Mushrooms and Lung Cancer: What the Human Evidence Actually Shows

Mushrooms & Cancer

3 species

Three mushroom species have published human lung cancer data: turkey tail, maitake and reishi. Only turkey tail has randomized evidence, only one of those trials is individually available in English, and the reishi result was null.

Fritz et al., Integrative Cancer Therapies, 2015; Tsang et al., Respiratory Medicine, 2003

1977

year PSK entered clinical use in Japan; the approved lung indication is small-cell only

5.9%

PSP patients withdrawing due to disease progression vs 23.5% on placebo (n=34/arm)

3

mushroom species with published human lung cancer data: turkey tail, maitake, reishi

Fritz et al., Integrative Cancer Therapies, 2015; Tsang et al., Respiratory Medicine, 2003

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Most of the writing about mushrooms and cancer is built on petri dish experiments. Researchers grow lung cancer cells in a dish, add a mushroom extract, and watch the cells die. The results are real, but they are not evidence that anything works in a human being with lung cancer.

The mushrooms lung cancer research that actually matters operates at a different level. Polysaccharide-K (PSK), a compound extracted from turkey tail mushroom, entered clinical use in Japan in 1977 and remains an approved adjunct in Japanese cancer care today.^[3] That is nearly 50 years of regulated clinical use — a longer track record than any other mushroom compound in oncology.

But the popular summary of that track record is consistently imprecise in ways that matter. The approved lung indication is narrower than "lung cancer." The most-cited systematic review is more hedged than its citations suggest. The largest survival numbers come from a study design that cannot establish cause. And a second species has human lung cancer data that almost never gets mentioned, because the result was null.

This article is part of our complete review of medicinal mushrooms in cancer treatment. Here we examine the lung cancer evidence specifically: which species have been tested in humans, what each study design can and cannot prove, and where the clinical picture ends and the speculation starts.

What Japan Actually Approved, and for Which Lung Cancer

Japan approved PSK as an adjunct cancer treatment in the 1970s. Not as a dietary supplement. Not as a functional food. As a pharmaceutical adjunct to standard cancer treatment, subject to the same kind of regulatory review Japan applies to pharmaceuticals. The compound is extracted from cultured mycelium of Trametes versicolor, the species sold in Western markets as turkey tail mushroom. The brand name is Krestin.

Maehara and colleagues documented this regulatory history in a 2012 review in Surgery Today.^[3] Clinical use began in 1977. Then, after a regulatory reevaluation in 1989, the approved indications were narrowed to three: use in combination with chemotherapy to prolong survival in resected gastric cancer, use in combination with chemotherapy to prolong survival in curatively resected colorectal cancer, and use to prolong remission in patients with small-cell lung carcinoma.

That third indication is where the popular summary goes wrong. "Approved for lung cancer" is close enough to be repeated, but the approved lung indication is small-cell only, and it is an indication for prolonging remission in patients who have already achieved it — not for treating or shrinking a tumor.

Regulatory Precision

What Japan Approved PSK For — and Which Lung Cancer

“Approved for lung cancer in Japan” is close, but the approved lung indication is small-cell only, and it is an indication for prolonging remission — not for treating the tumour.

1977

Clinical use of PSK (KRESTIN) begins in Japan.

1989

Regulatory reevaluation narrows the approved indications to the three listed above.

Post-1989 approved indications

PSK (KRESTIN), Japan — verbatim scope

●Gastric cancer

Prolong survival

Resected cases, with chemotherapy

●Colorectal cancer

Prolong survival

Curatively resected cases, with chemotherapy

●Small-cell lung carcinoma

Prolong remission

Patients already in remission

○Non-small-cell lung cancer

— not an approved indication —

The large majority of lung cancer diagnoses

The approved lung indication

Small-cell lung carcinoma, prolonging remission. Small-cell accounts for a minority of lung cancer diagnoses.

Where the cited lung data comes from

Tsang 2003 and Hayakawa 1997 — both non-small-cell. Real data, but outside the approved indication.

None of this makes the lung evidence worthless. It means the sentence “approved for lung cancer since 1977” compresses two different things — a 1977 market entry and a narrower 1989 indication — and then attaches them to trials in a lung cancer subtype the approval does not cover.

