I am a 75 yo white male. PSA 4.8 rose from 3.2 14 mos. previously. Sept. 28/24 I was diagnosed post biopsy of GL 4+4 , left sphere prostate cancer. Dec. 01/24, after a whole body bone scan which showed a suspicious lumbar flare and then a PSMA scan (neg. mets) I had a robot assisted laparascopic prostatectomy. {RALP} (my choice over radiation)
Post rp pathology as follows
Andenocarcinoma Gleason score 4+5 (Grade group 5),
Positive for tumor extension beyond the prostate gland at left apical and left posterior aspects. (also revealed on MRI)
Negative for bladder neck invasion
Negative for Seminal vesicle invasion (SVI)
Presence of perineural invasion. (PNI)
Presence of lymphovascular invasion (LVI)
Presence of intraductal carcinoma of the prostate (IDCP) p.s. I will ask if it is pattern 1 or 2.
Free all resection margins
Remaining prostate: nodular hyperplasia and atrophic change with patchy acute and chronic inflammation.
Lymph nodes left pelvic area ,dissection, negative for metatastic carcinoma in 4 nodes ( 0/4) {inguinal netting in the way}
Lymph nodes right pelvic area, dissection, neg. carcinoma in 10 nodes (0/10)
prostate wt. 64 gms.
Attached bladder neck muscle shows no gross tumor involvment.
Dec. 28/24 psa at <0.025 ng/ml by CMIA method. (at treatment center)
Jan. 27/25 psa at <0.003 ng/ml (at private lab)
Continence at 80% and improving each week. Have Urol. appt. c/w blood tests on Feb. 27/25
I should have added that on the Dec. 28 appt. (one month after rp) I asked about IDCP. He was more concerned about LVI and the need for radiation/ADT therapy when the post surgery symptoms settled down. He mentioned he could administer a 6 month Lupron shot right then. I declined thinking it may lead to faster castration resistence and I wanted to watch the natural progression of the PSA. He said "OK with me".
Feb 27. psa is unchanged.
Next appt. in 3 months.
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skiddles
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Thank you T_A. That is what my Dr. said Jan. 04/25. Adt 1st and then RT for the lymph nodes. Can always change direction to whole pelvic since I will be doing the drug regimen first. I would like your thoughts on which brand/type of ADT. I remember my Dr. mentioning Lupron (old school) but on researching this past week, there are some with less/different side effects. Appreciate your thoughts, again.
It has to be whole pelvic - individual lymph nodes don't work. You have to treat what you can't see, although you can get a boost to the individual nodes you can see, but they may be too small to see after ADT.
Most side effects from ADT are from castration-level testosterone -- all ADT meds do that.
Thanks. Urol. may well have said just that re whole pelvic. I just remember Adt/radiation/lymph nodes. That was two months ago (1 mo. post rp) and I was stoked about the good blood test results, psa <0.025 and being able to stay dry all night albeit having to void every 2.5 hrs. Next appt. Feb. 27/25.
Point taken. I was thinking if I was prescribed ADT for >1 year. Reported S.E. complaints re surgical castration seem to be few while ADT complaints are legion.
Had Urol. appt. 2 days ago.(Feb 27) PSA still at <0.025 CMIA method sensitive to 0.025. I also got an u.s. test at the same lab ... <0.003 ng/ml. Blood tests/urine test results normal. Next appt. in 3 months. (to consider srt) You mention starting ADT now. Is that neccesary with PSA being so low, for now anyway?
There is no mention of testosterone on my blood test although low creatinine at 0.71 mg/dl and high eosinophil at 8.7%. . I read that this is not related directly to testosterone. Giving it a mention because they were the only 2 abnormal blood results out of 32 items. Thanks for replying TA.
Do you mean at present? Next urol appt is May 29/25 (in 3 months)
Sorry, just re read your reply 11 days ago. Start adt now and then rt when continence returns. I wonder why my urol. didn't suggest to start adt, now? He only mentioned that he dosn't reccomend rt less than 6 mos. post rp.
As for your concern with IDP, you could ask for a test confirmation with an Immunohistochemistry (IHC) test. They can use the existing bio specimen. I've had a wide spectrum of pathology reports from simple Grade II to Grade III with cribriform and IDP. The IDP concerned me also with my own biopsy because of the aggressive characteristics. It sounds like your Dr is looking in the right direction with concern of LVI presence.
From ChatGPT...IHC (Immunohistochemistry) is crucial in diagnosing and characterizing IDC (Invasive Ductal Carcinoma) because it helps pathologists identify specific markers in tumor cells. Here’s how it helps:
1. Confirming Diagnosis – IHC stains for markers like cytokeratins to confirm that the tumor is of epithelial origin and invasive.
2. Hormone Receptor Status – IHC tests for estrogen receptor (ER) and progesterone receptor (PR) expression, which helps determine if hormone therapy (like tamoxifen or aromatase inhibitors) would be effective.
