PC-SPES (PDQ®): Complementary and alternative medicine - Health Professional Information [NCI]
This information is produced and provided by the National Cancer Institute (NCI). The information in this topic may have changed since it was written. For the most current information, contact the National Cancer Institute via the Internet web site at http://cancer.gov or call 1-800-4-CANCER
Purpose of This PDQ Summary
This PDQcancer information summary for health professionals provides comprehensive, peer-reviewed, evidence-based information about the use of PC-SPES as a treatment for prostate cancer. This summary is reviewed regularly and updated as necessary by the PDQ Cancer Complementary and Alternative Medicine Editorial Board.
Information about the following is included in this summary:
- A brief history of PC-SPES research.
- The results of clinical studies of PC-SPES.
- Possible side effects of PC-SPES use.
- Discussion regarding the contamination of PC-SPES and its withdrawal from avenues of distribution.
This summary is intended as a resource to inform and assist clinicians and other health professionals who care for cancer patients. It does not provide formal guidelines or recommendations for making health care decisions.
Some of the reference citations in the summary are accompanied by a level of evidence designation. These designations are intended to help the readers assess the strength of the evidence supporting the use of specific interventions or treatment strategies. The PDQ Cancer Complementary and Alternative Medicine Editorial Board uses a formal evidence ranking system in developing its level of evidence designations. These designations should not be used as a basis for reimbursement determinations.
This summary is also available in a patient version, which is written in less technical language.
This complementary and alternative medicine (CAM) information summary provides an overview of the use of PC-SPES as a treatment for cancer. The summary includes a brief history of PC-SPES research, the results of clinical trials, and possible adverse effects of PC-SPES. Included in this summary is a discussion of the contamination of PC-SPES and its withdrawal from avenues of distribution.
This summary contains the following key information:
- PC-SPES is a patented mixture of eight herbs.
- PC-SPES was sold as a dietary supplement to support and promote healthy prostate function.
- Each herb used in PC-SPES has been reported to have anti-inflammatory, antioxidant, or anticarcinogenic properties.
- PC-SPES was recalled and withdrawn from the market because certain batches were contaminated with Food and Drug Administration–controlled prescriptiondrugs.
- The manufacturer is no longer in operation, and PC-SPES is no longer being made.
- There is evidence from both laboratory and animal studies to suggest that PC-SPES had some effect in inhibiting prostate cancer cell growth and prostate-specific antigen (PSA) expression, but it is not known whether these results were caused by contaminants such as diethylstilbestrol (DES), which is an estrogenic compound, the herbs in PC-SPES, or their combination.
- Evidence from clinical trials has shown that PC-SPES lowers PSA and testosterone levels in humans, but it is not known whether these results were caused by contaminants, the herbs in PC-SPES, or their combination.
- There is some evidence to suggest that PC-SPES has some anticancer effects that are not related to estrogen-like activity.
- Although there are products that claim to be substitutes for PC-SPES, they are not the patented original formulation. Few of these products have been the subject of laboratory or clinical trials reported in the peer-reviewed medical literature.
Note: A separate PDQ summary on Prostate Cancer Treatment is also available.
PC-SPES is a patented herbal mixture that was sold as a dietary supplement and used as a complementary and alternative medicine (CAM) treatment for prostatecancer. It is a combination of eight herbs: baikal skullcap (Scutellaria baicalensis Georgi), chrysanthemum (Dendranthema morifolium [Ramat.] Tzvelev [synonym Chrysanthemum morifolium]), ganoderma (Ganoderma lucidum [Curtis:fr] Karst.), isatis (Isatis indigotica Fort.), licorice (Glycyrrhiza glabra L. or Glycyrrhiza uralensis Fisch. ex DC.), Panax ginseng C.A. Meyer or pseudoginseng(Panax pseudoginseng var. notoginseng Hoo & tseng [synonym Panax notoginseng (Burkill)] F.H.Chen), Isodon rubescens (Hemsl.) Hara (synonym Rabdosia rubescens [Hemsl.] Hara), and saw palmetto (Serenoa repens [Bartr.] Small). With the exception of saw palmetto, the herbs in PC-SPES have been used individually or in combination in Traditional Chinese Medicine (TCM) for a variety of health problems, including those of the prostate, for hundreds of years.[1,2]
PC-SPES is an herbal product that resulted from a collaboration between a chemist at the New York Medical College in Valhalla, New York, and a Chinese herbalist and doctor of TCM in China. Their idea was to combine TCM with the scientific techniques of Western laboratory research. In the United States, a series of in vitro and in vivo laboratory studies was started on the mixture of herbs used in TCM specially formulated to treat prostate problems. Researchers published the results of these studies, which showed promising anticancer activity from PC-SPES.[3,4,5,6,7,8,9,10,11]
In 1997, the herbal formula for PC-SPES was patented in the United States. A company, BotanicLab (Brea, California), was formed to produce, distribute, and sell the product. PC-SPES was sold through the BotanicLab Web site (the Web site was taken down after PC-SPES was recalled) and through selected distributors. Anecdotal information about the product and its positive effects was widely circulated on the Internet through Web sites that informed prostate cancer patients about new developments in treatment. At the same time, the published papers were being read by the scientific community, and the findings were presented at various conferences. As a result, clinicians and researchers began looking at PC-SPES as one of the first viable treatments to come out of the alternative medicine community.
