Started having intermittent sharp pain in groin area in March 2008. Had physical exam in July 2008, with first ever PSA of 136. DRE (Digital Rectal Examination) normal. Short course of antibiotics did not reduce PSA. Biopsy in September 2008 showed PC in three fourths of gland, with some cores as high as 80%, with PNI (perineural invasion), Gleason 7. Bone and CT scans negative. Typical urologist vs. radiologist recommendations. Urologist theory (admittedly unproven)was remove the gland as the "source" of the PC, then follow up aggressively with radiation and ADT (Androgen Deprivation Therapy). Radiologist theory was EBRT (External Beam Radiation Treatment) with ADT for at least three years. Both opined that the PC was ECE (extra-capsular extension), notwithstanding negative scans and normal DRE.

Because my life expectancy was about 30 years, still had to put kids through college, and I was otherwise in very good health, I decided on surgery (RRP), knowing that the possibility of cure was very slim, hoping (against hope?) to preserve erectile function, trying to avoid radiation and ADT, but leaving for salvage or adjuvant therapy (when necessary), radiation and ADT. I rejected radiation plus ADT as first line treatment because if that failed, surgery would probably not be possible, radiation (in my mind) was not likely to destroy all of the cancer cells, and ADT would ultimately fail. [There are examples of men whose ADT did not fail on the site - Doug Adams being the best example] Still don't know if that decision was correct.

Took 50 mg Casodex from October 2008 to April 2009. RRP December 2008. Stage pT3bNOMX. Gleason 7b (4 + 3, with tertiary grade 5, which some pathologists I was told would score as a Gleason 8 or 9). PSA < 0.1 through May 2009, then rose to 0.5 in August 2009. Had image guided radiation therapy September 2009 to November 2009 (49 sessions). PSA < 0.1 in December 2009,then rose to 1.1 as of July 2011. Enrolled in clinical trial for TARP vaccine in September 2011 (for Stage D0 PC). Scans still negative and asymptomatic. PSA was 2.68 on 01/09/12. PSADT (PSA Doubling Time) is about 6 months.

Side effects from surgery are complete ED (had no problems prior to surgery), minor incontinence, and penile "shortening". Side effects from radiation are slight lymphedema in left leg, slight rectal bleeding/proctitis, and most likely continued decline in erectile (dys)function (hard to measure that (no pun intended)). Side effect from Casodex is gynecomastia.

I have experimented with pomegranate juice and extract, green and black teas, no red meat, soy milk, almond milk, fish oil, vitamin D3, broccoli seed extract, eat more vegetables, and exercise. Can't determine whether its made a difference, but doesn't seem to have harmed me in any other respect.

Still have a goal of avoiding ADT for as long as possible (my rationale for my participation in the TARP trial). [Casodex is generally regarded as being an ADT therapy] Don't need more side effects, and from what I have read, ADT will ultimately fail, so I am saving it as a last resort before chemotherapy and last ditch biological or experimental drugs. I continue to work full time and cannot be sweating on the job or losing my memory, besides bone mass loss and possible cardiovascular problems ( I know side effects vary with the individual, but that's not enough comfort for me).

Other than ED (which is very troubling), larger breasts and a smaller penis, a little pee in my underwear, some blood out my ass on occasion, and the doctor appointments, life right now is normal and I physically feel great.

The TARP vaccines (a total of 7) ended in August 2012. The clincial trial continues, but only for observation. There is supposed to be a Phase II trial, but no specific word on when that might commence or whether I would be eligible for it. I added resveratrol (100mg)and curcumin (500mg) extracts to my daily supplements. PSA has continued to rise with a doubling time of between 5 and 9 months, depending upon what time period is used. PSA was 8.0 on 12/28/12. Still undecided on what to do next and when. Recent CT showed a doubling of size in one iliac lymph node, but the absolute size is small (8mm). Bone scans remain negative. Current thinking is to wait until PSA reaches between 15and 20 (which in all likelihood will be by the fall of 2013), and then decide whether to initiate some form of hormone therapy, find where the PC is (Na F PET, C-11 Choline PET, fereheme MRI) and attempt surgey or radiation to eradicate it, or continue with "active surveillance".

PSA continues to increase. 12.8 on 04/04/13. PSADT is about 5.8 mos. I have decided to have a C-11 Choline Pet Scan and endo-rectal MRI at Mayo Clinic in Rochester, MN. My thought process is if I can find a focal point of the PCa (e.g. in a lymph node), it might be treatable with surgery or radiation. That might set the PSA level back a bit and give me more time without using ADT. Or, if the scan shows no focal point, meaning it is just spread around in various micrometastic places, maybe it's time to commence ADT. I acknowledge the scan may show false positives and/or false negatives and a follow-up biopsy will probably be necessary to confirm the PCa, but I don't have any better ideas, except to continue to procrastinate.

