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Trametes versicolor

Turkey Tail Mushroom (Trametes versicolor) is a mushroom that is a source of a polysaccharide, known as polysaccharide K, that is established as a cancer adjunct therapy for the immune system.

Our evidence-based analysis on trametes versicolor features 15 unique references to scientific papers.

Research analysis led by and reviewed by the Examine team.
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Research Breakdown on Trametes versicolor

1Sources and Composition


Trametes versicolor, more commonly known as Turkey Tail Mushroom,

Historically, Turkey Tail polysaccharide (specifically PSK) have been used in Japan as anti-cancer adjuvants alongside other cancer therapies; first approved in 1977 as a prescription medication (in regards to isolated PSK) and in 1987 PSK itself accounted for more than 25% of total national expenditure for anticancer agents in Japan.[1]


The main bioactives in Turkey Tail are:

  • Polysaccharide K (PSK)[2][3]

  • Polysaccharide-peptide (PSP) from the water-soluble fragment[4][5]



PSP has been tested in rats to assess its interactions with pain (hot-plate test for tactile heat pain, acetic acid writhing test for chemical pain) and PSP appeared to have weak pain sensitizing effects relative to control.[6] This increase in pain sensitivity appears to have been related to pro-inflammatory effects of PSP, and was significantly inhibited by anti-inflammatories.[6]

3Inflammation and Immunology

3.1Mononuclear Cells

PSK may stimulate proliferation of PBMCs while inducing accumulation of interleukins (particularly IL-1α) within the cell.[6] Increased IL-8 levels result after stimulation of PBMCs by PSK, and this has been found in persons following oral ingestion of 1g PSK (with spikes appearing in 42-44% of persons within 3 hours, assay could not detect less than 25pg/mL) to a fairly variable level of 30-125pg/mL (data extracted from graph).[7]

3.2Natural Killer Cells

The polysaccharide PSK appears to be a TLR2 agonist, and can stimulate Natural Killer (NK) cells to produce IFN-γ and increase their cytotoxicity;[8] although it is contested as to whether this is direct or indirect NK cell activation (may be vicarious through Dendritic Cells).[9][10] Abolishment of the TLR2 receptor in mice abolishing NK cell activity induced by PSK.[8]

Interactions between tumors and Turkey Tail mushroom are partially dependent on NK cells, and mostly dependent on both NK cells and T-Cells.[7]

In women with breast cancer who had NK cell activity significantly reduced due to radiotherapy, a trend towards increasing NK cell activity was noted with 6g daily after 4 weeks but aside from not being present at 6 weeks nor being present with 9g ingestion this failed to be statistically significant.[11] This same trend existed for NK cell count.[11]


In vitro, incubation of 10-200ug/mL PSK appears to increase CD4+ and CD8+ T-cells and overall splenocyte proliferation.[8]

An increased level of cytotoxic T-cells against tumors has been noted in animals fed PSK (100mg/kg) after injection of tumor cells.[8]

Total levels of CD8 cytotoxic T-cells appear to increase after ingestion of 3-9g Turkey Tail over 6 weeks in women with breast cancer, but this was not statistically significant.[11]


Although increasing splenocyte proliferation, 10-200mcg/mL PSK appears to reduce the percentage of B-Cells in vitro from 46.8+/-0.6% to 22.4+/-1.9%[8] which may be related to the ability of PSK to suppress B-Cell growth via IL-15 secretion from T-Cells.[12]

A trend to increase CD19+ B-cells was noted in women given 6-9g Turkey Tail daily for 6 weeks.[11]

4Interactions with Cancer

4.1Breast Cancer

Mechanistically, the polysaccharide PSK appears to activate PBMCs via the TLR2 receptor directly and PBMCs then activate Natural Killer (NK) cells to release IFN-γ and lyse breast cancer cells.[13] TLR2 activation appears to enhance NK cell activity (as well as TLR8,9),[14] and PSK has once been demonstrated to enhance breast cancer therapries that target HER2 (a protein that is seen as a breast cancer therapeutic target[15]); with this study noting augmentation of Trastuzumab (Herceptin™).[13]