The manufacturing process for PC-SPES has been described by the manufacturer as follows: extracts of raw plant material were obtained from the specified plants, which were grown in particular geographic regions in China and harvested at certain times of the year to reduce the natural variation inherent in any biological product. The extracts were shipped to the United States, where high-performance liquid chromatography (HPLC) was used to monitor the key active compounds—which are believed to be directly related to the clinical effects—for batch-to-batch reproducibility. Activity-related biomarkers were kept in a constant concentration from lot to lot. A commercial testing laboratory (Truesdail Laboratory, Tustin, California) was used to guarantee that each batch was free from contamination with heavy metals, pesticides, microorganisms and products, and prescriptiondrugs. Each lot was standardized by an anticancer bioassay for an effective dose of 50% in vitro inhibition of cell growth using human LNCaP cells for androgen-dependent (AD) prostate cancer and DU-145 cells for androgen-independent (AI) prostate cancer. The powder was then encapsulated, bottled, labeled, and sterilized at the BotanicLab facility.
In 2001, allegations that PC-SPES contained the synthetic estrogendiethylstilbestrol (DES) started to appear on e-mail listservs used by prostate cancer patients and in online newsletters. Prostate cancer patients who were taking PC-SPES noticed that their recent medication was not as effective as the previous batches. A sample of PC-SPES submitted to a testing laboratory by BotanicLab in August 2001 found no DES. BotanicLab posted the letter from the laboratory on their Web site, claiming that PC-SPES contained no DES. However, in other tests of six different lots of PC-SPES received from two different sources in August 2001, Rocky Mountain Instrumental Laboratory found varying amounts of DES in three lots. More tests done for the California Department of Health Services in February 2002 did not find DES but did find warfarin, a prescription drug used as a blood thinner.
The presence of a synthetic estrogen such as DES was suspected early in the clinical use of PC-SPES after reports in the literature discussed the mixture's estrogen-like ability to lower prostate-specific antigen (PSA) levels in AD prostate cancer patients. In addition, the side effects of treatment were similar to those of estrogen therapy.[15,16,17] In one study, patients who showed the most response to PC-SPES were also those who were the most responsive to DES. Reviewed in [11,18] The same study also attempted to find out whether DES or similar compounds were present in PC-SPES. Transcriptional activation assays in yeast strain PL3 Saccharomyces cerevisiae using an ethanolic extract of PC-SPES showed estrogenic activity similar to 1nM estradiol. In addition, ovariectomized CD-1 mice showed substantially increased uterine weights. HPLC, gas chromatography, and mass spectrometry did not reveal the presence of DES but rather that of a compound with similar chemical characteristics. The authors of the report concluded that PC-SPES contains estrogenic compounds that are distinct from DES or other synthetic estrogens.
