don't have a visible metastasis. Maybe if I stay on bicalutamide long enough maybe I will develop a visible metastasis?
Super thanks Seaside! The podcast is a right-up-to-date and top quality report on the latest metastatic prostate cancer therapies.
OK, the "beyond counting metastases" headline is a cheap and misleading statement. But don't be discouraged.
Once you listen, you'll realize this discussion is in fact an important update on what we have learned from, and are building from, the CHAARTED, STAMPEDE and ARASENS clinical trials.
Everyone is encouraged to listen to the podcast - it's only 16 minutes. Also another benefit is how positive the speaker is.
I understand what you are saying (I also thought the same) but it looks different than the definition of micrometastasis after reading the Wikipedia article about micrometastasis:
Wikipedia
Micrometastasis
Article Talk
This article needs attention from an expert in Medicine. The specific problem is: Some content may not be easily understood by readers with no medical background. (February 2024)
A micrometastasis is a small collection of cancer cells that has been shed from the original tumor and spread to another part of the body through the lymphovascular system.[1] Micrometastases are too few in size and quantity to be picked up in a screening or diagnostic test, and therefore cannot be seen with imaging tests such as a mammogram, MRI, ultrasound, PET, or CT scans. These migrant cancer cells may group together to form a second tumor, which is so small that it can only be seen under a microscope. Approximately 90 per cent of people who die from cancer die from metastatic disease, since these cells are so challenging to detect.[2] It is important for these cancer cells to be treated immediately after discovery, in order to prevent the relapse (regrowth of the cancer) and the likely death of the patient.
Detection of micrometastatic cells
The major concern with micrometastases is that the only way to determine if they are present in distant tissue is to remove cells from where they are located and look at slices of the tissue under the microscope. The typical biopsy procedure involves hematoxylin and eosin (H&E) staining of specific markers that correspond to the particular tumor type.[3] Although surgeons are able to remove parts of a single lymph node from the body to screen, it is impossible to remove every lymph node and other organs (lungs, liver, bones, etc.) to look for spread.[2] Doctors must assume that the tumor cells have likely spread to other regions of the body if micrometastases are present in one of the lymph nodes. The presence or absence of micrometastases is crucial in choosing the right treatment option for cancer patients.[citation needed]
The detection of micrometastases in the sentinel lymph nodes (SLN) is the primary indicator of its spread to the regional lymph nodes, bone marrow, peripheral blood and ultimately to distant metastatic sites, since they are the first of the nodes that cancer would travel to.[3] This concept applies to melanoma, breast cancer, and other solid tumors, including colorectal, esophageal, stomach, lung, head and neck, vulvar, and penile cancers.[3] Therefore, the presence of these cells in the SLN can help make predictions regarding the patient’s diagnosis and prognosis. For example, it has been found that the prognosis of women who have micrometastases to the sentinel lymph node is poorer than that of women who do not have any evidence of tumor in these lymph nodes.[2] The same applies to patients with melanoma and the other solid tumor cancers.[citation needed]
Before the micrometastases colonize at a distant site, the tumor cells can be found in the bone marrow or peripheral blood.[3] Tumor cells found in the bone marrow are known as disseminated tumor cells (DTCs), and those found in the peripheral blood are known as circulating tumor cells (CTCs). These cells have successfully left the primary tumor microenvironment and the SNLs, and are able to survive in a non-native environment, which makes them more aggressive.[3]
Treatment of micrometastases
In breast cancer patients, if micrometastases are present in the SLN, removal of these nodes is often the next step in treatment. Axillary lymph node dissection involves the excision of the nodes from the armpit, or axilla, region. Depending on the progression of the cells, the surgeon will determine the level of dissection that is required. Level one is the least invasive, as it involves just the removal of tissue around the axillary vein, while level three is the most aggressive as it removes all of the nodal tissue from the axilla.[4] It may be necessary to remove other lymph nodes in addition to the SLN. Each woman has a different number of lymph nodes in her body, so determining how many nodes to remove is based on location, rather than number.[4] The lymph nodes serve as a filtering system for the lymphatic system, so it is important to preserve as many as possible, while also ridding the body of all cancer cells.[citation needed]
Learn more
This section may be confusing or unclear to readers. (February 2024)
In order to eliminate micrometastases that are not near lymph nodes and have traveled to distant regions of the body, chemotherapy and radiation therapies are necessary. However, since most micrometastatic tumor cells are in the nonproliferative G0 phase[clarification needed], standard cytotoxic chemotherapies may not be as useful.[5] Therefore, adjuvant chemotherapy and adjuvant radiation therapy[clarification needed] are more effective to eliminate micrometastases, since they are aimed to target dividing and quiescent cells[clarification needed]. Adjuvant therapies are administered after the removal of the lymph nodes. The significance of these therapies is to serve as a “clean up” method for those cells that have migrated elsewhere from the primary tumor.[2] Researchers still question whether this treatment method to rid the body of this small cluster of cells that may or may not progress is worth the side effects that it may cause.[6] Side effects include fatigue, hair loss, nausea, or vomiting. In addition, adjuvant therapies do not always result in a cure and they do not benefit all patients.[citation needed]
References
edit
Stephan, Pam (2017-12-08). "Micrometastases Meaning and Role in Lymph Nodes". very well health. Retrieved 2018-04-19.