The C-11 Choline PET "showed" 5 lymph nodes with PCa. Endorectal MRI was negative. A debate ensued about whether to irradiate the nodes, surgically remove them, continue to procrastinate, or commence ADT. I did not want to commence ADT, radiation could only be performed at a distant facility over a 6 to 8 week period (and more radiation was not recommended except by the radiologist who wanted to treat with radiation), and I didn't think waiting longer to do something was prudent. So I had a bilateral pelvic lymphadenectomy on July 15, 2013. PSA was 17.8 on July 12, 2013. 12 nodes were removed and 3 were positive for PCa, the longest being 5.1cm. Gleason was graded at 4 + 4. PSA on 07/29/13 was 2.04. PSA on 09/11/13 was 2.300. I now return to procrastination mode.

My last four PSA results were: 2.04 (07/29/13, down from 17.8 pre-surgery), 2.97 (11/12/13), 5.08 (02/17/14), and 7.80 (03/14/14). Based on these results, I have concluded that there are three most likely conclusions to be drawn from the 11C-Choline PET plus BLPND surgery:

1. Only three of the five scan detected positive nodes were removed by the surgery;
2. There were actually only three positive nodes, all of which were removed by the surgery, the scan had a 40% false positive rate, and there was distant metastasis which was not detected by the scan and not removed by the surgery; or
3. The remaining metastasis was actually located in other local nodes which should/could have been or were not detected by the scan and were not removed by the surgery (false negatives).

I won't know the answer until the remaining metastasis becomes evident by a future scan. My guess is I have other local nodes which have tumor and were not removed by the surgery (low alk phos, and no positives on bone scan, NaF-18 PET, MRI, or CT).

PSADT continues to fall post surgery from about 5.85 to 3.3 months. Not sure why. I didn't change supplements or diet. 06/11/14 PSA was 13.1. Looks like the time to start some form of ADT is approaching quickly, although my PSA target number for starting ADT is moving up as PSADT is falling.

PSADT has recently fallen to every three months, with a reading of 26.1 on 09/15/14, up from 13.1 in 06/14. No change in diet, exercise, or supplements. I guess it's just the natural course of the disease. Will consider commencing HT in December 2014 when PSA is about 50.

PSA rose to 47.93 as of 01/09/15. I commenced hormone lite therapy ("HLADT")on 01/10/15 with 50 mg bicalutimide, 0.5 mg dutasteride, and 1000 mg metformin, and had three EBRT 8 gy treatments to my breasts to hopefully prevent further enlargement. My breasts enlarged during my first 6 months of 50 mg bicalutimide 10/08 to 04/09. The goal is to reduce PSA to below 2.0, then decide whether to continue for a further reduction, to discontinue HLADT, or, if PSA does not fall sufficiently, to add an LHRH agonist or antagonist to the protocol.

After four months of 50 mg. bicalutamide, 0.5 mg dutasteride, and 1,000 mg metformin, PSA fell from 47 to 7.45. Not my goal of less than 2, but low enough that I felt it was in a range that the PCa could do little or no harm. Stopped all three drugs for three months and PSA rose to 35.5. Re-commenced 50 mg. bicalutamide and 0.5 mg. dutasteride for three months and PSA fell to 8.01 as of 11/18/15. I decided the metformin added nothing to the effectiveness of the protocol. I am now experimenting with only 0.5 mg. of dutatseride for the next three months to see if remaining on dutasteride in the off months slows the rise of PSA. The dutasteride is very effective in reducing my DHT from the 35 range to the 1.7 to 2.5 range, while at the same time increasing T from the mid 300's to about 625. A side effect of this hormone lite treatment is very tender nipples despite the EBRT I had to both breasts in January 2015. Apparently, it is commonly known that breast irradiation does not eliminate tenderness to the nipples. The breast irradiation also left about a 3 inch diameter area around each nipple of very slowly fading redness.

I continue with intermittent 50 mg bicalutamide monotherapy. PSA rose to 49.31 (from 8.01) from 11/18/15 to 02/11/16 (the off period). Recommenced 50 mg bicalutamide monotherapy from 02/11/16 to 06/10/16 which reduced PSA to 8.74. I am now in another off period. F18-NaF PET/CT in February 2016 has been interpreted alternatively as showing degenerative disease only (NIH) or bony metastasis in the spine and skull (local radiologist). 18F-DCFBC PET/CT and MRI ERC in April 2016 both confirm focal uptake in the retroperineal lymph nodes along the paraaortic chain consistent with PSMA over-expression, with no bony disease. As long as PSA continues to respond well to the bicalutamide, I remain asymptomatic, and metastasis is limited to the lymph nodes, I will continue with this therapy in my effort to delay as long as possible the use of LHRH agonists and antagonists, or estriadol patches.

Still on intermittent 50 mg. bicalutamide monotherapy. I have decreased the on and off periods to six weeks, respectively, due to the shorter PSA doubling time (about every 4 weeks). The range of PSA in the on and off periods is fairly consistent: between about 10 and 30. I am content to continue with this protocol indefinitely, until I see resistance.

Still on intermittent 50 mg bicalutamide monotherapy. However, the on period is now 7 weeks and the off period is 5 weeks. PSA is 12.5 to 40 at the end of the on period and off periods, respectively. NaF PET/CT in June 2017 showed no changes compared to 2016.