A definitive evaluation of PC-SPES analyzed specific lots of PC-SPES capsules manufactured from 1996 to 2001. In addition to using HPLC to isolate, identify, and quantify the synthetic drugs and active phytoestrogens, this study also identified components using proton nuclear magnetic resonance, gas chromatography/mass spectrometry, and mass spectra analysis. Tests showed the presence of the synthetic drugs indomethacin (a nonsteroidal anti-inflammatory drug not previously reported in the literature or found in other testing), DES, and warfarin. Testing was also done for concentrations of the two naturally occurring phytosterols, licochalcone A and baicalin. Test results indicated a history of rising and falling levels of contamination by the three synthetic drugs and a recent rise in the naturally occurring phytochemicals in PC-SPES. Lots of PC-SPES manufactured in 1996 through mid-1999 contained indomethacin ranging from 1.07 to 13.19 mg/g and DES ranging from 107.28 to 159.27 µg/g and were 2 to 6 times more antineoplastic and up to 50 times more estrogenic than lots manufactured after the spring of 1999. In vitro testing of ethanolic extracts of PC-SPES against LNCaP, PC-3, and DU-145 prostate cancer cell lines showed a decrease in both antineoplasticity and estrogenicity in lots of PC-SPES manufactured in June 1998 through August 2001, which correlated with the amount of DES and indomethacin contamination. Another in vitro test of suspected lots of PC-SPES manufactured from 2000 to 2001 also showed the presence of DES. The table below shows the lot numbers, date of manufacture, and amount of DES contamination.
Lot Numbers, Date of Manufacture, and Amount of DES Contamination
|Lot Number and Date||DES (µg mean/capsule)|
|5430125 (6/2000) ||46.36|
Refer to chart 1 below showing the lot numbers, date of manufacture, and amount of DES contamination.
Although the laboratory testing showed that certain lots of the mixture contained indomethacin, warfarin, and DES, the amount of DES present may not have accounted for all of the estrogenic effect of PC-SPES. There is some evidence that the mixture acts differently from DES at the molecular level.[7,21] In addition, its anticancer effects on both AI prostate cancer and AD prostate cancer may point to a mechanism other than estrogen-like activity.[19,22,23] The in vitro activity of PC-SPES against cancer cells other than prostate also gives rise to the speculation that its estrogen-like qualities might not account for all of the mixture's anticancer activity.[24,25]
Considerable research has been conducted on the anticancer properties of the eight individual botanicals in PC-SPES.
Baikal skullcap (Scutellaria baicalensis)—Chinese name huang qin—contains baicalin and wogonin, two active flavones. Baicalin converts to baicalein, which is another active flavone. In vitro, baicalin and baicalein inhibit cell growth of AD LNCaP and JCA-1 AI human prostate cancer cell lines [24,25], as well as inducing apoptosis in human LNCaP cells. Baicalin also shows antimutagenic and antioxidant activity in vitro as well as free radical scavenging ability.[27,28,29,30,31,32]
Licorice (Glycyrrhiza glabra or Glycyrrhiza uralensis)—Chinese name gan cao—contains the very active flavonoid licochalcone A, which has demonstrated in vitro estrogenic activity. This botanical shows a broad range of anticancer activity in vitro. It enhances the cytotoxicity of commonly used anticancer drugs and induces apoptosis in MCF-7 human breast cancer and HL-60 promyelocytic leukemia cell lines.[33,34,35,36]
Reishi mushroom (Ganoderma lucidum [Curtis: fr.] Karst.)—Chinese name ling zhi— has been shown to aid in the recovery of leukocyte counts in irradiated mice in a dose-dependent manner. It contains the polysaccharide G009, which has demonstrated antioxidant behavior against HL-60 cells in vitro and dose-dependent inhibition of lipid peroxidation in rat brain cells in vitro.[37,38,39,40,41]
Isatis (Isatis indigotica)—Chinese name da qing ve—contains active agents in each part of the plant. TCM has different names for the medicinals coming from the leaf, stem, and root and uses these plant products for different purposes. Indirubin, an active ingredient, and its analogs have demonstrated inhibition of cyclin-dependent kinases in human mammarycarcinoma cell line MCF-7 in vitro.
Ginseng (Panax ginseng or Panax pseudoginseng var. notoginseng)— Chinese name tianqi—contains ginsenosides and saponins. Of the 30 ginsenosides that have been isolated from Panax ginseng, only the 20(S)-protopanaxadiol type R3 has inhibited cell growth and suppressed PSA expression, androgenreceptor and 5-alpha-reductase activity, and PCNA production in vitro.[43,44,45]
Chrysanthemum flowers (Dendranthema morifolium)—Chinese name ju hua—contain triterpene diols and triols. Arnidiol exhibited cytotoxicity in vitro against 58 of the 60 human cancer cell lines developed by the National Cancer Institute (NCI) Developmental Therapeutics Program.