"Micrometastases in Lymph Nodes Need Treatment". breastcancer.org. 2009-06-04. Retrieved 2018-04-19.
Leong, Stanley; Tseng, William (2014-02-05). "Micrometastatic cancer cells in lymph nodes, bone marrow, and blood: Clinical significance and biologic implications". CA: A Cancer Journal for Clinicians. 64 (3): 195–206. doi:10.3322/caac.21217. PMID 24500995.
Pantel, Klaus; Kote, Richard; Fodstad, Oystein (1999-07-07). "Detection and Clinical Importance of Micrometastatic Disease". Journal of the National Cancer Institute. 91 (13): 1113–1124. doi:10.1093/jnci/91.13.1113. PMID 10393719.
Whittington, Elizabeth (2009-12-12). "The Implications of Micrometastases in Early-Stage Breast Cancer Revealed". curetoday.com. Retrieved 2018-04-19.
Last edited 4 months ago by Vanessa hexagon
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I would say that it is more precise than just stating that it is under the detection levels of most sensitive scans in my humble opinion. Anyhow people can read it here. I apologize for being to precise.
I don't understand your point. Your long post includes "Micrometastases are too few in size and quantity to be picked up in a screening or diagnostic test, and therefore cannot be seen with imaging tests such as a mammogram, MRI, ultrasound, PET, or CT scans. " which is exactly what I said.
This section may be confusing or unclear to readers. (February 2024)
In order to eliminate micrometastases that are not near lymph nodes and have traveled to distant regions of the body, chemotherapy and radiation therapies are necessary. However, since most micrometastatic tumor cells are in the nonproliferative G0 phase[clarification needed], standard cytotoxic chemotherapies may not be as useful.[5] Therefore, adjuvant chemotherapy and adjuvant radiation therapy[clarification needed] are more effective to eliminate micrometastases, since they are aimed to target dividing and quiescent cells[clarification needed]. Adjuvant therapies are administered after the removal of the lymph nodes. The significance of these therapies is to serve as a “clean up” method for those cells that have migrated elsewhere from the primary tumor.[2] Researchers still question whether this treatment method to rid the body of this small cluster of cells that may or may not progress is worth the side effects that it may cause.[6] Side effects include fatigue, hair loss, nausea, or vomiting. In addition, adjuvant therapies do not always result in a cure and they do not benefit all patients.[citation needed]"
I believe that we should understand better what micro Mets are than just saying that they can't be detected by the most sensitive scans. My aim is to clarify what micro Mets are so we can understand better micrometastases.
Another consideration might be the ability of surrounding tissue to induce dormancy. Research studies are ongoing to determine if the microbiome modulates dormancy in cells that were previously spread. This concept may also be supported by evidence that recurrence rates seem similar for both surgery and radiation. Hopefully ongoing research will inform us.
This phase 2 RCT is not proof, but surely it is an indication that SBRT can be of value? Addition of Metastasis-Directed Therapy to Intermittent Hormone Therapy for Oligometastatic Prostate Cancer: The EXTEND Phase 2 Randomized Clinical Trial | Oncology | JAMA Oncology | JAMA Network
PFS on combined SBRT + hormone therapy vs hormone therapy only
Progression-free survival mostly means that PSA hasn't increased. SBRT treats PSA by elimimating the largest mets which is the source of PSA. EXTEND proves that if you eliminate the largest metastases, you can go longer without ADT before your PSA increases.
But most patients want a way of extending survival, not just lowering PSA temporarily.
Right, PFS is mostly based on PSA in EXTEND, but not only. Radiographic progression, death and other clinical events were also followed. Of 7 such events, six were in the hormone therapy only arm, and one in the SBRT + hormone therapy arm.
Despite the small numbers, the large disparity means a statistical significance with a one-tailed test p = 0.02807 if my arithmetic is correct. Narrowly below significance with a two-tailed test.