Source: Maehara et al., Surgery Today, 2012 [ref 3]. Trial attributions: Tsang et al., Respiratory Medicine, 2003 [ref 2]; Hayakawa et al., Cancer Detection and Prevention, 1997 [ref 6].

This context matters when interpreting the broader research landscape. Supplement marketing often cites in vitro studies — results from cancer cells grown in a laboratory dish — as evidence that a product helps fight cancer. The PSK evidence base was built for a different purpose: earning and retaining pharmaceutical regulatory approval, which requires controlled human trials with prespecified endpoints and, in PSK's case, survived a formal reevaluation that narrowed what it could be sold for.

The Six-RCT Systematic Review, and What It Actually Concluded

Fritz and colleagues published a systematic review of PSK and Coriolus versicolor extracts for lung cancer in Integrative Cancer Therapies in 2015.^[1] It remains the only English-language synthesis of this literature, and it is the source behind nearly every "six randomized controlled trials" claim you will encounter.

Here is what the review contains. Searching six databases from inception to August 2014, the authors included 31 reports of 28 studies. Six were randomized controlled trials, five were non-randomized controlled trials, and 17 were preclinical. Nine of the reports were Japanese-language publications, which is part of why this literature is poorly known in English.

On results: 15 of the 17 preclinical studies supported anticancer effects through immunomodulation and direct tumor-inhibiting actions. The non-randomized controlled trials showed improvement in median survival and in one-, two- and five-year survival. The randomized controlled trials showed benefits across a range of endpoints — immune parameters, hematological function, performance status, body weight, tumor-related symptoms including fatigue and anorexia, and survival.

And then the sentence that gets dropped: "Although there were conflicting results for impact on some of the tumor-related symptoms and median survival, overall most randomized controlled trials supported a positive impact for PSK on these endpoints."

Fact Check

Myth vs. evidence

The claim

“A 2015 systematic review found that every one of six randomized controlled trials showed PSK benefits lung cancer patients.”

A compression of Fritz 2015's finding that six RCTs existed and that the overall direction was positive.

What research shows

Overstated

Fritz 2015 identified six RCTs and reported benefits across multiple endpoint categories, but explicitly noted conflicting results for some tumor-related symptoms and for median survival. Its own wording is that 'most' randomized controlled trials supported a positive impact.

The review's stated conclusion is that PSK 'may improve immune function, reduce tumor-associated symptoms, and extend survival in lung cancer patients' and that 'larger, more rigorous randomized controlled trials for PSK in lung cancer patients are warranted.' That is a call for better evidence, not a declaration of a settled question.

Fritz et al., Integrative Cancer Therapies, 2015 [ref 1]

The distinction is not pedantic. "Six out of six" implies a level of consistency that would be genuinely remarkable in oncology. "Most, with conflicting results on some endpoints" describes a real but ordinary positive signal — the kind that justifies more research rather than settling the question. Fritz's own concluding sentence asks for larger and more rigorous trials.

The Individually Citable Datasets, Side by Side

A caveat before the table. Fritz's review counted 11 clinical studies in lung cancer — six randomized and five non-randomized — but nine of the 31 reports were Japanese-language publications, and most of those individual trials are not accessible or individually citable in English. What follows is not the entire literature. It is the set of human lung cancer datasets that English-language writing on this topic actually cites, which is a different and much smaller thing.

Cited Human Datasets

The Cited Lung Cancer Datasets, Sorted by What Their Design Can Prove

These are the datasets English-language writing actually cites — not the whole literature, most of which is Japanese-language. One supports a causal claim. Two cannot, because of how patients were allocated. One is a null result.

Fritz 2015 · Turkey tail (PSK)

Synthesis

Lung, mixed · Systematic review — 28 studies / 31 reports · 6 RCTs, 5 non-randomised, 17 preclinical

What it found

RCTs showed benefits across immune parameters, haematological function, performance status, body weight, tumour-related symptoms and survival.

What limits it

The review reports conflicting results for some tumour-related symptoms and for median survival; its own summary is that MOST — not all — RCTs supported a positive impact.

Tsang 2003 · Turkey tail (PSP)

Randomised

Non-small-cell · Double-blind, placebo-controlled RCT, 28 days · 34 per arm

What it found

Fewer PSP patients withdrew due to disease progression: 5.9% vs 23.5% (P = 0.04, OR 4.00). Leukocyte and neutrophil counts, serum IgG and IgM, and percent body fat improved.