The botanical rabdosia rubescens (Isodon rubescens)—Chinese name dong ling cao—has two very active agents, oridonin and rubesencin b. Oridonin inhibits DNA synthesis in vitro Reviewed in , and rubesencin b inhibited cell growth in cancer cell lines in vitro and in a mouse model.
Saw palmetto (Serenoa repens) is the only botanical in PC-SPES that is not used in TCM. There is strong evidence from human trials that saw palmetto has some activity against benign prostatic hypertrophy (BPH), including improved urine flow and less erectile dysfunction when compared with placebo or finasteride.S repens also exhibits antiestrogenic activity in placebo-controlled BPH trials. In LNCaP cells, S repens produced apoptosis in vitro.[48,49,50,51,52]
Exactly how PC-SPES works in the body is still unknown. The presence of contaminants and varying amounts of the active agents in each lot of PC-SPES complicate the interpretation of any results from studies that might lead to an explanation of its mechanisms of action. More studies of the individual components of the mixture and testing of a standard formulation that is free of contaminants are needed before any conclusions can be reached about the level of cytotoxicity, antineoplasticity, or estrogenicity of PC-SPES.
The National Center for Complementary and Alternative Medicine (NCCAM) stopped funding to studies of PC-SPES after the drug contamination was detected and made public, although the laboratory studies were later resumed. Refer to The Future of PC SPES Research Funding by NCCAM.
Laboratory / Preclinical Studies
Before the discovery of diethylsylbestrol (DES), warfarin, and indomethacin contamination, PC-SPES appeared to have some efficacy as an antineoplastic agent in laboratory and animal studies. These studies are presented below. Due to the fact that there was no standardization of the composition of PC-SPES or any knowledge of the amount of contamination of each lot used in testing, it is difficult to interpret the data from these studies.
In one study that attempted to measure the effects of the whole PC-SPES mixture versus that of individual herbs of PC-SPES on prostate-specific antigen (PSA) expression and cell growth, LNCaP cells were treated with ethanol extracts of PC-SPES and each of the eight herbs. The PC-SPES mixture reduced cell growth by 72% to 80%, while Dendranthema morifolium (Ramat.) Tzvelev (synonym Chrysanthemum morifolium) (chrysanthemum) produced the highest reduction of the herb group at 85%. Panax pseudoginseng var. notoginseng Hoo & tseng (Synonym Panax notoginseng [Burkill] F.H.Chen) was next at 80.9% reduction, followed by Glycyrrhiza uralensis Fisch ex DC.(73%). The lowest reduction in cell growth was exhibited by Serenoa repens (Bartr.) Small (14.5%). Scutellaria baicalensis Georgi, Serenoa repens, and Glycyrrhiza uralensis lowered PSA expression, but each of the other herbs increased PSA expression. The ability of individual herbs to reduce PSA expression was not uniform, but the PC-SPES mixture as a whole exhibited a uniform response. The varying results with the individual herbs and the positive response of the cells (i.e., increased cytotoxicity and reduced PSA expression) to the aggregate PC-SPES mixture may suggest that the botanicals in PC-SPES work in concert and that no individual herb can account for the overall effects of the mixture.
In other studies, PC-SPES was found to inhibit clonal growth in three human prostatecancercell lines: LNCaP, PC-3, and DU-145. Cell cycle analysis showed cell cycle arrest at the G2 phase.Cell proliferation and reduced clonogenicity were observed in cancer cell lines other than those of prostate cancer: human breastcarcinoma lines MCF-7 and T47-D, SK-N-MC neuroepithelioma, COLO 38 melanoma, U937 histiomonocytic lymphoma, and HL-60 and MOLT-4 leukemias.Cytotoxic and cytostatic effects of PC-SPES were common to all tumor cell lines tested.
In another study evaluating regulation of PSA expression and androgenreceptor (AR) activity, LNCaP prostate cancer cell lines showed downregulation of both proliferating cell nuclear antigen (PCNA) and PSA expression. PSA changes occurred concurrently with the decrease of PCNA. The results suggest that PC-SPES modulates cell growth by changing PCNA expression and may decrease PSA levels indirectly by suppressing AR expression.
None of the studies above indicated lot number or year of manufacture of the PC-SPES used. Therefore, it is not possible to assess the amount of contamination of the mixtures used in the studies or whether the mixtures used were not in fact contaminated.