That's quite remarkable. I've read this old study (2017) which seems to indicate that gene TP53 is locally damaged way earlier than previously thought, and so it starts mutating protein p53, which in theory is what met cells need to thrive and expand. So it would be an early process it seems.oncotarget.com/article/2356...
I believe in the science as it guides our medical practitioners. The best medical advice on Prostate cancer (the condition at hand) should be guided by Standard Of Care (SOC) which uses outcomes of trials to obtain the highest level of evidence, and even proof, if such a concept can be so judged.
Subject to the foregoing I believe a prostate cancer medical oncologist could use his knowledge of the patient in his guidance and advice. The patient with whom he has had some period of time in consultation and an understanding of the patient view of disease and treatment can be incorporated into the medical advice; the age of patient, the patient response to previous treatment, the experience of the M. O. with out of SOC choices through trials yet to mature or out-of U. S. practices and publications. Not an experiment with the patient but an opportunity to expand boundaries with each patient as he is understood within the context of care. That is, some oncologists and some patients. Tailored and not uniform.
I would be (and am) interested in the ideas my M. O. has for my care that may be outside the S. O. C. tree which is the safest to follow. Honesty about the chance of side effects and limitations must be broached. In a sense this use of treatments that are not highest Level of Evidence but may extend current treatment or suspend current treatment are worthy of discussion. This includes oligo status as well as other stages. My comment is more broad than to reply strictly to TA and his topic above.
Doesn't sound good for whack-a-mole, although some say it has helped them.
I've wondered how there could be just one bone met without there being unseen cancer cells elsewhere (or at least without that being overwhelmingly likely), based on earlier remarks I've read here.
Thanks for this--very interesting. I note that re: the SABR-COMET trial, there is no hint of the particular cancer types in the abstract. I have no idea how one would compensate for the vastly different prognoses of the cancers studied in the trial and their distribution in the two cohorts.
The only other cancer I've heard of oligometastatic states being discussed is thyroid cancer, which shares the tendency with prostate cancer of being slow-growing--except when it ain't.
What I like about the approach proposed by Dr Scholz is that it is methodical and can help going through diagnostic/treatment in sequential order instead of immediately jumping to the worst conclusion.
I'll take my own situation as an example since it is pretty much what he's discussed in many of his videos.
A patient with cancer limited to the prostate area and pelvic lymph nodes goes through a treatment with curative intent (Lupron + Abiraterone + radiation in my case).
Once the curative intent treatment is over, we wait to see if Testosterone comes back and whether the PSA stabilizes after a few months or keeps going up.
My PSA went up every blood test and was now at 1.07 mid-May. We did a CT scan that showed nothing and a bone scan that showed a single met on the right shoulder blade.
What Dr. Scholz suggests doing in this situation is that rather than immediately electing to put the patient on ADT for life, perhaps needlessly, perhaps not, is to approach this by a process of elimination.
Step 1: You only ZAP the lone metastasis that has been discovered without giving ADT right away so that the ADT is not masking other potential areas of tumor growth.
Step 2: After the radiation, you monitor the PSA closely to see if it is now stable or if it is still rising.
Step 3a: If the PSA is still rising and a new scan reveals a meta that was missed on the previous scan, then you treat it locally and ZAP it and repeat step 2.
or
Step 3b: If the PSA is still rising and a new scan shows nothing new, then you treat it as a systematic issue and you take ADT until it becomes undetectable and then you stay on it two more months for good measure. Then you take a vacation and see if it is stable or rises and act accordingly.
or
Step 3c: If the PSA is now stable, then you assume that your initial curative intent treatment got rid of your systematic cancer burden aside of a metastasis that was initially missing during the original treatment because it was too small and away from the pelvic region treated. But now that it has been treated, you have a chance to be fine as your cancer load/burden is gone or small enough that your immune system can deal with it.
By approaching the issue procedurally like described above, I do not see why we'd be more at risk since all of this can be assessed in a relatively short time.
In my eyes, I do not see an immediate danger with this approach. And I do see a possible benefit because if you are lucky enough to fall into step 3c, then you won't shorten your life by taking ADT that you might not have needed. You only take ADT because you've confirmed that you need it.
It may be methodical, but it doesn't follow any known science. There certainly are safety concerns in allowing micromets to grow and multiply. It relies on treating PSA instead of treating the cancer.
I recently, after waiting a couple years , received a PSMA scan. Areas in the iliac lymp nodes lit up as well as a spot on my iliac bone. Oncologist and radiologist agreed that my best option was the radiate. So 38 sessions which were done on those identified areas and also added the prostate foscia for good measure. I had started back on ADT but they added Bicalutimide to the mix. This was to be done for six months past radiation. I am currently in holding pattern not taking any medication and watching for PSA rise. I am still T sensitive so that should be a good indication. That said, this was the first breakthrough in my journey haven gone 8 years being told the treatments were palatine and now curative. Time I’ll tell but if not for the PSMA scan it would have continued to be undetected and thought micrometastatic.
