Initial PCa Diagnosis, the Journey be... - Advanced Prostate...

Advanced Prostate Cancer

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Initial PCa Diagnosis, the Journey begins...

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Diagnosed with the terminology language: Advanced Prostate Cancer, Metastatic, Stage 4. This will overwhelm generic Medical Oncologists, getting a PCa Oncologist is best choice...

Patient Encounter Stats: Age 58, PSA 1000+, GS 8, Extensive Pelvic tumors, Metastasis throughout Thoracic and Lumbar Vertebrae findings. Biopsy pending for Vertebrae findings...

Excerpt from prostate MRI:

"TECHNIQUE: Multi-parametric MRI of the prostate gland and pelvis was performed at 3.0T, with a phased-array surface coil. Sequences utilized included T1WI, T2WI, diffusion weighted imaging (DWI and ADC mapping) and dynamic contrast-enhanced (DCE) imaging in multiple planes. Post-processing and 3-D image evaluation was performed using DynaCAD software on an independent 3-D workstation."

"FINDINGS: The calculated volume of the prostate gland is 137 cm3. There is a large mass infiltrating the prostate gland encompassing the entire gland but more on the right than the left with dimensions of this is great as 6.3 cm in diameter.

The mass demonstrates restricted diffusion. Extends into the right periprosthetic softt issues and is invading the floor of the bladder..."

"IMPRESSION:

1. There is a large mass in the prostate gland predominantly on the right side of the gland with extensive pelvic metastatic disease, there is invasion of the bladder and metastatic disease involving sacrum. All these findings are new compared to the prior examination from 2013 (Age 53, GS 7)."

My Current State:

After 2 months of Lupron (6 months dose), Daily Zytiga 1000 mg/Prednisone twice daily 50 mg and daily Casodex. I have no pain, just some fatigue and mental acuity issues, no symptoms with as my work is software development, ironically, in bioinformatics domain.

Current PSA 2.1 from initial dx of PSA 1000+

I've been posting here, but have not established my own base situation, the journey starts.

I'm in the Boston area, have the Lahey Health Systems as front line healthcare and Dana-Farber as my second opinion team.

I'm going to challenge my medical teams to consider BAT and other treatments, engage!

11 Replies

I don't think you are a good candidate for BAT. In the pilot trial for men with mHSPC, 10/29 had a low met burden and 19/29 were recurrent with no detectable mets. You have a heavy metastatic burden. I think you should be very wary of throwing gas on the fire.

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Hidden in reply to Tall_Allen

Understood, at least I'm responding to metastatic hormone sensitive prostate cancer (mHSPC) treatment. Hence my PSA from 1000+ to 2.1 in two months of ADT + Abiraterone (Zytiga). Although, must say, started with Casodex for two week, then my symptoms of weak urine stream with burning pain subsided.

But, it seems there's no proactive treatment to prevent castration resistance, so currently its ADT + Abiraterone until PSA starts rising again.

Basically, putting out the prostate cancer metastasis is like trying three buckets to put out a fire!

First try the bucket of water, then try the bucket of foam, then, finally, try a bucket of sand. Is this it, after about 70 years from Dr Charles Huggins ADT (water bucket) Treatment?

Tall_Allen profile image
Tall_Allen in reply to Hidden

Yeah. Sadly, the cancer is smarter than we are. It progresses to castration resistance no matter what.

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Have you seen this report:

journals.lww.com/oncology-t...

William K. Oh, MD, from Mount Sinai School of Medicine:

"Oh also said that the development of neuroendocrine prostate cancer is a function of treatment..."

Others claim the same assertions, a Catch 22 proposition!

jmurgia profile image
jmurgia in reply to Hidden

WOW. This confirms what I've always suspected: "Treatment makes the cancer mad."

Thanks for the link to the report.

Joe

Tall_Allen profile image
Tall_Allen in reply to Hidden

Fortunately, it is a rare occurrence. UCSF researchers found its presence in 14% of heavily pre-treated men. No one can say whether those 14% had small amounts of NEPC from the start, waiting for the chance to multiply, or whether they were the product of adaptation. Oh is just expressing his opinion, not a fact, and definitely not an inevitability. It is certainly true that that the incidence of mixed type NEPC increases over time. It is also true that ADT increases selective pressure to adapt, and NEPC is one of many adaptive pathways.

Fairwind profile image
Fairwind in reply to Tall_Allen

Does this theory have any validity ? Dr. Walsh at J-H feels (or felt) that prostate cancer is either hormone sensitive or, usually a much smaller cell volume, are not hormone sensitive. ADT KILLS the hormone sensitive prostate cancer cells. They are gone. But the remaining cancer cells that are not hormone sensitive are not effected by ADT. They continue to multiply, once again become detectable, and must be treated by means other than ADT. The ratio of hormone sensitive to hormone insensitive cells varies greatly among patients. Hence the effectiveness of ADT treatment varies greatly..Dr Walsh rejected the theory that PC cells BECAME hormone refractory after treatment, he felt some cells always were immune to hormone treatment and that's why it always fails in the end.. Has this thinking changed ?

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Tall_Allen in reply to Fairwind

For the same reasons I mentioned above, how can one really know? We know that there are a half a dozen mechanisms by which a prostate cancer cell can become castration resistant. But WHEN exactly they kick in is anyone's guess. Maybe the Guardant 360 database will someday offer clues because it tells us the genomics of the cell fragments in circulation.

I would guess that BAT is out of the question unless and until your PSA gets down well below 1.0 and stays there for a year, but the oncologists will know more about that than I do.

In the meantime I would expect that very aggressive therapy will be proposed - an LHRH agonist like Lupron, Zoladex, or Eligard, or perhaps better still Firmagon (degarelix), plus either docetaxel chemotherapy or Zytiga (abiraterone acetate + prednisone) - they appear to have similar benefits for aggressive PCa.

Ideally you want your treatment plan to be by a medical oncologist with a specialty in prostate cancer. If Lahey doesn't have one, or if their medical oncologist is not recommending the aggressive therapy described above, I would get an opinion from Dana-Farber. I would also start the androgen deprivation therapy (ADT) mentioned above, i.e., the Lupron, Zoladex, Eligard or Firmagon, ASAP. Hopefully, it will temporarily reverse the growth of the cancer and give you some time to learn more and setup the additional treatments.

Best of luck.

Alan

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Hidden in reply to AlanMeyer

Hi Alan,

About two months ago started Lupron (6 month dose), Casodex and Zytiga/Prednisone daily - scheduled to get Zometa infusion in two weeks. This seems to be standard ADT aggressive therapy as result from the STAMPEDE and LATITUDE Clinical Trials.

Excerpt from 09/19/2018 CT abdomen pelvis:

"There is significantly enlarged retroperitoneal and pelvic metastatic lymphadenopathy with some metastatic nodes appearing to be necrotic..."

Currently being treated by an Hematology Oncologist from Lahey Health Systems. My second opinion team is from Dana-Farber Genitourinary Cancer Center with Mark Pomerantz, MD, specializing in prostate cancer and is the principal investigator for the regional IRONMAN (advanced prostate registry) Clinical Trials:

clinicaltrials.gov/ct2/show...

ironmanregistry.org/

Since my initial PSA 1000+ is now PSA 2.1, shows I'm metastatic hormone-sensitive prostate cancer (mHSPC) at the moment.

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Hidden in reply to Hidden

And hopefully it stays that way for many more years to come..

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