Sorry me again, I'm a neurotic wife!
Husband's been on HT for 2 months after a PSA of 167, just heard PSA is now 0.2. Chemo to start in 3 weeks time.
Is this a good sign?
First PSA: Sorry me again, I'm a... - Advanced Prostate...
First PSA
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Fdccs
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Yes, a good response to HT bodes well.
Very good response
Are you still considering brachy boost therapy? Not sure if there's a threshold period when treatment cannot be performed. Perhaps. Tall_Allen can chime in on this...
By the way, great response, nice to know he's hormone sensitive!
Can't ask for a better response. Good move to do early chemo to beat it down as much as possible at the beginning. That's what I did and I would do it again. Don't be afraid of the chemo, it's really tolerable for most people. I felt crappy for about a week in each cycle, but even then I could still do things around the house etc. as long as they weren't physically demanding. After the first week of the cycle, it was pretty much back to normal. My pain was also improving during chemo which was an added plus. Good luck with treatments.
Fdccs• in reply to
Ok thanks guys. Early days but I'll take some heart in this
• in reply toFdccs
What's happening now isn't everything, it's the only thing.
MarkBC• in reply to
I agree completely. I had the same experience.
Yes! Great news!
Wish my husband had that response. Praise God that he's responding well- y'all need to kick cancers butt!
Of course, that’s excellent news😀
relax i'm on my 11 year and i'm at 38 so don't worry
charlie
Charles 11 year of prostate cancer. and 38 what psa
Hi everyone...this seems impossible given my recent diagnosis and creaky aching bones...my initial PSA two and a half months ago crashed from 900+ to .79.....and the medoncs cannot establish any involvement of lymph node metastasis!...but it turns out the bones were far more colonized than just the hips and femur. Talk about bad news being flattened by good...I’m very much relieved. I took my first dose of dukarol on the way to traveling to fly to see the Docs yesterday. I left that tidbit out of the history...I sure like the inferred odds of a 7 year survival. Cancer’s a fickle bitch who needs to be reminded constantly that we’re not her’s. Ran into a 30 year’s past darling acquaintance at our celebratory dinner....do these coincidences have deeper meanings?
Excellent ! My PSA went from 550 to 6.5 in 10 months .
Didn’t mean to be sexist with my analogy...also read...cancer’s a brutal thug who needs to know that any punch it throws will feel it’s return in bloodied flurry....?
I think that is good news
Sounds like a great sign
PSA drops are good indicators of response so my oncologist says
Good luck
Hi Fdccs,
I don't think you are neurotic. Congratulations for being a very nice lady concerned about a husband's problem.
Psa of 167 to 0.2 is what my onco doc would call a good response to ADT. But the Pca is now in a kind of coma state, alive, but unconscious, and we could only hope that chemo, ie Docetaxel might kill it, but this type of chemo kills cells that divide fast, and theory is that cancer cells divide fast so chemo zaps them. I have always questioned this where ADT has put cells to sleep. And if there is Pca in bones, chemo is not so good, so I can only wish good luck.
I had initial Psa of 6 at diagnosis in Dec 2009, then attempted open RP in April 2010 when Psa was 8.8. Docs found too much cancer outside capsule so could not do RP.
I began ADT and had EBRT and there was never any intention to use chemo which is usually used here only after Psa rises above say 10 when all forms of hormone manipulation drugs have become ineffective. So my ADT was from April 2010 to June 2016 when Psa began rapid rise, then I had Cosadex added which gave 6 more months, then Zytiga, gave 8 months, and then I had chemo in July 2018, and after 5 shots the Psa went from 12 to 45, so I am now having Lu177, and Psa is now maybe 20.
Every man has a different journey with Pca, and a different amount of time where ADT works well to suppress cancer growth. My Pca had probably spread to many places by the time I was diagnosed a bit too late to be able to have a successful outcome after an RP. The result is a long battle over many years.
The spread spots, aka metastases or mets, were all too small to be seen in scans until 7 years after diagnosis in 2016.