3. HER2 Status – HER2 protein overexpression is checked via IHC (or FISH if results are equivocal). If HER2 is positive, targeted therapies like trastuzumab (Herceptin) may be beneficial.
4. Ki-67 Proliferation Index – Measures how rapidly the cancer cells are dividing, helping to assess tumor aggressiveness.
5. Basal-like and Triple-Negative Identification – If ER, PR, and HER2 are all negative, IHC can help classify triple-negative breast cancer and identify basal-like subtypes that might respond to chemotherapy or immunotherapy.
6. Identifying Other Molecular Subtypes – Additional markers like p53, E-cadherin, and androgen receptor (AR) can provide insights into prognosis and potential treatment options.
End of ChatGPT
My last Pathology report came back with IDP, which was surprised me with such aggressive characteristics. I had 3 other reports with no mention of this and (2) of the reports were favorable at 3+4 only and no need for any ADT or any of the other aggressive treatments that IDP can require.
Unfortunately, after I requested this test conformation, I was told there was not enough specimen left to do the test after my RO agreed it should be done. BTW, this is another example of the patient having to be the advocate.
More specific regarding treatment plan.IHC (Immunohistochemistry) results play a direct role in shaping the treatment plan for IDC (Invasive Ductal Carcinoma) by identifying key biological markers that determine therapy options. Here's how:
1. Hormone Receptor Status (ER/PR) → Endocrine Therapy
ER+/PR+ (Hormone Receptor-Positive):
Treated with endocrine therapy like tamoxifen (pre-menopausal) or aromatase inhibitors (post-menopausal) to block estrogen and slow tumor growth.
These tumors tend to grow slower and have better long-term outcomes.
ER-/PR- (Hormone Receptor-Negative):
Hormone therapy is ineffective.
Chemotherapy is typically required.
2. HER2 Status → Targeted Therapy
HER2+ (HER2 overexpression):
Treated with HER2-targeted drugs like trastuzumab (Herceptin) or pertuzumab (Perjeta), often combined with chemotherapy.
HER2+ cancers are more aggressive but respond well to targeted therapies.
HER2- (No HER2 overexpression):
No benefit from HER2-targeted therapy.
Treatment depends on hormone receptor status and tumor aggressiveness.
3. Ki-67 Index → Chemotherapy Decision
High Ki-67 (≥20%)
Indicates a fast-growing, aggressive tumor.
More likely to require chemotherapy.
Low Ki-67 (<20%)
Suggests a slower-growing tumor.
Chemotherapy may not be necessary if hormone receptor-positive.
4. Triple-Negative Breast Cancer (ER-/PR-/HER2-) → Chemotherapy & Immunotherapy
No targeted hormone or HER2 therapies available.
Standard treatment is chemotherapy (e.g., anthracyclines, taxanes).
Some cases may benefit from immunotherapy (e.g., pembrolizumab/Keytruda) if PD-L1 positive.
5. Other Markers Affecting Treatment
p53 mutation: May indicate more aggressive behavior and influence chemotherapy choices.
Androgen receptor (AR): Some triple-negative cancers respond to androgen-targeted therapies.
Summary
IHC results help oncologists determine:
✅ Whether hormone therapy will work (ER/PR status)
✅ If HER2-targeted therapy is needed
✅ Whether chemotherapy is required (Ki-67, triple-negative status)
Are you sure that Invasive Ductal Carcinoma is the same as Intraductal Ductal Carcinoma? I know that Invasive ductal Carcinoma comes up as a very common feature of invasive breast cancer back when I was researching the term. That could be why your AI is misleading a bit??
Yes, you are correct in that 2nd post. However, it did point me to referenced papers that outline the importance of identifying molecular and protein-level information about prostate tumors that can aid in diagnosis and treatment.
I think ChatGPT is wrong as usual. IDP is diagnosed by pathologists, not stains. This is another example of AI making patents agnorant. Probably, a good start is understanding that all carcinomas are not the same. IDC-P is easily identified by a pathologist looking at a biopsy core through a microscope.
“Immunohistochemistry (IHC) is also considered helpful in establishing a diagnosis of IDC-P in terms of confirming the presence of at least an incomplete or partial basal cell layer around the atypical glands.”
My IDP report was from a Pathologist via slide review only. When I asked for confirmation via an IHC test, he agreed it should be done but did not have enough specimen to complete. So, unfortunately, I have no results to give from my experience.
I was only suggesting this might be a useful test to address the OP's concern of IDP. It’s just another tool in the toolbox to help find the “true” risk characteristics.
Your comment on ChatGPT seems harsh to me. I find it a very useful tool and the results can always be crossed-checked.
From your link: "IHC for basal markers (p63, CK5/6 and high molecular weight cytokeratin) is performed in the setting of IDC-P where there is a need to distinguish IDC-P from invasive carcinoma for quantification of tumor volume or the presence of IDC-P potentially affects the Gleason score"
IDC-P is usually well-diagnosed based on cellular morphology with a microscope. Differential diagnosis is seldom needed.
