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In the short time the study has been running (median follow-up a little over one year), a total of 261 men had repeat biopsies. To be accepted for the study, the initial diagnosis required was clinical stage T1c or T2 disease, PSA level 10ng/ml or less, PSA density of < 0.2ng/ml/ml, Gleason score 6 or less, and 2 biopsy cores or less involved with cancer. The repeat biopsies showed no PCa in 34% of the men and PCa in one or two cores with Gleason score less than 6 in 44%. In other words the biopsy showed no worsening of the situation in 78% of the men – quite the contrary, in most cases the result was significantly better. Presumably these men would lave had ‘favorable criteria’ since the other 22% of the men had what was termed in the Abstract as “unfavorable criteria”.
Of course, given the ‘hit and miss’ nature of prostate biopsy procedures, these results may mean that the needles just missed dangerous parts of the gland – but then again maybe not. I have long held the view that the development of the atypical cells that are labeled as ‘prostate cancer’ is a natural process. Like all other natural processes, there is no stasis: in nature there is always growth or retreat, nothing stands still. When cancers retreat the process is termed spontaneous remission or spontaneous regression. A definition might be A complete or partial, temporary or permanent disappearance of all or at least some relevant parameters of a soundly diagnosed malignant disease without any medical treatment or with treatment that is considered inadequate to produce the resulting regression. So could the absence of any sign of prostate cancer in the second biopsy needles, or the lower Gleason Grades be a demonstration of spontaneous regression?
Most men and medical people will tend to refute this thought with the reaction that there are no studies that demonstrate this possibility for prostate cancer. And they would be right, depending on their definition of what an appropriate study is – as far as I know there are no specific, prospective, double blinded, peer reviewed studies that demonstrate that prostate cancer can spontaneously regress. But that really means that the possibility may not have been studied. I don’t think it should mean we should ignore all evidence that points to a possibility of a spontaneous regression of prostate cancer.
When I first started my investigations of the possibility of spontaneous regression (SR), one of the first abstracts I found was this one which speculates on possible causes of SR. I found it particularly pertinent to note that SR is reported in virtually all types of human cancer and that one of the mechanisms proposed for SR was psychologic factors - an interesting thought for those who feel that attitude has nothing to do with healing. Immune mediation is another contentious issue since it was a long held belief that the immune system could not recognise tumour cells.
Papac RJ.: Spontaneous regression of cancer: possible mechanisms. In Vivo, 1998 Nov-Dec, 12(6):571-8. Abstract: Spontaneous regression of cancer is reported in virtually all types of human cancer, although the greatest number of cases are reported in patients with neuroblastoma, renal cell carcinoma, malignant melanoma and lymphomas/ leukemias. Study of patients with these diseases has provided most of the data regarding mechanisms of spontaneous regression. Mechanisms proposed for spontaneous regression of human cancer include: immune mediation, tumor inhibition by growth factors and/or cytokines, induction of differentiation, hormonal mediation, elimination of a carcinogen, tumor > necrosis and/or angiogenesis inhibition, psychologic factors, apoptosis and epigenetic mechanisms. Clinical observations and laboratory studies support these concepts to a variable extent. The induction of spontaneous regression may involve multiple mechanisms in some cases although the end result is likely to be either differentiation or cell death. Elucidation of the process of spontaneous regression offers the possibility of improved methods of treating and preventing cancer.
Another study which seems to me to be pertinent is this one. I noted with interest that SR is said to be well documented and is said to be commonly attributed to the activation of the immune system. I was somewhat surprised to see the suggestion that tumours are inherently prone to SR since the odds of SR occurring have been calculated in one report as only occurring once in 80,000 cases. Mind you it is as difficult to identify how much SR there is as it is to calculate how many perfect murders occur. The definition of a perfect murder means that it was never identified as a murder. If a tumour occurs, is not diagnosed and is overwhelmed by the immune system, it could not be identified as a SR case. But I digress – here’s the second study:
Yakovlev A; Boucher K; DiSario J. Modeling insight into spontaneous regression of tumors. Mathematical Biosciences, 1999 Jan 1, 155(1):45-60.
The abstract opens by saying
The phenomenon of spontaneous regression of benign and malignant tumors is well documented in the literature and is commonly attributed to the induction of apoptosis or activation of the immune system. We attempt at evaluating the role of random effects in this phenomenon. To this end, we consider a stochastic model of tumor growth which is descriptive of the fact that tumors are inherently prone to spontaneous regression due to the random nature of their development.
When I have raised the issue of SR as a discussion point previously, the concept has either been ignored or shot down because of the stated lack of specific prostate related studies. I did find one study that referred specifically to prostate cancer:
Bissada NK; Kaczmarek AT. Complete remission of hormone refractory adenocarcinoma of the prostate in response to withdrawal of diethylstilbestrol. Journal of Urology, 1995 Jun, 153(6):1944-5.
Abstract: The phenomenon of regression of adenocarcinoma of the prostate after the withdrawal of antiandrogens is well documented. However, to our knowledge we report the first case of durable complete remission of hormone refractory prostate cancer after cessation of diethylstilbestrol. The drug was discontinued because the patient had disease progression while on diethylstilbestrol and withdrawal resulted in durable remission. In more than 3 years of followup since discontinuing diethylstilbestrol there has been no evidence of clinical or biochemical recurrence.
Of course this is not conclusive, but there are anecdotal reports of PSA not rising after intermittent ADT (Androgen Deprivation Therapy). This would, I think qualify as SR because the general view ADT is not curative. It is because of these incidents that I have wondered why early stage PCa is not treated with what I refer to as ADT Lite – limited shots of Zoladex for instance. If the colony is small enough, the combine effects of ADT and the immune system might wipe it out permanently.
I am not suggesting in any way that anyone should rely on SR as a potential ‘cure’ , but I think it is important to bear in mind that those men – the substantial majority in the US especially – who have a diagnosis that fits the criteria for this study would probably not lose anything – and might gain confidence in the Active Surveillance option if they followed the suggested PRIAS protocols.