A 1998 study that evaluated estrogenic activity of extracts of PC-SPES, ginseng (Panax ginseng C.A. Meyer), saw palmetto, DES, and estrone (estradiol-17 beta) in vitro reported on the estrogenic response of ovariectomized CD-1 mice to PC-SPES extract as well as the response to PC-SPES capsules in eight prostate cancer patients who had received previous therapy. This study used four samples of PC-SPES ordered in separate purchases from BotanicLab. No lot numbers were supplied in the study. Lot numbers from October 1996 through July 1998 were later tested for contamination and had DES levels of 114.74 µg/g to 159.27 µg/g, as well as the highest detected levels of indomethacin of the PC-SPES lots tested.In vitro tests of PC-SPES extract or estradiol showed estrogenic activity similar to 1 nM estradiol on estrogen receptor Y253 yeast strain. Transcriptional activation assays in yeast strain PL3 Saccharomyces cerevisiae with ethanolic extract of PC-SPES exhibited estrogen-like effects. In the eight prostate cancer patients, serumtestosterone concentrations decreased during the use of PC-SPES and increased within 3 weeks after treatment was discontinued. PSA levels decreased in all eight patients. Side effects in all eight patients were similar to those seen after treatment with estrogen: breast tenderness and loss of libido. One patient had superficial venous thrombosis.
By incorporating PC-SPES into the rat diet, researchers conducting an in vivo study showed antitumor effects using a Dunning R3327 rat prostatecancer model. Levels of 0.05% and 0.025% of dietary PC-SPES were fed to the rats over a 6-week period. No toxicity was seen, nor was there a difference in the food intake of the rats during this time. Pulmonarytumors were induced by intradermalinjections of MAT-LyLu cells, which are particularly resistant to many forms of treatment. Tumor incidence was inhibited in a dose-dependent manner, and the rate of tumor growth showed the same dose-dependent response.[1,2]
In another study, which used male BNX nu/nu immunodeficient nude mice, PC-SPES was also administered orally, but in suspension. The mice received 300 rad of whole-body irradiation, after which they were inoculated with either PC-3 or DU-145 prostate cancer cell lines. Treatment with PC-SPES began the day after injection. Results showed that PC-SPES suppressed the growth of DU-145 tumors compared to tumor growth in the control group. Cytological analysis showed apoptosis in the treated group that was not apparent in controls.
In two other studies, clinical studies of patients were initiated along with in vitro and in vivo research. The results of these two patient groups are discussed in the Clinical Trials section. The first study, preceding more extensive research, examined in vitro activity of PC-SPES against LNCaP, LNCaP-bcl-2, PC-3, and DU-145 cells lines. Results showed that PC-SPES was active in suppressing both hormone-sensitive and -insensitive prostate cancer cell lines. In the subsequent study, research was conducted in vitro on the ability of PC-SPES to induce apoptosis in androgen-independent (AI) prostate cancer cell lines, and in vivo on the effect of oral PC-SPES on the growth of xenographed PC-3 tumors in immunodeficient male mice. Mice in the treatment arm—in which treatment was started 1 week after implantation—showed a significant decrease in tumor weight when compared with mice in the control arm. PC-SPES showed activity against both androgen-sensitive and AI prostate cancer in the patients and suppressed tumor growth in AI tumors in mice. Reviewed in [3,4,5] In both studies, the patients were given capsules manufactured between 1996 and 1999, a time when contamination levels of DES were highest.
Another study in rats demonstrated that PC-SPES (one lot contaminated with DES and one lot without DES) causes some decrease in the activity of a liverenzyme involved in drugmetabolism (CYP3A).
One published randomized cross-over study of patients with androgen-independent (AI) prostate cancer who initially received either 960 mg PC-SPES 3 times a day or 3 mg DES once a day before crossing over to the other regimen when disease progression occurred reports data demonstrating the presence and levels of contaminants in the four lots of PC-SPES used in that trial. The lots were manufactured by BotanicLab (Brea, California). The study was halted and chemical analyses of the lots were performed. The analyses showed that all four lots of PC-SPES contained amounts of DES ranging from 0.1 µg/g to 32.7µg/g, and that one lot contained varying amounts of ethinyl estradiol. The authors concluded that the presence of these contaminants rendered their results inconclusive.
Several nonrandomized clinical studies published between 1999 and 2003 described the results of clinical trials conducted before contaminants had been conclusively identified in PC-SPES lots and before it was known that there was significant variation in naturally occurring active agents, such as baicalein and licochalcone-A, in the lots. These studies, many of which enrolled small numbers of patients, did not identify the source of the lots that were used in the trials, nor did they identify where patients acquired PC-SPES.
