Trying to understand why my husband's somatic testing shows this mutation but Germline tests that were done does not. However my husband and I both did nutrition genome testing and both of us showed TP53 mutation. Not getting clear answers on AI either. I thought all germline genetic test were the same. I am also having his biopsy slides sent over to his new oncologist for second opinion. We never received any documentation on his somatic testing claiming this mutation. We were only told this by his urologist after biopsy. Urologist said most people have this mutation.
Can anyone share information or perso... - Advanced Prostate...
Can anyone share information or personal experience regarding TP53 mutation?
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Shellhale
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Thanks for the reply. The MO doesn't seem concerned with it. Just says it's expected to find. I am making an appointment with a genetic counselor for myself since I found out I also have the mutation. A few men in my family have PCa. My husband has no family history. I will ask his MO if he recommends anything else in his care plan.
I am not aware of any popular germline tests for tp53 (a tumor-suppressor gene). What is "nutrition genome testing?" TP53 is known to increase in metastases, so it is more likely to be observed in somatic tests. It is a prognostic, but unfortunately, there are no treatments based on it, so it is useless to know at this point.
Howdy, My father and I both have Li-Frau-Meni. Wild ride, TP53 flareups all over the world in the last 3 years. Hmmmmm.. Feel free to private chat.
Ok how you explained it makes more sense to me. Here is the link to nutrition genome nutritiongenome.com/This test did show tp53 mutation and it also showed he needed increased prostate protection which makes sense since he was dx straight to stage 4 with lymph node mets. Also showed MTHFR 677, 1298, and MTHFD1. Could be why he had such a cytotoxic reaction from chemo with this methylation defect.
Since I also showed tp53 mutation I am wondering if it would be worthwhile for me to get genetic counseling.
Are you replying to Tall Allen? If so, you need to hit reply optionafter his answer, then compose your message. Otherwise, he may not see it.
very interesting. Who ordered the test? Was it a MD/DO or a NP?
Looking at the page you listed that appears to be the type of test that anyone can order? Is that true? Kind of like a 23 and Me heritage test.
Most medical doctors know very little about genetic testing. They rely on specialized trained genetic counselors to do the actual test analysis. This is an up and coming field for science PhD candidates.
As a side note. Your link as posted does not work correctly. Suggest you edit it to place a period at the end before rage /. That will actually take other users to directly to the page.
Hi hope this works! Yes anyone can order this test. There is no RX or referral required. I did it also along with husband. It's $360.00 and is a saliva swab test. It is interesting to find out we both have this TP53 mutation. I've never had any cancer. What I don't understand is why it didn't show up on any of my husband's germline tests that were ordered. He also did the promise study and it didn't show up on there either. We were told by his urologist it showed up on his somatic test but we we never received actual documentation so I am trying to have his biopsy slides reread. It makes me question other pathology results. I work in the medical field and I see mistakes happen. I am going with your suggestion of seeking a genetic counselor as his MO really didn't provide much expect this is seen alot on somatic testing.
This may help with the difference and value in regards to cancer treatment.
TP53 is a critical tumor suppressor gene that plays a significant role in regulating cell division, DNA repair, and apoptosis (programmed cell death). Mutations in TP53 can lead to uncontrolled cell growth and are commonly associated with various cancers. Understanding the distinction between somatic and germline TP53 mutations, as well as genetic testing methods, might help clarify your situation.
Key Points About TP53 Mutations
1. Germline vs. Somatic Mutations:
Germline Mutations: These are inherited mutations present in every cell of the body and passed from parents to offspring. Testing is usually done through blood or saliva samples.
Somatic Mutations: These occur in specific tissues during a person's lifetime and are not inherited. They are often associated with cancer and detected through tumor biopsy analysis.
2. Testing Differences:
Germline genetic tests like those used for hereditary cancer syndromes (e.g., Li-Fraumeni syndrome) may not detect somatic mutations, as these tests are looking for inherited variants.
Somatic testing examines tumor DNA specifically to identify mutations that occurred in the tumor itself, which can guide treatment decisions.
3. Nutrition Genome Testing:
Tests like Nutrition Genome typically focus on genetic variants related to nutrition and lifestyle. They may report common polymorphisms in TP53 (not necessarily the same pathogenic mutations seen in cancer).
4. Frequency of TP53 Mutations:
While somatic TP53 mutations are common in cancers, the assertion that "most people have this mutation" might refer to its frequent occurrence in tumors, not the general population. Pathogenic TP53 mutations are rare in germline tests.