What limits it

PSP was given AFTER patients had completed conventional treatment, not alongside it. Evaluable PSP patients did not improve on NSCLC-related symptoms. 34 per arm is small.

Hayakawa 1997 · Turkey tail (PSK)

Not randomised

Non-small-cell · Non-randomised comparison after radical radiotherapy · 225 patients

What it found

Among the 170 patients (76%) with squamous cell carcinoma, five-year survival was 39% (stage I–II) and 26% (stage III) with PSK, vs 17% and 8% in responders not given PSK.

What limits it

PSK was given only to patients whose tumours had already shrunk after radiotherapy. Allocation followed response, so the survival gap cannot be attributed to PSK alone.

Hayakawa 1993 · Turkey tail (PSK)

Not randomised

Non-small-cell · Non-randomised comparison after radical radiotherapy · 185 patients

What it found

Among patients with epidermoid carcinoma, five-year survival was 39% (stage I–II) and 22% (stage III) with PSK, vs 16% and 5% without.

What limits it

Same design and same selection issue as the 1997 series, from the same centre and overlapping years.

Gao 2005 · Reishi (Ganopoly)

Null result

Advanced lung cancer · Open-label, uncontrolled, 12 weeks, 5.4 g/day · 36 enrolled / 30 completed

What it found

No significant change in mitogenic reactivity, CD3/CD4/CD8/CD56 counts, IL-2, IL-6, IFN-gamma, or NK activity — though results were significantly variable and some patients did respond.

What limits it

This is the counterexample to "every other species is preclinical." Reishi has human lung cancer data; the primary immune endpoints were null.

Read as a set, the citable lung evidence is thinner than the headline suggests: one small randomised trial with a withdrawal-based endpoint, one systematic review whose own conclusion is hedged, two non-randomised series with response-based allocation, and one null trial in a second species.

Sources: Fritz et al., Integrative Cancer Therapies, 2015 [ref 1]; Tsang et al., Respiratory Medicine, 2003 [ref 2]; Hayakawa et al., Cancer Detection and Prevention, 1997 [ref 6]; Hayakawa et al., Anticancer Research, 1993 [ref 10]; Gao et al., Journal of Medicinal Food, 2005 [ref 9].

1. Cell studiescompleted

   Extensive across many species; 15 of 17 preclinical studies in Fritz 2015 supported anticancer effects.

2. Animal studiescompleted

   PSK inhibits tumor growth in mice via TLR2, CD8 T cells and NK cells (Lu 2011) — though the tumor model was breast, not lung.

3. Case seriescompleted

   Maitake MD-fraction plus whole powder, uncontrolled, 62.5% composite response in lung cancer patients (Kodama 2002).

4. Small randomized trialscurrent

   Tsang 2003: 34 patients per arm, 28 days, withdrawal-due-to-progression endpoint. This is the current frontier.

5. Large modern RCTsmissing

   No adequately powered randomized trial of any mushroom compound in lung cancer alongside targeted or immune-based therapy.

6. Meta-analysis of lung trialsmissing

   Fritz 2015 is a systematic review that reports results narratively; it does not pool the lung trials into a meta-analytic estimate.

Mushroom lung cancer research has cleared the preclinical and small-trial rungs but has never reached an adequately powered modern randomized trial. The approval that anchors the topic predates the ladder's upper rungs entirely.

Fritz et al., 2015 [ref 1]; Tsang et al., 2003 [ref 2]; Lu et al., 2011 [ref 7]; Kodama et al., 2002 [ref 4]

The Randomized Trial: What Tsang 2003 Measured

The single randomized, placebo-controlled trial of a turkey tail compound in lung cancer is Tsang and colleagues' study of PSP in advanced non-small cell lung cancer, published in Respiratory Medicine in 2003.^[2] PSP is a closely related compound extracted from the same mushroom species using a different process.

