PSA rockets up to 344

[Arcticfox44]

Hello - I received quite shocking news during my visit to the Mayo Clinic last week. My PSA has jumped to 344 from a low of 3.6 last November, when I completed chemo with cabazitaxel. PSA did start to rise quite soon, into double digits, but this is by far my highest PSA ever.

Dr. Kwon recommended starting chemo with taxotere plus carboplatin and this is scheduled to start in Cyprus on 17 June (the earliest appointment I could get). He also recommended adding Xtandi or Nubeqa, but the "protocols" at the oncology center here in Cyprus would not permit that, so we have agreed to skip it for now and see how the chemo goes. As noted in my previous postings, I had chemo with docetaxel in 2022, when PSA started at 62 ng/ml and fell to 8 ng/ml after six cycles. I started chemo with cabazitaxel in July 2023 when PSA was 83, and as reported above it had fallen to 3.6 by November 2023. I am on Zoladex shots every three months.

The latest Mayo report sums up: "Interval progression of intensely PSMA avid nodal and peritoneal metastases since 11/06/2023. miPSMA Expression Score 3."

PROSTATE BED: No abnormal PSMA uptake to suggest locally recurrent disease.

LYMPH NODES: Interval increase PSMA uptake of pelvic sdewall soft tissue left worse than right, with the most prominent soft tissue in the left posterior pelvic sidewall (SUV max: 15.2)

New PSMA avid left para-aortic lymph node (SUV max: 13.5)

OSSEOUS DISEASE: No PSMA avid osseous lesion.

OTHER METASTATIC DISEASE: Multifocal PSMA avid peritoneal and mesenteric nodularity, most prominently seen along the hepatic surface and the small bowel mesentery, highly suspicious for peritoneal metastases. For example, linear perihepatic lesion along the right hemidiaphragm (SUV max: 5.4) and focal soft tissue anterior to the left lateral hepatic lobe (SUV max 10.4)

Multifocal porta hepatis, periportal and gastrohepatic PSMA uptake without definite corresponding CT abnormality, indeterminant for nodal metastases versus peritoneal metastasis. For example, PSMA focus anterior to the caudate lobe (SUV max 11.7) and PSMA avid focus along the gastrohepatic ligament (SUV max: 9.5)

Stable PSMA activity within the bilateral thyroid lobes.

Reference SUV max:

- Parotid gland: 13.1

- Liver: 4.1

Additional findings on the noncontrast low-dose CT: Gynecomastia. Atherosclerotic calcification including coronary artery calcification. Pulmonary atelectasis. Colonic diverticulosis. Advanced musculoskeletal degenerative change with thoracolumbar curvature. Compression deformities of T11, T12, L4, L5. Transitional lumbosacral vertebra. Hepatic cysts. Colonic diverticula.

The Mayo report adds:

He will repeat genetic testing to determine if he has any targetable genetic mutations or high tumor burden for which he could qualify for potential treatment with a PARP inhibitor or immunotherapy in the future. (I gave a blood sample for testing before leaving the Mayo.)

I was instructed to return for follow-up after 3 to 4 cycles of chemo to assess treatment response to perform the following tests: PSA, Testosterone, Alkaline phosphatase, AST, ALT, Total Bilirubin, and Direct Bilirubin. In addition PSMA PET to identify sites of prostate cancer relapse after failed treatment, per medical necessity and per FDA, NCCN and CMS guidelines.

I would be interested in any comparable experiences. It seems quite unusual that PSA would make such a powerful comeback after last year's chemo with cabazitaxel and I wonder whether there's anything we could or should have done to ensure it stayed lower for longer.

[GP24]

I would try to get Pluvicto or Lutetium 177 therapy instead of the next chemo. Taxotere plus Carboplatin after you had Cabazitaxel will not be very effective.

[Arcticfox44 in reply to GP24]

Thanks. This is the kind of feedback I need. I'll run it past the Mayo.

[Wynnsts]

Sorry for the delay in replying, my experience with Xtandi was a good experience, no harsh side effects. It quickly reduced my PSA from 7.1 to >.03 in about 8 weeks and kept it there. They’ve switched me to Erleada ilo Xtandi after a 7 mo vacation and my PSA elevated to 3.8 and probably a bit higher along with new metastasis and prior ones grew, probably my last med vacation in my lifetime. I started back on Orgovyx along with Erleada on 06/01 and we’ll see where I am the first week of July. Keep battling the beast and may God continue to Bless You!!

[Arcticfox44 in reply to Wynnsts]

Thanks. We considered Erleada before I had the chemo with cabazitaxel but it was complicated to get it, given that I live in Cyprus. I will raise this again with the Mayo doctors.

[Seasid]

This post highlights a complex and challenging journey with prostate cancer, characterized by aggressive PSA increases and treatment-resistant progression. Your experience, as shared here, raises key considerations and potential strategies:

1. Rapid PSA Rise: A jump from 3.6 to 344 after a prior response to cabazitaxel suggests a highly resistant disease variant. Progression in PSMA-avid metastases, despite no bone lesions, indicates unusual aggressiveness.

2. Chemotherapy Adjustments: Moving to Taxotere (docetaxel) plus carboplatin aligns with treating neuroendocrine or aggressive variant prostate cancer. However, some in the prostate cancer community suggest Lutetium-177 (Pluvicto) as a potential alternative if disease remains PSMA-avid.

3. Androgen Receptor Therapy: While protocols in Cyprus restrict combining Xtandi (enzalutamide) or Nubeqa (darolutamide) with chemotherapy, these agents can significantly prolong responses post-chemotherapy in sensitive patients. Reevaluating access may benefit future treatment.

4. Emerging Therapies: Repeating genetic testing to explore mutations like BRCA or ATM may uncover options for PARP inhibitors like olaparib or rucaparib. Similarly, high TMB (tumor mutational burden) might enable immune checkpoint inhibitors (e.g., pembrolizumab).

5. Alternative Treatment Paths: If feasible, discussing Lutetium-177 PRRT (targeted radionuclide therapy) with your Mayo team might open another avenue. The community feedback here about its potential efficacy after chemo is worth pursuing.

6. Monitoring & Support: Your plan to retest markers and perform a PSMA PET scan after a few chemotherapy cycles ensures close monitoring. Sharing experiences, as seen here, builds an understanding of how others manage advanced disease and navigate systemic limitations.

If you need further information on Lutetium-177, accessing Xtandi/Nubeqa, or a specific aspect of treatment, let me know.

ChatGPT said

Did you also perform FDG pet CT scan? How many lutetium psma treatment did you have in Istanbul? Was it effective?

[Seasid]

I really don't understand why nothing was done when your PSA rocketed to 300+ and they know that you are BRCA positive? Your oncologist should contact Astra Zeneca and maybe you could get the New less toxic Astra Zeneca parp inhibitor clinical trial drug plus nubeqa even outside of the clinical trial?