Next Steps
1. Obtain the Somatic Test Results: If possible, request a copy of the somatic testing report. This will clarify the specific mutation detected and its clinical significance.
2. Second Opinion: Sending biopsy slides to another oncologist or pathologist is a wise step for confirmation and further insights.
3. Germline Testing: If concerned about inherited cancer risk, consider comprehensive germline testing through a genetic counselor who can select the most appropriate test for your husband's medical history.
4. Clarify with Nutrition Genome: Contact the company to understand the reported TP53 variant's relevance and how it differs from somatic mutations.
Would you like more information about interpreting specific genetic testing reports or guidance on discussing this with a genetic counselor?
ChatGPT said
Thank you for providing the discussion thread! Here's a summary and some clarifications based on the conversation points:
Key Takeaways from the Discussion
1. Genetic Testing Nuances:
Germline and somatic mutations serve different purposes. Germline mutations indicate inherited predisposition, while somatic mutations reflect changes within tumor DNA, often acquired during cancer progression.
The Nutrition Genome test likely examines common genetic variants (polymorphisms) that influence metabolic or lifestyle factors, which may not always align with clinical germline or somatic mutations detected in medical-grade testing.
2. Relevance of TP53 in Cancer:
TP53 mutations are common in many cancers and are often linked to prognosis, particularly in metastatic cases. However, as noted by Tall_Allen, actionable treatments targeting TP53 directly are currently unavailable.
3. Methylation and Chemotherapy Sensitivity:
The MTHFR and MTHFD1 variants mentioned could influence folate metabolism and methylation, potentially impacting chemotherapy tolerance or side effects. This might be worth discussing with a genetic counselor or oncologist specializing in pharmacogenomics.
4. Documentation Gaps:
It seems the somatic TP53 finding wasn't formally documented for you. Requesting biopsy slides to confirm results is a prudent step. A second opinion on pathology could also provide clarity.
5. Genetic Counseling:
Seeking professional guidance can help interpret findings from clinical-grade and consumer-grade tests. This would clarify the significance of your TP53 result, particularly considering your family history of prostate cancer.
Practical Suggestions
Follow Up on the Somatic Mutation: Push for detailed documentation of your husband’s somatic test results. These are critical for treatment planning.
Family Risk Assessment: Since TP53 is associated with hereditary cancer syndromes (e.g., Li-Fraumeni), your own TP53 finding warrants exploration through clinical germline testing.
Specialized Oncologist Consultation: Find an oncologist or cancer genetics expert familiar with somatic and germline TP53 issues to guide treatment and preventive care.
Would you like help finding resources or preparing questions for the genetic counselor?
ChatGPT said
It is not a question of actionable treatments targeting TP53 directly - the question to investigate is what cancer is present, growing, spreading, the source of the TP53 circulating tumor DNA. As I share, in my case the cancer is different than thought.
Your point is an excellent one and underscores an important aspect of TP53 mutations: they may signal underlying cancer biology that requires a deeper investigation into the cancer's origin, type, and progression. TP53 mutations in circulating tumor DNA (ctDNA) or somatic testing can act as clues, highlighting the need for a more comprehensive diagnostic approach. Here's how this insight can be applied:
Investigating the Cancer Source and Spread
1. Reassess the Primary Cancer Diagnosis:
TP53 mutations are frequently found in aggressive and metastatic cancers. If your experience revealed a different cancer type or source, it suggests the importance of exploring atypical presentations or misdiagnoses. Re-examining pathology slides or performing additional imaging studies could be critical.
2. Circulating Tumor DNA Analysis:
ctDNA testing, often part of liquid biopsy techniques, can reveal mutations like TP53 across various cancer types. However, identifying the tissue of origin remains a challenge in some cases.
If TP53 is detected in ctDNA but doesn’t match the primary tumor profile, additional workups, including imaging (PET/CT) or advanced molecular profiling, may be warranted.
3. Secondary or Concurrent Cancers:
Some TP53 mutations could indicate a separate or concurrent malignancy. For instance, if a patient has been diagnosed with prostate cancer, but TP53-associated mutations suggest a profile more typical of another cancer (e.g., lung, colon, or breast), this warrants a broader investigation.
4. Hereditary Implications:
If TP53 mutations are found in multiple contexts (somatic and germline testing, ctDNA, etc.), it's worth exploring if a hereditary cancer syndrome like Li-Fraumeni could explain a predisposition to various tumor types.