But my lifestyle has remained quite good despite the Pca. I know I cannot live forever, and I am 71, and have not been married for 40+ years so there is nobody else to get upset by my sickness. It would have been nice to have had family support, but it just was not to be. I quite love life while I have it.
So always look on the bright side of life. Any one of us could be so much worse off, but here we are, able to "hold each other's hands" in our time of trouble, via this marvellously cheap telegram sending app on our PC.
If ever there's a time when love needs to find a way, its now.
Patrick Turner.
Regarding chemo's ability to attack "unconscious" cancer cells while on ADT, I've wondered the same thing myself. The studies do show a survival benefit when chemo is used while ADT is still effective. One theory is that some portion of the cancer won't respond to the ADT, and early chemo kills off those cells before they have a chance to start multiplying.
I'm on ADT and chemo right now. The ADT had lowered my PSA to about 2 at the start of chemo. It's continued to drop since then, and I've noticed that alkaline phospohatase (a marker of cancer activity in bone) seems to drop a little steeper the week after each chemo infusion.
• in reply totom67inMA
Regarding both comments on ADT putting cancer to sleep. My two cents.... Wrong. It reduces the ability to make testosterone. Chemo kills the little bastards floating around in the highways and byways of the lymphatic and vascular system and their colonies.
This is a good question for your Medical Oncologist.
Gourd Dancer
Patrick-Turner• in reply to
Hi gourd_dancer,
ADT turns off the ability of testicles to make testosterone. Its the chemical equivalent of having orchiectomy, ie, balls removed. Big Pharma makes pile selling ADT but a cheaper alternative is ball removal.
When normal ADT with Lupron, Eligard, Lucrin Zoladex et all begin to fail, one of these 3 things, bicalutamide, enzalutamide, abiraterone are added to normal ADT to interfere with adrenal gland which makes a small amount of testosterone, plus interfere with the cancer's ability to make its own testosterone. Chemo with Docetaxel kills fast dividing cells. If Pca is a slow growing cancer, then it may not seem to divide very often but when it does, its quick, and if there's chemo in the blood it kills the dividing cell but chemo cycles are 3 weeks chemo remains at high levels for only a week so some cancer cells die, but may keep growing in the 2 weeks up to next chemo shot.
My chemo seemed to fail, Psa went up and stayed up, and never went below what it was when I began.
The behaviour of Pca cells in mets is different to the original tumour, and the chemo effect of bone mets is often not successful.
Oncologists often do not really know what's going on at cellular level.
Their job here in our medical system is to follow protocol and in nearly all cases where Psa rises after RP or if Psa was so high or Gleason score was so high, ADT is tried and with one of the other 3 blocker drugs added, and when all that fails to stop Psa rising, its time for chemo or what I am having - Lu177.
The docs here do not try chemo early here because they know many cells will survive chemo and grow anyway, just like many survive radiation. What survives becomes a killer.
But one man's Pca is different to the next. The only common thing is that it begins in the prostate gland and the range of overall survival time from diagnosis can vary between 2 years and 25years.
And I was diagnosed too late because although Psa had only just gone over 5.0, the tumour at PG had come outside the capsule and adhered around all nerves, and so RP was abandoned after attempting it, and the Gleason 9 meant Pca had spread widely already. Where I read stories about Psa over 100 at diagnosis, it probably means Pca has spread widely, but the many mets are too small to show up in any scans until years later. And they are suppressed by ADT for awhile as well as the primary tumour.
• in reply toPatrick-Turner
Exactly! It’s why over six months I had 18 infusions of Taxotere alternated with 18 infusions of Adriamycin; plus Ketozonale, Estramine, and Prednisone. Patrick, one day standard of care will change.
GD
Hi tom67MA,
I hope the combination of chemo with ADT that is working does work for you, but not all is known that could be known about what is going on in any one man. I made some other comments about all this to gourd_dancer below.....
Its too late for me to change course. There is no Back button for life, to allow a different set of treatments to be tried.
Patrick Turner.
I agree there is a lot that is not known about how treatments actually work at the cellular level. Usually, it's easier to just run a scientific study and prove that a given treatment protocol works in general (ie, for more men in the test group than in the control group), and then afterwards they might figure out how it works.