Tsang et al. (2003) · Respiratory Medicine

Population

34 patients per arm with advanced NSCLC who had completed conventional treatment; no significant baseline differences between arms

Intervention

Polysaccharide peptide (PSP), 28 days, administered after conventional treatment was complete

Comparator

Double-blind placebo

Finding

Significantly fewer PSP patients withdrew due to disease progression: 5.9% versus 23.5% (P=0.04, OR 4.00). Blood leukocyte and neutrophil counts, serum IgG and IgM, and percent body fat improved significantly in the PSP arm but not the control arm. No adverse reactions were attributed to the trial medication.

preliminary The evaluable PSP patients did not improve on NSCLC-related symptoms. The primary positive endpoint is trial withdrawal attributed to progression, not a direct measure of tumor progression, and 34 per arm is a small sample. The authors' own conclusion is that PSP 'appears to be associated with slower deterioration.'

Tsang et al., Respiratory Medicine, 2003 [ref 2]

Three details in this trial are routinely lost in summary.

The first is the endpoint. The 5.9%-versus-23.5% figure describes patients withdrawn from the study due to disease progression — not a measured disease progression rate in the whole cohort. Withdrawal is a composite of the disease worsening and of a clinical judgment that the patient should come off study. It correlates with progression but is not the same measurement.

The second is the timing. PSP was given for 28 days to patients who had completed conventional treatment for advanced NSCLC. This was not a test of PSP added to concurrent chemotherapy. It is a test of PSP in the period after treatment ended.

The third is the null within the positive. The trial's own abstract states that the evaluable PSP patients did not improve in NSCLC-related symptoms. The immune and hematological markers moved; the symptoms did not.

None of this makes Tsang 2003 a bad study. It was double-blind, placebo-controlled, showed no attributable adverse reactions, and found a statistically significant difference on a clinically relevant endpoint. It is the best randomized evidence in this topic. It is also a 34-per-arm, 28-day trial from 2003 that has not been independently replicated by a separate research team.

The Biggest Survival Numbers Have the Weakest Design

The most impressive figures in the mushroom lung cancer literature do not come from the randomized trial. They come from two series at Gunma University Hospital in which PSK was given after radical radiotherapy for non-small cell lung cancer.

In the larger of the two, Hayakawa and colleagues analyzed 225 NSCLC patients treated between 1976 and 1989, of whom 170 (76%) had squamous cell carcinoma.^[6] Among those squamous cell patients, five-year survival was 39% for stage I–II and 26% for stage III patients receiving PSK, against 17% and 8% in the comparison group. The differences were statistically significant. An earlier report from the same group, covering 185 patients treated between 1976 and 1985, found 39% and 22% against 16% and 5% in patients with epidermoid carcinoma.^[10]

Those are large gaps. They are also produced by a design that cannot attribute them to PSK.

The 1997 paper states the allocation rule directly: PSK "was given only when the tumor showed satisfactory shrinkage (complete or partial response) after completion of RT," and the outcomes "were compared with those of the responders to RT not receiving PSK."

The authors themselves treated the work as hypothesis-generating rather than conclusive, writing that improvement "is anticipated in the future" and that when trials of these agents are conducted, patients with satisfactory tumor regression after radiotherapy should be the study population. They were describing a trial that should be run, not reporting one that had been.

PSK and PSP: Two Extracts, Two Research Lineages

Both PSK and PSP come from Trametes versicolor, but they are chemically distinct preparations produced from different fungal strains by different national research programs.

Fisher and Yang laid this out in a 2002 review in Anticancer Research.^[5] PSK and PSP are both protein-bound polysaccharides, but PSK is derived from the CM-101 strain by Japanese researchers, while PSP is derived from the COV-1 strain by Chinese researchers. PSK has been researched longer and has undergone more thorough laboratory, animal and clinical testing. Randomized trials across both compounds have produced positive results in adjuvant treatment of gastric, esophageal, colorectal, breast and lung cancers.

This matters for reading the literature: PSK and PSP results are not interchangeable. They are different preparations from different strains with partially separate evidence bases, and in lung cancer specifically, the randomized evidence sits with PSP while the regulatory approval sits with PSK.

The practical implication is more direct. The lung cancer evidence base was built for pharmaceutical-grade standardized extracts, not for turkey tail mushroom powder, capsules, or tea sold in health food stores. The extracts used in these trials went through controlled production from specified strains with defined polysaccharide concentrations. How much active compound a consumer supplement delivers, and whether that concentration resembles what was tested, varies by product and is not guaranteed.

This is a calibration note, not a dismissal of turkey tail supplements as a category. It is a statement about what the clinical evidence specifically supports: Krestin and PSP in standardized pharmaceutical form, tested in controlled conditions.