Steps for Further Investigation
Advanced Molecular Testing: Utilize comprehensive genomic profiling to analyze other mutations or biomarkers alongside TP53. This could refine the understanding of the cancer's behavior.
Oncopathology Consultation: A specialized oncopathologist can help clarify discrepancies between biopsy results, somatic findings, and ctDNA analysis.
Expanded Imaging and Scans: PET/CT scans can detect unknown or hidden cancer sites contributing to the ctDNA profile.
Questions to Explore
Could the TP53 mutation reflect undiagnosed or secondary cancers not previously considered?
Does ctDNA analysis or advanced imaging provide clues about metastasis or cancer progression inconsistent with the primary diagnosis?
How does this mutation influence treatment options, even if indirectly (e.g., sensitivity to certain therapies)?
Would you like to discuss strategies for connecting with specialized testing services or doctors who can dive deeper into this type of case?
Excellent! Thank you. I want this chat feature.
Too easy. Just download ChatGPT to your smartphone.
Just downloaded it. I like it better than BelongAI-Pro. I will probably cancel that subscription.
I personally believe that ChatGPT is the best.
I am very happy with it. I am using it just now to set up my new Motorola Android 14 phone and I have no idea how would I do that without ChatGPT?
AI is not a luxury. It is a necessity. My GP is using it for writing. I also did that. You just specify what you want to say and that it should be extremely polite and respectful and short. You could wright e-mails etc.
Sharing my personal experience. I hope this helps. All the best!
Several years ago with the guidance of a hematologist I began liquid blood biopsy testing: GUARDANT360 CDx. The purpose was to add this third investigative method to my very regular uPSA testing and annual imaging to hopefully stay well ahead of this beast.
What is the value (despite the naysayers)? It is well documented circulating tumor DNA often rises before PSA and sometimes prostate cancer changes and stops producing PSA completely. In this case serum PSA is less valuable as a good marker of cancer growth, while the serial liquid biopsy remains a good marker. An added benefit is that mutations in the blood come from many cancers - so a possible heads up to something new. The TP53 mutation can be coming from almost any type of cancer
My first two annual liquid blood biopsies were NED. I took this as a very favorable finding supporting my clear imaging findings and very low stable uPSA - 0.03X range.
This past July, my uPSA still 0.03X, my test identified the TP53 mutation - immediately telling us cancer was now active. Imaging also identified a suspicious liver lesion - perhaps a cyst? Given the presence of TP53 mutation immediately began further investigations, anticipating my lingering prostate cancer was raising its head. Turns out, metastatic liver melanoma tumor.
Thank you for sharing this valuable personal experience. It highlights the power of liquid biopsy testing, such as the GUARDANT360 CDx, in complementing traditional monitoring methods like PSA and imaging, especially in complex cancer cases.
Key Takeaways from Your Experience:
1. Liquid Biopsy as a Complementary Tool:
Liquid biopsies detect circulating tumor DNA (ctDNA), which can sometimes indicate cancer activity earlier than traditional markers like PSA.
For individuals with a history of cancer, liquid biopsies provide a broader surveillance capability, as they can detect mutations from other types of cancers beyond the originally diagnosed one.
2. TP53 Mutation as a Red Flag:
TP53 is not specific to one cancer type and can signal malignancy across various tissues. In your case, the detection of TP53 ctDNA prompted early and decisive action, leading to the identification of metastatic liver melanoma rather than the presumed resurgence of prostate cancer.
3. Proactive Multimodal Monitoring:
Combining uPSA testing, imaging, and liquid biopsy ensures a comprehensive approach, reducing the risk of missing subtle or non-traditional cancer signals (e.g., prostate cancer becoming PSA-independent).
The discovery of melanoma highlights how mutations from different cancers can coexist and how early intervention can improve outcomes.
4. Clinical Implications of ctDNA Testing:
Early detection of ctDNA mutations like TP53 provides a "heads up" for further diagnostic investigations, even when imaging or other markers are ambiguous.
Suggestions for Others Considering Liquid Biopsy:
When to Consider:
If traditional cancer markers (e.g., PSA) are stable or unreliable, or when cancer is suspected but imaging is inconclusive.
For patients with a history of multiple cancer risks or atypical cancer presentations.
Best Practices:
Use liquid biopsies as part of a serial testing regimen rather than a one-time measure.