Hi tom67inMA,
Yes, getting a good result without too many side effects is about all pharmaceutical companies can do to help anyone. It means that there will always be a large number who don't get a benefit or who have serious side effects. There is usually some pure research which works out how something might work if it is made, and many chemicals are found to be just no good in the development process.
Nothing seems to prevent research doctors trying out combinations of more than one chemical or therapies; there is a trial starting in Australia soon of Lu177 + ketruda. The docs want Lu177 to work better for higher % of men, same goes for keytruda, so why not try both at same time?
Nobody knows if this will work, or if it just causes side effects that are worse than having only one of these treatments.
Patrick Turner.
Wonderful result! Great News!
I should add..as a matter of fact, that I’ve learned to much enjoy my morning coffee with a tsp of turmeric with a pinch of cardamom and cinnamon and a dash of pepper since I started my other treatments (Eligard and bicalutamide).....we shouldn’t neglect disclosing anything possibly vital on our journeys of recovery.
Above all...do no harm as we seek to do our best.
Congrats on the good response.
Excellent response. 22 months ago I started my treatment with lupron and chemo for 6 cycles. I'm happy to hear that you are hitting it hard early. I believe you will have great results and your PSA will remain low. Mine had been holding steady from 0.1-0.3. As gregg57 said, chemo is tolerable for most men. I continued to work full time and it did not impact my decision making. It will just be a bumpy road and later on you will feel great. Kerp us posted on his progress.
Nick
Great response!
don't know what ht is i went the normal way when found out i had it. been 11 years now
charlie
Same here just did fourth round of chemotherapy..90day of ADT and my psa was 50.now its Down to. .3 going on bicalutamide today to see if I can knock it down below. .2
If you have access to the New England Journal of Medicine, here is an article that may be useful.
medscape.org/viewarticle/58...
If not, I copied key points:
In the setting of hormone naïve M1 metastatic prostate cancer, is achieving a low testosterone level really important? Up until several years ago, any answers to this question were completely unknown as testosterone levels were rarely measured in the setting of follow-up of advanced prostate cancer patients. In men that undergo bilateral simple orchiectomy, the mean testosterone level was approximately 20 ng dL However, the traditional testosterone level to define a castrate state has been 50 ng dL−1 . In fact, all contemporary clinical trials related to prostate cancer have used the level of 50 to define castrate-resistant disease. In 2007, Morotefurther reported patients that failed to achieve testosterone levels below 20 had a more rapid progression toward castrate-resistant disease Examined another way Morote et al. found that patients who had a testosterone level above 32 ng dL − 1 had a more rapid course toward castrate-resistant disease. In contrast, patients who achieved a testosterone level < 32 enjoyed an additional 4 years on average until castrate-resistant progression. In 2010, Perachino et al. reported similar findings which the testosterone level measured after 6 months of hormone therapy was a strong predictor of progression to castrate-resistant disease. More recently, Pickles et al. studied 2196 patients treated with LH-RH agonist during and after radiation therapy. Five to 8% of patients experienced breakthrough testosterone levels above 50 ng dL − 1 . Importantly, young age < 70 predicted higher risk for testosterone breakthrough above 50. Pickles also demonstrated patients that experienced no testosterone breakthrough levels above 50 enjoyed a better disease free survival after external beam therapy treatment. Finally, and most recently, Klotz studied 626 patients on the continuous hormonal therapy arm of PR-7. The PR-7 trial was a Canadian study of intermittent versus continuous hormonal therapy in M1 metastatic hormone naïve prostate cancer. These authors looked at serum testosterone levels and time to the development of CRPC and studied patients after a median follow-up of 8 years. For those men who had testosterone levels that measured > 50 the hazard ratio for CRPC was 1.91 compared to a control group of men who maintained testosterone levels < 20. For the group who had testosterone levels that measured between 20 and 50 the hazard ration for CRPC was 1.41. In summary, these multiple lines of investigation suggest that the level of testosterone suppression during the initiation and early course of ADT for hormone naïve metastatic prostate cancer is a powerful prognostic factor.