In women with breast cancer (Stage I-III) consuming Turkey Tail mycelia powder at 3, 6, or 9g daily (two divided doses) over 6 months resulted in normalization of lymphocyte counts that were reduced by radiotherapy at only 6-9g daily (3g not being significantly different than placebo) with the measurement after 6 weeks exceeding pre-radiation levels.[11]


In promyelocytic leukemia cells (HL-60), incubation of various extracts of Turkey Tail resulted in both the ethanolic and water extracts suppressing cell viability in a concentration dependent manner with more efficacy in the water extract; with 7.5-10mcg/mL suppressing viability to lower than 25% of baseline.[5]

Proliferation also appears to have been reduced at 5-10mcg/mL water extract of Turkey Tail that was associated with a decrease of cells in S phase (41.2% to 11.3%) with concomitant increases in G1 and G2/M phases.[5]

In regards to cytokines, a suppression of IL-8 was noted in HL-60 cells.[5]

5Safety and Toxicicity

Up to 9g of Turkey Tail daily for 6 months in women with Breast Cancer has failed to note any significant side effects and was deemed well tolerated.[11]


  1. ^ Sullivan R, Smith JE, Rowan NJ. Medicinal mushrooms and cancer therapy: translating a traditional practice into Western medicine. Perspect Biol Med. (2006)
  2. ^ Fisher M, Yang LX. Anticancer effects and mechanisms of polysaccharide-K (PSK): implications of cancer immunotherapy. Anticancer Res. (2002)
  3. ^ Sakagami H, et al. Stimulation by PSK of interleukin-1 production by human peripheral blood mononuclear cells. Anticancer Res. (1993)
  4. ^ Zaidman BZ, et al. Medicinal mushroom modulators of molecular targets as cancer therapeutics. Appl Microbiol Biotechnol. (2005)
  5. ^ a b c d Hsieh TC, et al. Effects of extracts of Coriolus versicolor (I'm-Yunity) on cell-cycle progression and expression of interleukins-1 beta,-6, and -8 in promyelocytic HL-60 leukemic cells and mitogenically stimulated and nonstimulated human lymphocytes. J Altern Complement Med. (2002)
  6. ^ a b c Chan SL, Yeung JH. Polysaccharide peptides from COV-1 strain of Coriolus versicolor induce hyperalgesia via inflammatory mediator release in the mouse. Life Sci. (2006)
  7. ^ a b Kato M, et al. Induction of gene expression for immunomodulating cytokines in peripheral blood mononuclear cells in response to orally administered PSK, an immunomodulating protein-bound polysaccharide. Cancer Immunol Immunother. (1995)
  8. ^ a b c d e Lu H, et al. Polysaccharide krestin is a novel TLR2 agonist that mediates inhibition of tumor growth via stimulation of CD8 T cells and NK cells. Clin Cancer Res. (2011)
  9. ^ Azuma M, et al. The peptide sequence of diacyl lipopeptides determines dendritic cell TLR2-mediated NK activation. PLoS One. (2010)
  10. ^ Martinez J, Huang X, Yang Y. Direct TLR2 signaling is critical for NK cell activation and function in response to vaccinia viral infection. PLoS Pathog. (2010)
  11. ^ a b c d e f Torkelson CJ, et al. Phase 1 Clinical Trial of Trametes versicolor in Women with Breast Cancer. ISRN Oncol. (2012)
  12. ^ Liu A, et al. PSK and Trx80 inhibit B-cell growth in EBV-infected cord blood mononuclear cells through T cells activated by the monocyte products IL-15 and IL-12. Blood. (2005)
  13. ^ a b Lu H, et al. TLR2 agonist PSK activates human NK cells and enhances the antitumor effect of HER2-targeted monoclonal antibody therapy. Clin Cancer Res. (2011)
  14. ^ Moreno M, et al. Toll-like receptor agonists and invariant natural killer T-cells enhance antibody-dependent cell-mediated cytotoxicity (ADCC). Cancer Lett. (2008)
  15. ^ Pathmanathan N, Bilous AM. HER2 testing in breast cancer: an overview of current techniques and recent developments. Pathology. (2012)