The below 2023 article contends that not only is there an oligometastatic state for colon cancer, but that in the context of liver mets treated by metastasectomy, 10 year survival reflects cure.
Furthermore, this concept has been around for a long time. See below 2007 article.
Moreover, surgical excision of limited liver metastases, is standard of care, not alternative medicine. From up To Date, arguably a repository of standard of care information.
"Sometimes surgery is an option for a person whose colorectal cancer has spread in a limited way outside of the intestine to an area such as the liver. Up to 30 percent of people may be cured if metastases in the liver can be completely removed (the medical term for this is "resected"). In order for surgery to be considered, there must be no evidence of cancer outside of the liver, and there must be an adequate amount of normal liver left behind after the resection to sustain life."
Note: Up to Date uses the term: "cured"
Quote from the below 2022 article: "Survival beyond 10-years after resection of colorectal liver metastases (CRLM) reflects cure in most (98%) patients "
Maybe it's true for colorectal cancer. But clearly, there's no such thing as an oligometastatic state that applies to all cancers. The breast cancer case is especially disappointing because, like prostate cancer, it is an adenocarcinoma.
Minor point: The usual colon cancer that is the subject of the above articles is also an adenocarcinoma.
I acknowledge your cautionary notes regarding prostate and breast cancer and the concept of oligometastatic state. But both colon cancer and renal cell carcinoma data indicate the oligometastatic state is not just wishful thinking but for real.
There is no reason to think the same state may not exist in other solid cancers. The TNM staging system which applies to all solid cancers is a testament to a common pathway view. Perhaps both prostate and breast cancer will be better subcategorized, perhaps by number, size, and location of metastases, even if only 1 small distant lymph node, the latter currently placed in M1 disease, in combination with biomarkers, whether driver mutations, etc., into a more restricted sub-category that will be responsive to metastasis-directed therapy in a phase 3 statistically significant study, proving a restrictive oligometastatic state in those cancers.
Concerning your statement: "there is no oligometastatic state for lung cancer." I provide you with the below reference: a June 2024 article that reports on an oligometastatic state in lung cancer: admittedly one defined as having only 1 metastatic site. With this number restriction, they reported significant HR values and CI intervals.
That is just a retrospective database analysis, which is only useful for raising hypotheses. NRG Lu-002 was an actual prospective trial to test such hypotheses.
If you learn about "levels of evidence," there is no conflicting data.
Debulking the primary has proven value in oligometastatic prostate cancer, but there is no such proof for met-directed therapy.
I acknowledge that the study is just a retrospective database analysis, though the large National Cancer database and propensity matched. But the NRG study is of those with up to 3 metastases, so it has not proven that 1 is not the magic number or that some other, yet-to-be-determined, combination of restrictive clinical or biomarker factors will define an oligometastatic state. This intermediate step has to exist, just as fledgling birds exist, informed by the incremental nature of genomic evolution as modeled by the "Hallmarks of Cancer", the incremental acquisition of phenotypic capabilities.
You can imagine all kinds of hypotheses, but until they are clinically tested, they are only figments of one's imagination. Also, remember that observable metastases is a very different thing from actual metastases.
It is a joint clinical guideline by American Society for Radiation Oncology (ASTRO) and the European Society for Radiotherapy and Oncology (ESTRO). They are the experts; are they not?
Good, but I asked you to look up the dates (plural). And the first author of the article you referenced is Iyengar. Do you see where it says,"Based on the lack of significant randomized phase 3 trials, a patient-centered, multidisciplinary approach was strongly recommended for all decision-making regarding potential treatment." ? That was the best anyone could do in September2023.
I will tell you the date of the trial I referenced (NRG-Lu002). The link and date is in my article, but I will tell you. It was published May 29, 2024. And the author is (wait for it)- Iyengar -the same guy! And in it, he reports the results of the first randomized Phase 3 trial that he lacked the previous year. Here is the link if you truly want to learn:
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Radiotherapy in the Definitive Management of Oligometastatic Prostate Cancer
TACE (transarterial chemoembolization) for prostate cancer mets to liver or lung?
not PCa related but promising in vivo therapy for cancer metastasis 
Can oligometastatic prostate cancer be ‘cured’ with ‘total therapy’? This paper suggests there is a sliver of hope. 
Phase 1 study SBRT for bone metastases in oligometastatic patients. So far, "few toxicity events and high local control rate" 