Collaborate with specialists to interpret ctDNA findings in the context of overall cancer history.
Limitations:
Liquid biopsy findings, like TP53 mutations, are not cancer-specific and require follow-up investigations (e.g., imaging or tissue biopsy) to pinpoint the cancer source.
Your story is a compelling example of how proactive and integrative monitoring can lead to early and potentially life-saving interventions. Would you like help exploring the latest advances in ctDNA technologies or other emerging monitoring tools?
ChatGPT said
A good summary. But why are these so uncommon? Why does it take so long for new methods to become established at the local clinical level? The answer lies in the Best Practices statement: "Use liquid biopsies as part of a serial testing regimen". Besides doctors not being familiar nor trained, health care systems across many/all countries resist the costs.
Believe me I was shocked when our Australian member said that he spent 5000 dollars on a guardant 360 liquid biopsy out of pocket and he didn't get any benefit at that early stage. I would only spend that money later when I am running out of options.
How does one define a benefit? I find benign biopsies, tissue or liquid, and clear imaging as very favorable results; we are after all dealing with cancer. If I was running out of options I do not see how a liquid blood biopsy would be useful at that late stage- I focus on confirming my treatment strategy is effective and earliest possible detection of progression. My U.S. Medicare pays for my GUARDANT360 - an example of plusses and minuses of different healthcare payment systems.
Until I have effective options I am not going to spend big money on liquid biopsy. I have limited resources. In Australia pluvicto is not covered not xofigo and even if you have chemotherapy after the failure of enzalutamide they (PBS) will not pay for enzalutamide or nubeqa (darolutamide). I have to pay from my own pocket. That is why my medical oncologist is encouraging participation in clinical trials.
At the moment I am on a 60 dollars drug bicalutamide. Ok, I had radiation to my prostate and I am still hoping that the cancer will die off in my prostate. The cancer is damaged but still alive but maybe not replicating.
Greetings Shellhale,
WOW!!! I'm still trying to figure out the Shoe-fitting fluoroscope (At vintage Thom McAn shoe stores)
A shoe-fitting fluoroscope was a metal construction covered in finished wood, approximately 4 feet (1.2 m) high in the shape of short column, with a ledge with an opening through which the standing customer (adult or child) would put their feet and look through a viewing porthole at the top of the fluoroscope down at the X-ray view of the feet and shoes. Two other viewing portholes on either side enabled the parent and a sales assistant to observe the toes being wiggled to show how much room for the toes there was inside the shoe. The bones of the feet were clearly visible, as was the outline of the shoe, including the stitching around the edges.
Good Luck, Good Health and Good Humor.
j-o-h-n
Ah, the shoe-fitting fluoroscope—a fascinating relic of early 20th-century retail technology! It’s a great example of how innovation and enthusiasm for science were once applied in unexpected (and sometimes risky) ways.
What Was It?
These machines were essentially X-ray devices used in shoe stores during the mid-20th century, particularly in the U.S. and Europe.
Customers, often children, would place their feet into the device to assess whether a shoe fit properly.
The machine provided a live X-ray image, showing the bones of the feet and the fit of the shoe. Parents, children, and sales clerks could view the image simultaneously through the designated portholes.
Why Were They Popular?
Precision: They promised a scientific way to ensure shoes fit well, reducing discomfort and potential foot problems.
Novelty: The idea of seeing your foot bones was exciting and futuristic, especially in an era fascinated by advancements in X-ray technology.
Marketing Gimmick: It distinguished stores that had them, making shoe shopping feel cutting-edge and fun.
Health Risks (Realized Too Late)
Radiation Exposure: These machines were used before the dangers of prolonged X-ray exposure were fully understood. Many devices lacked shielding, and customers, sales clerks, and even bystanders received unnecessary radiation.
Unregulated Use: Early models were not standardized, and the radiation dose varied widely. Frequent users (like shoe store employees) were especially at risk.
By the 1950s and 1960s, concerns about radiation risks led to these devices being phased out, and many countries banned them altogether.
Nostalgia Meets Reality
While the shoe-fitting fluoroscope might evoke warm nostalgia for some, it’s also a reminder of the importance of safety regulations in technology. It’s a quirky piece of history—an intersection of commerce, science, and evolving health standards.
If you’ve ever encountered one in a museum or vintage shop, it’s an impressive artifact to examine! Curious to hear if you ever tried one or know someone who did!