The Mechanism: A TLR2 Agonist, Demonstrated in Mice

The mechanism behind PSK's clinical effects is immunomodulatory rather than cytotoxic. These compounds do not appear to kill lung cancer cells the way chemotherapy does. They act on the immune system.

Lu and colleagues identified the specific receptor in 2011 in Clinical Cancer Research.^[7] PSK is a selective agonist of Toll-like receptor 2 (TLR2). Activation of dendritic cells and T cells by PSK depends on TLR2; oral PSK inhibited tumor growth in mice; selective depletion experiments showed the antitumor effect required CD8 T cells and NK cells but not CD4 T cells; and PSK did not inhibit tumor growth at all in TLR2-knockout mice. That last result is the strongest part of the finding — remove the receptor and the effect disappears.

The important calibration on this mechanism work: the tumor model was breast cancer in transgenic mice, not lung cancer in humans. It is a well-controlled demonstration of a receptor-dependent mechanism, and it is the most rigorous mechanistic account available for PSK. It is not lung-specific and it is not human.

Maehara's 2012 review describes the mechanism in a broader clinical frame: recovery from immunosuppression induced by humoral factors such as TGF-β or by surgery and chemotherapy; activation of antitumor immune responses including dendritic cell maturation, correction of Th1/Th2 imbalance, and promotion of interleukin-15 production by monocytes; and enhancement of chemotherapy's antitumor effect through induction of apoptosis and inhibition of metastasis.^[3]

The adjunct framing across all of this is not incidental. No trial tested PSK or PSP as a standalone lung cancer treatment. Japan's approval is specifically as an adjunct in combination with chemotherapy. The question the evidence addresses is not whether mushrooms treat lung cancer, but whether adding PSK or PSP to standard care improves outcomes compared to standard care alone.

Beyond Turkey Tail: Maitake and Reishi

Two other species have published human data touching lung cancer. Both are weaker than the turkey tail evidence, and one of them is negative.

Maitake: real numbers, uncontrolled design

Kodama, Komuta and Nanba published a 2002 analysis of maitake in cancer patients across multiple tumor types in Alternative Medicine Review.^[4] The widely-quoted figures come from this paper: cancer regression or significant symptom improvement in 58.3% of liver cancer patients, 68.8% of breast cancer patients, and 62.5% of lung cancer patients, with less than 10–20% improvement in leukemia, stomach and brain cancer patients.

Case Series Anatomy

The Maitake Numbers, With Their Study Design Attached

These percentages are quoted accurately almost everywhere. What gets dropped is that they come from an uncontrolled series using a composite endpoint.

Breast

68.8%

Lungthis article

62.5%

Liver

58.3%

Leukaemia

<10–20%

Stomach

<10–20%

Brain

<10–20%

What the percentages rest on

Design

Non-random case series. No control group.

Intervention

MD-fraction combined with whole maitake powder — not MD-fraction alone.

Endpoint

A composite: "cancer regression OR significant symptom improvement." These are very different outcomes counted as one.

Population

Patients aged 22–57, cancer stages II–IV.

The one comparative signal in the paper

When maitake was taken in addition to chemotherapy, immune-competent cell activities were enhanced 1.2–1.4 times compared with chemotherapy alone. This is the only figure in the study with a stated comparison, and it is an immune marker — not a survival or tumour outcome.

Without a control arm, a 62.5% composite response rate in lung cancer cannot be separated from the conventional treatment these patients were also receiving, from the natural course of the disease, or from which cases got written up. The number is real. What it measures is not what the phrasing implies.

Source: Kodama, Komuta & Nanba, Alternative Medicine Review, 2002 [ref 4].

Two calibration points are essential here, and a third correction.

The correction first: this paper is routinely attributed to "Nanba et al." The first author is Kodama; Nanba is the last author.

The first calibration point is design. This is a non-random case series with no comparison group. Patients received maitake alongside conventional care, and outcomes were tracked. This design cannot distinguish the effect of the mushroom preparation from the effect of the concurrent treatment, from natural disease fluctuation, or from which cases get written up.

The second is what was actually tested. The intervention was not D-fraction alone. It was, in the paper's own description, a combination of MD-fraction and whole maitake powder. Supplement marketing that cites these percentages for a purified D-fraction product is citing a different intervention than the one studied.