I’m sorry, but I do not agree that I was misled. I think you are doing readers a disservice to suggest a test (that my pathologist agreed is useful) is not useful. A preponderance of evidence can be useful especially in view of the subjective nature of a pathologist “reading the tea leaves”.
And before any disciples mention Epstein…”In God we trust, All others must bring data”
I agree with the other comments here. My surgery was in 2019 with no apparent spread of the cancer outside of the prostate, so I have no experience with these post op treatments. Good luck...this is a great site with great contributors.
congrats on your successful RALP. It appears you are an intelligent and resourceful person. I seem to have won my battle against prostate cancer and would enjoy sharing my story with you offline. I invite you to visit my page on Facebook (Carl Gay in Port Angeles, Washington) in order to contact me and perhaps we can chat by phone.
Agreeing with comments above and emphasizing the benefits of early radiation following RALP for complex cases, ie high Gleason scores. In this regard publications by Dr Anthony D’Amico of Dana Farber may be helpful and reinforcing. I had similar pathology to yours and am same age and had RALP followed by full pelvic radiation in 20/21. Fortunately so far no recurrence. I had Lupron annd Casodex and side effects lifted six months following last treatment. Good luck with the journey. Sounds like you are in a good track.
Thank you for replying. Your positive treatment results are very reassuring. Any chance of you sharing the specifics of your treatment course.? Lupron/Casodex concurrent or consecutive? Also knowing the radiation regime would be helpful. I have started reading your publication referrals.
Here is my recollection of therapy which took place in fall of 21 and spring of 22. 2 Lupron shots. First one at beginning of treatment and second one three months later. Casodex daily pill began on day one (day of first Lupron shot) and continued for following 6 months. First of 40 daily radiation treatments began 10-12 weeks after initial Lupron shot. Most oncologists recommended Casodex continue for up to 2 years but in my case my Oncologist was fine with 6 months.
Any thoughts? I would be very pleased with the "Jan. 27/25 psa at <0.003 ng/ml (at private lab)". A benefit with RP is we can, if we choose, utilize uPSA testing and get an earlier look at remaining cancer and spread, well ahead of general guidelines for biochemical and clinical recurrence. Nine years ago I chose to rely on <0.010 as best indicator post RP and to this day I am strong advocate for ultrasensitive testing and this threshold.
With the concern for spread I would be testing monthly to see if your uPSA rises. Based on my experiences with liquid blood biopsy testing I would add this to your investigations - especially with the identified LVI and clear lymph nodes. Before I did any treatments I would have multiple imaging methods for comparison. Hope this helps. All the best!
Yes, totally agree. I was happy with the <0.025 ng/ml result, sensitivety 0.025 by CMIA method. I was curious about "how much less than?" so waited 1 month and had a u/sPSA test resulting in <0.003 ref. range 0.000-4.000 ng/ml. I will do another same private lab test just before my Feb. 27 Urol. appt. at which time blood tests inc. PSA will be done.
That said, my psa was (only?) 4.8 ng/ml at diagnosis (5 months ago) and 3.2 ng/ml 15 mos. before that. That has taught me to be a lot more pro-active.
In my research....and I use the term loosely, I remember a report indicating that anything equal/less than .006 at 3 months after RP is excellent concerning BCR and/or metastatic situation in the future. I would see what an RO says about the situation regarding the low USPSA and LVI. At this point, the IDC is pretty much a moot point and I wouldn't waste my time worrying about it. It is treated pretty much as any G4 disease based again on my "loose" research. I have/had it as well in my pathology and it's one of the biggest unknowns on it's actual effect concerning PC and treatment options. Still at <.02 at the 41 month mark. Good luck to ya.
I apologize for my delayed response. I’m fairly new at this too. My only treatment has been the single-port robotic (transvesicle) prostatectomy in Jan 2024, whereby my seminal vesicles were also removed. My PSA post-surgery was .3 and has remained stable for a little over a year now. My oncologist and I agree to hold off on ADT until there is a reason to start. I don’t think another PSMA scan will be ordered unless my PSA rises to 2.0. Your PSA is very low now, but your biopsy report suggests to me the importance of staying vigilant. If you haven’t already it’s good to let this forum know of your situation. So many members here are far more knowledgeable than me about the various therapies available as well as recommendations for where you are now.
I did state that incorrectly. My PSA post the prostatectomy was 2.0. It turned out the prostate cancer was found in my j-pouch—a j-pouch is the end of the small bowel (large colon was excised as a result of ulcerative colitis). It was after removing my j-pouch and that met that my PSA dropped to 0.3.
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Reviewing my final Path report, post RP
Post RALP path report 
Treatment after RP with affected lymph nodes
Is Super Testosterone treatment appropriate or a viable option for me going forward? Should I just wait for an inevitable BCR and more ADT?