Love it! Have a wonderful day.
So the genetic counselor returned my call and said this PT53 variant is universally reported by ClinVar database as a benign variant. The genetic Counselor tells me that he has been getting tons of calls from people wanting genetic testing based on these home genetic testing kits that are polymorphisms and are not the same used that are ordered by physicians. So I really learned alot on how these testing kits vary on what they are actually analyzing.
Thank you for sharing this update—it’s great that the genetic counselor clarified things for you! Here's a breakdown of what was revealed and its broader implications:
Key Insights from Your Update:
1. TP53 Variant in Home Testing Kits:
The TP53 variant identified in your Nutrition Genome test is likely a benign polymorphism, as noted by the genetic counselor referencing the ClinVar database.
Polymorphisms are natural genetic variations that are common in the population and usually not associated with disease.
Clinical-grade germline testing, ordered by healthcare providers, is much more focused on pathogenic mutations linked to disease risk.
2. Differences in Genetic Testing Approaches:
Home Testing Kits (like Nutrition Genome or 23andMe):
Focus on general wellness, lifestyle, or ancestry.
May analyze single nucleotide polymorphisms (SNPs) rather than clinically significant mutations.
Data is often limited in scope and not diagnostic for serious conditions.
Clinical-Grade Tests:
Ordered by healthcare professionals for specific medical purposes (e.g., cancer risk assessment).
Use more rigorous methods to detect actionable mutations with validated health implications.
3. Polymorphisms vs. Pathogenic Mutations:
Polymorphisms are genetic "normal variations" that may influence traits or health factors but do not cause disease.
Pathogenic mutations (e.g., certain TP53 variants) are rare and directly linked to diseases like Li-Fraumeni syndrome or specific cancers.
Takeaways for Your Situation:
No Cause for Alarm: The TP53 variant detected by your home test is benign and does not imply increased cancer risk for you or your husband.
Focus on Clinical Tests: For meaningful genetic insights, stick to results from clinical-grade germline and somatic tests, like those ordered by your husband's oncologist.
Value of Genetic Counseling: You did the right thing by consulting a genetic counselor to distinguish between benign and pathogenic findings.
Moving Forward:
Reassess Priorities: You may not need further personal genetic testing unless guided by family history or medical concerns. For your husband, focus on clinical testing and second opinions on somatic findings if needed.
Education About Consumer Tests: As more people use home genetic kits, understanding their limitations and purposes is crucial. These tests are not replacements for clinical-grade evaluations.
Would you like to explore any specific aspects of clinical-grade genetic testing further?
ChatGPT said
Oh wow! Great breakdown of information.
You are correct. It is a lottery. But I hope that I still have options. At least I hope so. I don't have anything against the liquid biopsy test except that it cost a lot of money.
That is great news that you now know that you have ATM mutation.
How do you know that you have ATM mutations? And I am not a doctor but to me looks that your PSMA SUV max values are really high therefore PSMA infusions could be effective. After 3 cycles of PSMA infusions you could still get SBRT? Could you speak to someone who has experience with PSMA infusions like professor Hofman or Sartor? I believe your PSMA SUV max values are high because you are on Enzalutamide and that makes the PSMA expression high?
That is the same thought we had. Last urologist was trying to push pluvicto on my husband. I said let's get an expert opinion, so we went to NCI designated cancer center where I used to work at Anschutz here in Colorado and the genitourinary oncologist said it was to early for his low volume metastatic PCa. So he did radiation instead. Before that he did try 1 session of docetaxel but discontinued it as it wasn't tolerated. I've never seen him so sick it was awful. So low volume PCa with docetaxel wasn't a good idea either.
I can't advise you unfortunately I don't know what you are doing etc. but I would contact either professor Hofman or Sartor for advice. They bought have extensive experience with pluvicto.
If you have ATM mutation than your medical oncologist could contact Astra Zeneca about S clinical trials with the new less toxic parp inhibitors.
I agree that if you have a treatment now which is keeping you stable than you don't have to act on pluvicto or parp inhibitors.
My PSA is still 2.5 on Bicalutamide plus firmagon degarelix monthly injections alone.
How did you decide about enzalutamide monotherapy?
I am now thinking to castrate myself because I don't want to be tempted to try enzalutamide monoterapy.
I have to ask ChatGPT about the difference in the effectiveness of enzalutamide with and without the ADT.