I continue with intermittent 7 weeks on six weeks off 50 mg bicalutamide monotherapy, keeping PSA in the range between 12 and 50. No new scans.

As expected after four years, the 50 mg. bicalutamide IADT monotherapy is exhibiting increased resistance. The androgen receptors are very smart, adaptable, and devious. PSADT is now about 0.7/mos. and the PSA range is about 35 to 70. I have shortened the on period to 3 weeks and the off period to 2 weeks to compensate for the decrease in PSADT. Otherwise, I am asymptomatic, physically active, and working full time, and glad I have not yet used any other type of first line hormonal agents, second line hormonal therapies, or chemotherapy.

Intermittent 50 mg bicalutamide monotherapy has become ineffective (PSA rising to 87 in a two week off period). Increased dosage to 100 mg intermittent in June 2019, then continuous in August 2019. I may try another three week on off protocol just to see what happens.

I learned I have the ATM DNA repair defect gene, although I do not know if it is biallelic (my genetic test was by blood sample with Guardent Health). Guardent Health advised that the tumor itself has to be tested to determine whether it is biallelic.

I am participating in the Phase II TARP vaccine clinical trial at the NIH, for men who had participated in Phase I. My arm is to observe the long term effects of repeated vaccination. Recent bone, CT, and Axumin scans have confirmed metastatic disease in the para-aortic and other lymph nodes, and two suspicious nodules in the lungs.

All in all, I am very pleased the 50 mg intermittent bicalutamide monotherapy protocol lasted over five years, I am still hormone naive, and have a good quality of life. My immediate plan is to continue with bicalutamide, eventually increasing the dose to 150 mg. Then . . . . . .?

Still on continuous 100mg bicalutamide monotherapy. PSA has a slight upward trend over the past 9 months. I completed the Multi-Epitope TARP (T-cell Alternate frame Reading Protein) vaccine clinical trial at the NIH. I will re-evaluate treatment when I have my next scans in September 2020. If stable, I will continue with bicalutamide notwithstanding rising PSA. I hope the FDA approves relugolix because I would like to try that when the bicalutamide (up to 150 mg dose) completely fails. As an oral antagonist, I could control the relugolix dose in a further effort to avoid treatment mediated selection pressure. COLOR germline genetic test showed no mutations (compared to Guardent360 somatic test which showed ATM and two other mutations).

I increased bicalutamide continuous monotherapy to 150 mg, but it failed - PSA rose to 108. I commenced one month Lupron depot monotherapy on off for 5 months. PSA dropped to 21, but it is doubling about every 10 days in the off period. Commenced apalutamide monotherapy on May 1st and intend on using it intermittently like bicalutamide, possibly alternating with relugolix monotherapy in keeping with my "game theory"/ avoid castration resistance approach. Latest Axumin PET shows no bone metastasis but does show para-aortic, retroperitoneal and abdominal lymph node metastasis.

I continue to use apalutamide monotherapy, 30 days on, 30 days off, with PSA predictably falling and rising correspondently. I used apalutamide plus relugolix the past 30 days which brought my PSA down from 65.9 to 5.48. I remain castrate sensitive with metastasis only to para-aortic lymph nodes, per the latest Aximun scan. Looking into SBRT to attack the lymph nodes.

A Ga68 PSMA PET scan detected a "duodenal mass" and distant LNs, and an endoscopic biopsy in July 2022, confirmed the mass was "high grade adenocarcinoma" GS(4+5). I commenced combo apalutaime and relugolix in August 2022 and then had proton RT to the LN chains. PSA fell to 6.4. At the conclusion of the PRT on October 22, 2022, I stopped all treatment for 4 weeks and PSA rose to 14.3. Since then, I have been on intermittent apalutamide monotherapy. Compared to pre-PRT, PSADT fell from 11 days to 22 days. I am not sure how beneficial the PRT was, but a slower PSADT is not a bad thing.

PSADT is now about 50 days, a substantial slowing from 13 days pre-proton RT. I continue on intermittent apalutamide monotherapy, with one month on, three months off. I will stretch this out as long as possible. The duodenal mass is still present. The October 2023 PSMA scan showed it had not increased in size, but SUVmax had doubled. If I could participate in a pluvicto or actinium 225 trial, I would attack the duodenal mass with radioligand therapy. I believe the duodenal mass is really just a LN pushing against the duodenal wall. Unfortunately, because I am still hormone sensitive and chemo naive, I do not qualify for any trials, and insurance will not cover this non-standard of care approach. On the other hand, I could also say "fortunately", because after almost 16 years post diagnosis, I am still hormone sensitive. My original plan to remain hormone sensitive for as long as possible by avoiding continuous ADT (and stress on the cells due to lack of T), and using anti-androgen monotherapy intermittently, with occassional metastasis directed therapy, is catching on as reflected in the NCCN guidelines, chatter in support groups, and the De-Escalate clinical trial. That said, because prostate cancer is such a heterogenous disease, what may work for one patient may not work for another.

Richard's e-mail address is: notsdr AT aol.com (replace "AT" with "@")