Interesting Theory on Chemo and Tumour Load

Having had PCa for nearly 3 years now (doesn’t time fly…) certain questions always appear to crop up.  One that I have always wondered focuses on the effect tumour load has on survival given that sometimes oncologists allow (unnecessary) tumour growth and that this can then limit the effectiveness of the treatment, especially in advanced cases.

 

Last night at our monthly prostate support meeting an urologist, who offers to keep the group updated, gave a presentation of the implications of ADT on men and their partners.  During the questions session I asked him why this was the case and he gave a standard reply.  Then he said something which I thought was quite interesting.  In the context of locally advanced PCa’s, he theorised that PCa should be treated in a same way to BCa.  Primary treatment should be given inconjunction with adjunct ADT until, I assume, a stable (and ideally undetectable) nadir was established for a period of time and then the patient should undergo chemo.  He believed that this would do the most damage to any remaining PCa cells and given the light tumour load would possibly reduce the need for longer cycles and offer longer remissions.  Have any other oncologists/ urologists mentioned this?

 

Paul

BB- I also know of a guy whom I have corresponded with before and he is one on the rear cover of Dr. Strum's book (I believe), whom did chemo as primary treatment and then followed by I think it was brachy and IMRT. Not real long ago emailed him and all was still looking as cured, which looks good of course. I rememer his postings on a forum way back then about doing chemo first, it was bizzare to hear as we almost never hear of anyone getting this treatment as primary or firstly done.

Myself not a huge fan of chemo in general (but we almost always see it given late in hrpca patients), but perhaps there is something to this concept when used in unison with other therapies immediately after or within conjuction (perhaps LHRH or combos thereof or estrogen drugs, etc may prove of value.)

Also, shows why questioning protocols is worthwhile as there are many ways to fight PCa, the one size fits all playbooks are not the gospel on PCa, but are treated like it usually. Dr. Fred Lee an incureable himself still alive 33+ yrs. later, using a somewhat bizzare approach with emcyt as his main PCa drug therapy and I believe only drug he has used over alot of years.

SC,

Did Dr. Lam indicate the criteria for this or was it because of the high risk of spread in your case?

Southern comfort, did the doc wait until your PSA rose post-surgery, or did they just begin the ADT right away after surgery? My dad hasn't had his first post-op PSA check yet, but his gleason was upgraded to a G9 after surgery and he also has SVI. Negative margins I think. He is 73.  But his PSA never rose above 4.5 I think.  And I've read two different (exact opposite) opinions on high grade, low psa... one camp says that's not good, and another camp says that the outlook is better than if it were a really high psa. 

I imagine at his appt the doc will talk about options. And at his age, it might be prudent to just wait and see if the PSA rises rather than do any adjuvant treatments. We'll see what they say.

I am curious-- how were the side effects of the chemo for you? Tolerable? Terrible?

Post Edited (Skooley) : 4/25/2013 11:14:22 AM (GMT-6)

Hi Paul,
In the case of BCa, combined treatment for high-risk disease includes surgery, radiotherapy and chemotherapy (including hormone therapy in some cases of hormone-receptor-positive disease). Both surgery and radiation are cancer volume reducing strategies by potentially eliminating the oldest PCa tumor present. This tumor tends to be a mixture of dedifferentiated cells in the normal carcinogenic progression process. In BCa (unlike PCa) combination therapies have been proven to improve survival in high-risk patients.

In the UK at diagnosis there is presently more PCa advanced disease than here in the US. This is related to the limited use of PSA testing there. The urologist making the presentation there probably sees this all the time. Advanced disease at diagnosis is limiting as to what treatments are available for the patient. Metastatic disease in PCa is not typically treated with surgery or radiation since these are considered treatment for localized disease.

For many years it has been known that systemic treatment (hormonal treatment) for PCa is more effective when the disease is lower in volume. Survival is directly related to treating the disease at the lowest metastatic involvement possible. That is when the disease is more androgen-dependent and androgen deprivation is capable of inducing the most cell death. In theory at this point when most androgen-dependent tumor volume is depleted, the residual androgen-independent tumor load (not responding to deprivation) could be addressed with chemotherapy which is capable (because of its action mechanism) to kill those androgen-independent tumor cells. It all makes sense, but because these therapies are not inconsequential in nature, clinical trials (like those done with BCa) are needed for PCa.

That said, many patients cannot afford to wait for clinical trials as their survival is on the line and they adopt treatments not clinically certified by trials. Success is not predictable, but many do succeed (at least in my observations throughout the years).
In my view, early detection gives the patient the most flexibility to decide on treatment. This includes early detection of advanced disease. The flexibility comes (in my personal view) to treat aggressively when dealing with high-risk disease or to slow down and observe when the disease is low-risk and slow progressing.

From your signature we see you have been there, done that. We wish you continued success in your fight with PCa. Cheers!

RalphV