The one figure in the paper with a stated comparison is the immune marker: when maitake was taken in addition to chemotherapy, immune-competent cell activities were enhanced 1.2–1.4 times compared with chemotherapy alone. That is a comparative result, and it is about immune markers, not tumors or survival.

Reishi: a human lung cancer trial that found nothing

The claim that all non-turkey-tail evidence is preclinical is not accurate, and the counterexample is worth knowing precisely because it is negative.

Gao and colleagues ran an open-label study of a water-soluble Ganoderma lucidum polysaccharide preparation in patients with advanced lung cancer, published in the Journal of Medicinal Food in 2005.^[9] Thirty-six patients were enrolled at 5.4 g/day for 12 weeks; 30 completed. Treatment did not significantly alter mean mitogenic reactivity to phytohemagglutinin, mean CD3, CD4, CD8 or CD56 counts, mean plasma IL-2, IL-6 or IFN-gamma, or NK activity.

The authors noted that results were significantly variable and that some individual patients showed markedly modulated immune function, suggesting subgroups might be responsive. That is a reasonable read of a null primary result with heterogeneity. It is not evidence that reishi helps lung cancer patients, and the study was uncontrolled, so even the subgroup observation carries little weight.

For a deeper look at how mushroom polysaccharides interact with cancer cells through these immune pathways, see our article on how mushroom polysaccharides kill cancer cells.

What Independent Review Says About the Same Compound

The most rigorous independent assessment of turkey tail extract in cancer is not in lung cancer — it is Cochrane's 2022 review in colorectal cancer.^[8] It is worth reading across, because it grades the same compound and the same national trial program using formal evidence-certainty methods.

Pilkington and colleagues included seven randomized trials with 1,569 participants, six conducted in Japan. They found low-certainty evidence of a small effect on five-year survival (RR 1.08, 95% CI 1.01–1.15; 1,094 participants; three studies; number needed to benefit 16). Every adverse-event outcome — withdrawal due to adverse events, neutropenia, oral cavity disorders, nausea, diarrhea, fatigue — was graded very low certainty. The review also flagged that the chemotherapy regimens used in these trials "do not reflect current preferred practice."

That is what happens when this trial program is graded formally: a real but small survival signal at low certainty, uncertainty about everything else, and an applicability warning about the age of the chemotherapy backbones. There is no equivalent Cochrane review in lung cancer, but there is no reason to expect a more favorable grading, given that the lung evidence base is smaller and includes fewer randomized trials.

What the Evidence Doesn't Answer Yet

Research Gaps

What would it take?

What would it take to know whether turkey tail compounds help people with lung cancer today?

◑

An adequately powered randomized trial in non-small cell lung cancer

Tsang 2003 exists but enrolled 34 patients per arm over 28 days. Nothing larger has been published.

○

Independent replication by a separate research team

The Tsang PSP result has not been reproduced by an unaffiliated group.

○

Trials alongside modern lung cancer treatment

The PSK lung trials predate targeted therapies and checkpoint inhibitors. Whether an immunomodulator adds anything to treatments that already activate the immune system is untested.

○

Direct tumor-progression endpoints rather than withdrawal proxies

The headline randomized finding rests on trial withdrawal attributed to progression, not scheduled imaging.

○

Evidence for the products people can actually buy

All clinical data uses standardized pharmaceutical extracts from specified strains, not consumer turkey tail supplements.

○

A randomized trial of any non-turkey-tail species in lung cancer

Maitake data is an uncontrolled case series; the reishi trial was uncontrolled and null.

One small randomized trial completed in 2003; nothing larger since.·A single adequately powered adjuvant lung cancer trial would typically take 5–8 years from funding to publication.

Fritz et al., 2015 [ref 1]; Tsang et al., 2003 [ref 2]; Pilkington et al., 2022 [ref 8]

The PSK lung cancer evidence base is among the stronger bodies of work in the mushroom-cancer literature. Six randomized trials, a regulatory approval that survived a formal reevaluation, and decades of clinical use represent institutional confidence that most botanical compounds never earn. That is worth stating plainly.

But the gaps are structural, not incidental. Most of the PSK lung trials were conducted between the 1970s and 1990s, against cytotoxic chemotherapy and radiation. Lung cancer care has since been reorganized around targeted therapies for specific tumor mutations and immune checkpoint inhibitors. Whether an immunomodulatory adjunct stacks with, does nothing to, or interferes with treatments that already work by activating the immune system has not been tested in a published controlled trial.