In addition to the confounding effects of contaminants on the clinical trial results discussed below, the fact that an optimal dose of PC-SPES remains undetermined and that dose varies among these studies makes it difficult to compare their findings.
In a retrospective study of 23 consecutive patients with AI disease, charts were evaluated for patients' responses to PC-SPES and the occurrence of any toxicity. There is no report of where the patients acquired their PC-SPES or what lots were used. Patients were all seen between February and November in 1999. Patients ranged in age from 51 to 88 years, with a median age of 70 years. All had previous initial androgen ablation for a period of 6 months to 144 months. Ten patients had received chemotherapy, 13 had not. More than half the patients with AI showed a post-therapyprostate-specific antigen (PSA) decline of 50% or greater. Median time to PSAprogression was 6 months. The side effects were similar to those of estrogen therapy: gynecomastia and impotence. Other side effects were nausea/vomiting and diarrhea and to a lesser extent, allergic reactions, leg cramps, and leg swelling.
In a prospective clinical trial of 16 men with stage D3 metastaticprostate cancer in which all patients had failed therapy and had disease progression, the effects of PC-SPES on pain, quality of life, and side effects were assessed. Previous therapy was either orchidectomy or a luteinizing hormone–releasing agonist with or without antiandrogen.Hormonal therapy was continued throughout the trial to avoid the known withdrawal effect of antiandrogen on PSA levels. There was a significant decrease in pain scores such that the 14 patients on analgesics required an average of 40% less analgesics while taking PC-SPES. PC-SPES treatment was associated with improved function and emotional and physical well-being. PSA levels declined significantly after PC-SPES therapy (>50%). Side effects were breast tenderness, deep venous thrombosis, and mild dyspepsia. Reviewed in [3,4]
In a study of 70 patients, 37 with androgen-dependent (AD) disease and 33 with AI disease, the AD cohort was treated with PC-SPES only or after an initial treatment with prostatectomy,radiation,cryotherapy, and/or hormonal therapy. Median duration of PSA response was greater than 57 weeks. All patients in the AD cohort had PSA declines within a range of 80% to 100%, and two patients with bone metastases showed improvement on radiographic analysis. Within the AI cohort, 54% (19 of 35) had a PSA decrease of greater than 50%, with median time to nadir of 10 weeks and a median duration of 18 weeks. Eight of the 16 patients who had received ketoconazole therapy prior to PC-SPES also obtained a decrease of greater than 50% in their PSA values. Testosterone levels within the AD group decreased to castrate levels (<50 ng/mL) in 94% of patients (31 of 33), and libido (25 of 25) and potency (15 of 15) were lost in all patients who entered the study. Side effects were hot flashes, gynecomastia/gynecodynia, and thromboembolic effects in 3 of 70 patients. Although the results of this trial were promising for the treatment of both AI and AD prostate cancer, it is not possible to assess what was responsible for these effects. This trial used PC-SPES from one single lot, but the published study does not indicate the lot number. The research was completed before 2000. No attempt was made to assess the possible contamination of the product.Reviewed in [3,5]
A prospective clinical series assessed the ability of PC-SPES to lower serum PSA levels in 33 prostate cancer patients. The patients had either refused conventional therapy or had failed previous cryosurgery,radiation therapy, and/or hormonal therapy. No overt signs of disease progression were found in any of the patients. At 2 months, PSA levels had decreased by a mean of 52% in 27 of the 31 patients and had increased in two patients. Of the five patients who had hormone-refractory disease, all had decreased serum PSA levels. Reviewed in [3,6]
In a continuation of the previous study, a total of 69 patients with either AI or AD disease were separated into three study groups. Group one (43 patients) had undergone previous therapy, including hormonal; group two (22 patients) developed AI after treatment; and group (four patients) had not undergone previous therapy. The study assessed PC-SPES activity in suppressing PSA levels. Patients were given three capsules of PC-SPES 3 times per day. PSA levels and side effects were observed for 24 months.