In the setting of traditional metastatic prostate cancer, a number of key questions arise with regard to the use of hormone therapy in hormone naïve disease.
The first key question: is the PSA response to initial ADT important to predict response and survival?
The second question: does the type of ADT matter for maximal response?
And the third question: is achieving a very low testosterone level really important in the setting of M1 metastatic prostate cancer?
As early as 1990, it was shown in a small study that PSA declined after the initiation of hormone therapy predicted survival in patients with metastatic prostate cancer. Patients who enjoyed a > 80% PSA decrease in the first month of ADT enjoyed a significantly longer progression-free survival compared to those patients who had a < 80% PSA decrease in the first month.
In a study published by Fowler in 1995, PSA nadir was a very significant predictor of response to hormone therapy. In this study, after patient exclusions, 245 patients with localized and 78 patients with newly diagnosed metastatic prostate cancer were treated with ADT in the form of orchiectomy or LH-RH agonist. PSA regression, nadir and doubling times were calculated for the patient cohorts. For the metastatic patients who reached a PSA nadir < 1.0 ng ml − 1 , they experienced a statistically significant longer time to biochemical recurrence. These authors further stratified PSA nadir on initial ADT from 1 to 1.9, 2 to 3.9, and a PSA nadir of > 4. Patients whose nadir was < 1 enjoyed a much greater disease-free interval compared to patients who experienced a PSA nadir > 4.
The largest and most noteworthy study to look at PSA levels after initiation of ADT for new M1 prostate cancer was published by Hussain et al. in 2006. Specifically in this large Southwest Oncology Group (SWOG) trial, the authors showed that initial PSA nadir 7 months after initiation of LH-RH agonist was a strong predictor of median overall survival . Specifically, patients who enjoyed a PSA nadir ≤ 0.2 at 7 months after the initiation of therapy had a median overall survival of 75 months. In contrast, patients who had a PSA nadir of > 0.2 but < 4.0 had median overall survival of 44 months. Finally, the patients who experienced a PSA nadir at 7 months that were > 4.0 ng ml − 1 had a median overall survival of only 13 months. In my practice, I use these publication data to help counsel patients who I initiate on ADT for traditional M1 prostate cancer. I attempt to defer discussion regarding prognosis with these patients until I have been able to examine a 7-month PSA level. Once the patient and I have the 7-month PSA nadir value in hand, we will use the aforementioned survival data to counsel them on prognosis and future treatment strategies. In fact, many of those patients who have suboptimal PSA nadir > 4 at the 7 months interval after starting ADT will have impending CRPC and may benefit from early novel therapeutic agents. Unfortunately, from this SWOG study in 2006 by Hussain et al., we do not have the serum testosterone levels at the 7-month point. It is possible that a combination of PSA response as well as testosterone response at 7 months or even an earlier interval may provide additional prognostic information to help guide future treat strategies for these patients.
Great news. Meds are doing what there supposed to do ❤️🙏🙏🙏
Super!
Excellent. Took me 16 months to get from 59.9 to 0.2 Have been at 0.2 for 6 months. Extensive bone mets and abdominal lymph nodes. Did lupron, xgeva, 8 cycles taxotere and xtandi. Except for getting up many times a night, urinary problems went away 1st week of chemo. About 3rd cycle very heavy night sweating stopped. That was lymph node issue being resolved. Still had hot flashes. Quality of life pretty darn good for almost 2 years now. I am unfortunately incurable. Best of luck to you.
You guys are all amazing and I wish you all the best. Keep fighting X
You know what your husband needs now? Is a lap dance...
Good Luck, Good Health and Good Humor.
j-o-h-n Friday 01/25/2019 6:21 PM EST
I started with the same treatment and am now in complete remission only after 12 months Keep up the fight!! gods speed!!
Great
yes it is and it will go down further as long as he is on ht. it means he is hormone sensitive which means he's safe from cancer growth at this point. It takes the edge off and you shouldnt be frantic or overly concerned.
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