Safety

Moderate

Mushroom compounds and lung cancer treatment

Concern

PSK, PSP and other mushroom polysaccharides act on immune function. Modern lung cancer care frequently includes immune checkpoint inhibitors, which also act on immune function. No published controlled trial has tested whether these interact.

What the research says

Every positive finding in this literature comes from mushroom compounds used as an adjunct to standard treatment, never as a replacement. Nothing in this evidence base supports substituting a mushroom product for lung cancer treatment, and no mushroom product is approved for lung cancer outside Japan's narrow small-cell remission indication.

Particularly relevant for: Anyone undergoing or considering treatment for lung cancer

What to do

Discuss any mushroom supplement with your oncology team before starting it, particularly if you are receiving immunotherapy. This article is a review of published research, not medical advice, and it is not a treatment recommendation.

Maehara et al., 2012 [ref 3]; Fritz et al., 2015 [ref 1]; Pilkington et al., 2022 [ref 8]

For species other than turkey tail, there is no lung cancer randomized trial at all. Maitake has an uncontrolled case series. Reishi has an uncontrolled trial that found nothing on its primary measures. Other species that appear in the broader cancer literature have not been tested in lung cancer with controlled designs. The gap between preclinical evidence and human trial evidence is large, and most mushroom species have crossed only the first threshold.

For context on how mushroom research compares across cancer types, see our reviews of mushrooms and prostate cancer, mushrooms and liver cancer, mushrooms and pancreatic cancer, and mushrooms and ovarian cancer.

The Bottom Line

Turkey tail compounds PSK and PSP have more human lung cancer evidence than any other mushroom intervention, but the popular summary overstates it in three specific ways. Japan's 1989-reevaluated lung indication for PSK is small-cell only and covers prolonging remission, while nearly all cited lung data is non-small-cell. The 2015 systematic review that anchors the topic concluded that most of its six randomized trials showed benefit, with conflicting results on some endpoints. And the largest survival figures come from non-randomized series in which PSK was given only to patients who had already responded to radiotherapy. The strongest randomized result — Tsang 2003, 5.9% versus 23.5% withdrawal due to progression — comes from 34 patients per arm over 28 days, given after conventional treatment ended. Maitake's lung numbers come from an uncontrolled case series of MD-fraction plus whole powder, and reishi's one human lung cancer study found no significant change in any primary immune measure. The mechanism is immunomodulatory: PSK is a selective TLR2 agonist whose antitumor effect depends on CD8 T cells and NK cells, demonstrated in mice.

Frequently Asked Questions

Can turkey tail mushrooms help with lung cancer?

The clinical evidence is for PSK and PSP, standardized pharmaceutical extracts from turkey tail mushroom, not for turkey tail supplements sold in stores. PSK entered clinical use in Japan in 1977 and, after a 1989 regulatory reevaluation, is approved there to prolong remission in small-cell lung carcinoma (Maehara et al., 2012). A 2015 systematic review identified six randomized controlled trials in lung cancer and concluded that most supported benefit, with conflicting results on some tumor-related symptoms and median survival (Fritz et al., 2015). PSP reduced withdrawal due to disease progression from 23.5% to 5.9% in a 34-per-arm randomized trial (Tsang et al., 2003). These results come from pharmaceutical-grade extracts of specified fungal strains; consumer supplements vary substantially in active compound content. This is a research summary, not medical advice — discuss any supplement with your oncology team.

Is PSK approved for non-small cell lung cancer?

No. After Japan's 1989 regulatory reevaluation, PSK's approved indications are resected gastric cancer, curatively resected colorectal cancer, and prolonging remission in small-cell lung carcinoma (Maehara et al., 2012). Non-small cell lung cancer is not an approved indication, which is notable because most of the frequently cited lung data is in NSCLC: Tsang's 2003 randomized PSP trial and Hayakawa's radiotherapy series are both NSCLC. Those are real studies, but they sit outside what the approval covers.

Which mushrooms have been studied in humans for lung cancer?