In group one, 82% of patients (32 of 39) had a decrease in PSA levels, with 20 patients having a decrease of greater than 50% at 2 months' follow-up; the decrease lasted for 24 months in two patients. In group two (AI patients), 90% (19 of 21) had a decrease in PSA at their 2-month follow-up, with 66% (14 of 21) having a decrease of greater than 50% in PSA levels. At 24 months, two patients had a decrease of 20% to 50% in pretreatment PSA levels. In group three, 50% (2 of 4) had a decrease of greater than 50% in PSA levels at 2 months, and the remaining two patients had an increase at 2 and 6 months. Eighty-two percent of study patients had a decreased PSA level after 2 months of therapy. Side effects included nipple tenderness (42%), gynecomastia (8%), hot flashes, and deep venous thrombosis.
Adverse effects of PC-SPES treatment were similar to those of hormonal drugs. The percentages indicate the approximate low-to-high range of side effects reported in the studies. It is difficult to compile accurate numbers from all studies reporting side effects because they are not consistently reported. Some studies concatenated categories of side effects, some did not report specific numbers or percentages, and some reported a few side effects while not reporting others. The following references indicate the studies from which the percentages come:
- Gynecomastia (8%–8.7%).[1,2,3,4,5,6]
- Nipple tenderness (34.8%–100%).[1,2,3,4,5,6,7]
- Dyspepsia/nausea (15.7%–21.7%).[2,3,4,5,6,7]
- Fatigue (8%–17.1%).[1,2,3,4,5]
- Diarrhea (13%–38.6%).[1,2,3,4,5]
- Leg cramps/swelling (2%–68.5%).[1,2,3,4,5]
- Cardiovascular problems/angina (4.3%–7%).[1,2,3,4,5]
- Hot flashes (4.3%–34%).[1,2,3,4,5]
- Decreased libido (6.2%–100%).[5,7]
- Erectile dysfunction (single case report).
- Thromboembolic effects (5%–6.2%).[5,6]
Substitutes for PC-SPES
No substitutes are available for the original PC-SPES. Although manufacturers are selling supplements purporting to be substitutes, the PC-SPES mixture is patented and cannot be duplicated. There are no published reports of clinical trials of herbal mixtures that claim to be substitutes for PC-SPES. The only company that had a license from the patent holder to manufacture PC-SPES is no longer in business, and the product cannot be legally manufactured in the United States without the patent holder's permission. PC-SPES is not legally available in the United States.
Overall Level of Evidence for PC-SPES
To assist readers in evaluating the results of human studies of complementary and alternative medicine (CAM) treatments for cancer, the strength of the evidence (i.e., the levels of evidence) associated with each type of treatment is provided whenever possible. To qualify for a level of evidence analysis, a study must:
- Be published in a peer-reviewed scientific journal.
- Report on therapeuticoutcome or outcomes, such as tumorresponse, improvement in survival, or measured improvement in quality of life.
- Describe clinical findings in sufficient detail that a meaningful evaluation can be made.
The lack of consistent composition of PC-SPES due to varying concentrations of contaminants makes it difficult to determine the effects of PC-SPES in humans; therefore, no level of evidence analysis is possible for this treatment. At this time, the use of PC-SPES as a treatment for cancer cannot be recommended outside the context of well-designed clinical trials.
For additional information about levels of evidence analysis, refer to Levels of Evidence for Human Studies of Cancer Complementary and Alternative Medicine.
Changes to This Summary (09 / 04 / 2008)
The PDQcancer information summaries are reviewed regularly and updated as new information becomes available. This section describes the latest changes made to this summary as of the date above.
An image was added to this summary.
ADDITIONAL INFORMATION ABOUT CAM THERAPIES
- The National Center for Complementary and Alternative Medicine (NCCAM).
- The National Cancer Institute Office of Cancer Complementary and Alternative Medicine (OCCAM).
- CAM on PubMed, a special subset of the PubMed scientific literature database created through a partnership between NCCAM and the National Library of Medicine.
- PDQ® - NCI's Comprehensive Cancer Database
Full description of the NCI PDQ database.
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Tests or procedures that detect specific types of cancer.
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- PDQ® Cancer Information Summaries: Genetics
Genetics of specific cancers and inherited cancer syndromes, and ethical, legal, and social concerns.
- PDQ® Cancer Information Summaries: Complementary and Alternative Medicine
Information about complementary and alternative forms of treatment for patients with cancer.
This information is intended mainly for use by doctors and other health care professionals. If you have questions about this topic, you can ask your doctor, or call the Cancer Information Service at 1-800-4-CANCER (1-800-422-6237).
Date Last Modified: 2008-09-04