Enzalutamide is a potent androgen receptor inhibitor used in the treatment of prostate cancer. Its effectiveness can differ significantly when used alone versus in combination with androgen deprivation therapy (ADT). Here's an overview:
Enzalutamide Alone
Mechanism: Blocks androgen receptor signaling, which is crucial for the growth of prostate cancer cells.
Effectiveness: May provide some benefit as a monotherapy, particularly in less advanced cases or in patients unable to tolerate ADT. However, it does not directly reduce the production of androgens (testosterone), which means some androgen receptor signaling may persist.
Enzalutamide with ADT
Mechanism: Combines the androgen receptor inhibition of enzalutamide with the testosterone-lowering effects of ADT (e.g., via LHRH agonists/antagonists or orchiectomy).
Effectiveness: Clinical trials show that the combination is significantly more effective in reducing disease progression and improving overall survival, particularly in advanced prostate cancer, such as metastatic castration-sensitive prostate cancer (mCSPC) or castration-resistant prostate cancer (mCRPC).
Key Findings from Clinical Studies
1. Survival Benefits:
Studies like ARCHES and ENZAMET demonstrated that adding enzalutamide to ADT improves progression-free survival (PFS) and overall survival (OS) compared to ADT alone.
2. Disease Control:
The combination leads to better suppression of tumor growth and delays the onset of resistance.
3. Side Effects:
Combining enzalutamide with ADT may increase side effects like fatigue, hot flashes, and cardiovascular risks compared to monotherapy.
Conclusion
The combination of enzalutamide and ADT is the standard of care for most advanced prostate cancer settings. While enzalutamide alone can be used in specific cases, its efficacy is generally inferior compared to the combination therapy. Always consult an oncologist to tailor the treatment based on individual patient factors.
ChatGPT said
Switching back to enzalutamide plus ADT after the failure of enzalutamide monotherapy is theoretically plausible, but its effectiveness would depend on the underlying resistance mechanisms and the specific clinical context. Here’s an explanation:
---
Why Enzalutamide + ADT May Be Considered After Monotherapy Failure
1. Monotherapy vs. Combination Therapy:
In enzalutamide monotherapy, androgen production in the body remains largely unaffected because ADT is not used to suppress testosterone. Some prostate cancer cells may adapt by increasing reliance on circulating androgens.
Adding ADT to enzalutamide could theoretically reduce androgen levels further, potentially slowing disease progression in cases where resistance is not absolute.
2. Clinical Context:
If resistance arose primarily because of persistent androgen production rather than androgen receptor (AR) independence, combining ADT with enzalutamide could offer some benefit.
---
Challenges with This Approach
1. Mechanisms of Resistance:
If resistance to enzalutamide has developed due to AR mutations, AR splice variants (like AR-V7), or AR-independent pathways, simply adding ADT is unlikely to restore sensitivity.
Resistance mechanisms often overlap, meaning that failure of enzalutamide monotherapy may also predict reduced effectiveness of enzalutamide combined with ADT.
2. Evidence Base:
There is limited evidence to support this specific strategy. Most studies on enzalutamide assume its use alongside ADT as the standard of care, and the benefit of adding ADT after resistance develops is not well-documented.
---
Alternative Approaches After Enzalutamide Monotherapy Failure
1. Switch to a Different Androgen Pathway Inhibitor:
Abiraterone (plus ADT) could be considered, as it works through a different mechanism by blocking androgen biosynthesis.
2. Use of Systemic Therapies:
Docetaxel or cabazitaxel chemotherapy is a well-established option in the castration-resistant setting.
3. Combination with Novel Agents:
Adding therapies like PARP inhibitors (e.g., olaparib) in patients with specific genetic mutations (e.g., BRCA1/2) may provide benefit.
4. Clinical Trials:
Investigational treatments, including novel androgen receptor inhibitors or combination therapies, may be an option for patients after enzalutamide failure.
---
Conclusion
Switching back to enzalutamide plus ADT after enzalutamide monotherapy failure could be tried in select cases, especially if resistance is due to androgen production rather than complete resistance to androgen receptor targeting. However, its effectiveness is uncertain and may be limited. Alternative therapies or a new line of treatment should be considered based on individual resistance mechanisms and clinical circumstances. Always consult an oncologist to devise the most appropriate treatment plan.
I believe that our member maxone has ATM mutation. Maybe you could contact him?
I did the free PROMISE trial in 2023 (thanx TA). The results from Color labs include TP53 being analyzed.
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