Three species have published human lung cancer data. Turkey tail (Trametes versicolor) has the most: six randomized trials of PSK identified in a 2015 systematic review, plus a separate randomized PSP trial and two non-randomized radiotherapy series (Fritz et al., 2015; Tsang et al., 2003; Hayakawa et al., 1997). Maitake (Grifola frondosa) has an uncontrolled case series reporting a 62.5% composite response rate in lung cancer patients using MD-fraction combined with whole maitake powder (Kodama, Komuta & Nanba, 2002). Reishi (Ganoderma lucidum) has an open-label trial in 36 advanced lung cancer patients that found no significant change in any primary immune measure (Gao et al., 2005). No randomized lung cancer trial exists for any species other than turkey tail.

Can medicinal mushrooms be used alongside chemotherapy for lung cancer?

PSK was developed and approved specifically as an adjunct used in combination with chemotherapy, and no trial has tested it as a replacement for standard treatment. One important detail is often reported incorrectly: the Tsang 2003 PSP trial gave PSP for 28 days to patients who had completed conventional treatment, not concurrently with it (Tsang et al., 2003). Whether these compounds interact with modern lung cancer treatment — particularly immune checkpoint inhibitors, which also act on immune function — has not been tested in any published controlled trial. Anyone in active treatment should discuss supplements with their oncology team before starting them.

Did a trial really cut lung cancer progression by 75%?

That framing overstates what was measured. In Tsang's 2003 randomized trial, 5.9% of PSP patients versus 23.5% of placebo patients were withdrawn from the study due to disease progression (P=0.04, OR 4.00). That is withdrawal attributed to progression, not a measured progression rate across the whole cohort, and the trial enrolled 34 patients per arm over 28 days. The same trial found that evaluable PSP patients did not improve on NSCLC-related symptoms. The authors' own conclusion was the more measured statement that PSP "appears to be associated with slower deterioration" in advanced NSCLC (Tsang et al., 2003).

Sources & References

1. 1RTHM-00684·Fritz, Heidi et al. (2015). “Polysaccharide K and Coriolus versicolor extracts for lung cancer: a systematic review..” Integrative cancer therapies.Study breakdown →PubMed →↩
2. 2RTHM-00124·Tsang, K W et al. (2003). “Coriolus versicolor polysaccharide peptide slows progression of advanced non-small cell lung cancer..” Respiratory medicine.Study breakdown →PubMed →↩
3. 3RTHM-00475·Maehara, Yoshihiko et al. (2012). “Biological mechanism and clinical effect of protein-bound polysaccharide K (KRESTIN(®)): review of development and future perspectives..” Surgery today.Study breakdown →PubMed →↩
4. 4RTHM-00095·Kodama, Noriko et al. (2002). “Can maitake MD-fraction aid cancer patients?.” Alternative medicine review : a journal of clinical therapeutic.Study breakdown →PubMed →↩
5. 5RTHM-00089·Fisher, Monte et al. (2002). “Anticancer effects and mechanisms of polysaccharide-K (PSK): implications of cancer immunotherapy..” Anticancer research.Study breakdown →PubMed →↩
6. 6RTHM-00049·Hayakawa, K et al. (1997). “Effect of Krestin as adjuvant treatment following radical radiotherapy in non-small cell lung cancer patients..” Cancer detection and prevention.Study breakdown →PubMed →↩
7. 7RTHM-00419·Lu, Hailing et al. (2011). “Polysaccharide krestin is a novel TLR2 agonist that mediates inhibition of tumor growth via stimulation of CD8 T cells and NK cells..” Clinical cancer research : an official journal of the American Association for Cancer Research.Study breakdown →PubMed →↩
8. 8RTHM-01600·Pilkington, Karen et al. (2022). “Coriolus (Trametes) versicolor mushroom to reduce adverse effects from chemotherapy or radiotherapy in people with colorectal cancer..” The Cochrane database of systematic reviews.Study breakdown →PubMed →↩
9. 9RTHM-00152·Gao, Yihuai et al. (2005). “Effects of water-soluble Ganoderma lucidum polysaccharides on the immune functions of patients with advanced lung cancer..” Journal of medicinal food.Study breakdown →PubMed →↩
10. 10RTHM-00033·Hayakawa, K et al. (1993). “Effect of krestin (PSK) as adjuvant treatment on the prognosis after radical radiotherapy in patients with non-small cell lung cancer..” Anticancer research.Study breakdown →PubMed →↩