Lion's Mane for Gastric Cancer: From History to Research

Lion's Mane and Cancer

Zero human trials of lion's mane in gastric cancer. Every quantified finding in this article comes from a cell line or a mouse.

Lion's mane has a genuine claim on stomach research: a centuries-old traditional indication for gastric complaints, and a modern mechanism that is unusually specific — erinacine S switches on the cell's own death-receptor genes by trimethylating histone H3 at their promoters. What it does not have is a single patient outcome.

Tung et al., Food & Function, 2021; Gravina et al., World Journal of Gastroenterology, 2023

H3K4me3

the specific epigenetic mark erinacine S places on the FasL and TRAIL promoters in AGS gastric cancer cells, raising expression of two apoptosis-triggering ligands (Tung 2021)

3 of 5 stages

of the Correa gastric carcinogenesis cascade have any lion's mane evidence at all; intestinal metaplasia and dysplasia — the two stages where the progression becomes hardest to reverse — have none

Least sensitive

of the four gastrointestinal cell lines Li 2014 screened, the gastric line was the one that required the highest extract concentration to halve cell viability (Li 2014)

Tung et al., Food & Function, 2021; Gravina et al., World Journal of Gastroenterology, 2023

View as image ↗

The dominant pathway to gastric cancer begins with a bacterial infection. Helicobacter pylori colonises the stomach lining, triggers chronic inflammation, and sets off an ordered progression: chronic gastritis, then atrophy, then intestinal metaplasia, then dysplasia, then carcinoma. This sequence — the Correa cascade — is the reason gastric cancer is considered, in principle, a preventable disease.

Lion's mane has preclinical evidence at three of those five stages. It inhibits H. pylori at the start, it has a single cell-model study at the atrophy stage, and it kills gastric cancer cells at the end. What it has never been tested against — in any model, at any dose — is intestinal metaplasia or dysplasia, the two stages in between where the tissue changes become hardest to reverse. For the broader cancer overview, see lion's mane and cancer: what the research shows.

The Traditional Use Context: Centuries of Gastrointestinal Application

Gravina and colleagues (2023) published a review in the World Journal of Gastroenterology documenting the long history of H. erinaceus as a medicinal fungus for digestive disease.^[6] In traditional Chinese medicine the mushroom was used for gastritis and for stomach complaints generally; the review's authors, gastroenterologists surveying the modern evidence, concluded that several of its components appear to have antineoplastic capabilities against gastric and colorectal cancer.

This traditional record is not evidence of efficacy against gastric cancer. What it explains is the shape of the research literature. Modern investigators looking for a place to start with this mushroom started where the tradition pointed — the stomach and the gut — which is why the gastrointestinal cancer work is more developed than, say, the lung or breast work. Convergence between a traditional indication and a modern pharmacology programme generates research attention. It does not, by itself, generate results.

The Prevention Chain: H. Pylori, Atrophy, and What Comes After

Gastric cancer is not primarily a disease of isolated genetic bad luck. H. pylori infection is the dominant risk factor for non-cardia gastric cancer; the International Agency for Research on Cancer's updated estimate, based on immunoblot rather than ELISA serology, puts the population attributable fraction at roughly 89% worldwide.

The progression runs in stages. The bacterium colonises the epithelium and provokes sustained inflammation. That inflammation destroys gastric glands, producing chronic atrophic gastritis — the recognised precancerous stage. In some patients atrophy progresses to intestinal metaplasia, where stomach lining cells are replaced by intestine-like cells; then to dysplasia, where cells become frankly abnormal but stay confined; then to invasive carcinoma.

The distinction that matters for evaluating any prevention claim is that these stages are not interchangeable. Acting on the bacterium at stage one is upstream prevention. Killing a tumour cell at stage five is treatment. Neither one demonstrates anything about the stages in between, where the tissue changes become progressively harder to reverse.

Evidence Coverage · The Correa Cascade

The Research Clusters at Both Ends and Thins Toward the Middle

Gastric cancer develops through an ordered sequence of tissue states. Laid against that sequence, the lion’s mane research is heaviest at stage 1 and stage 5 — acting on the bacterium at the start, on tumour cells at the end — thins to a single cell model at stage 2, and disappears entirely at stages 3 and 4. Those two empty stages are where a prevention claim would have to be earned, because they are where the progression becomes hardest to reverse.

1. Stage 1

   Chronic gastritis

   Animal modelRefs 7, 8

   H. pylori colonises the gastric epithelium and sets up sustained inflammation.

   Ethyl acetate fractions of the fruiting body inhibited 9 clinical H. pylori isolates at 62.5–250 µg/mL. A separate ethanolic extract inhibited all six strains tested at about 2 mg/mL, blocked bacterial adhesion to human gastric AGS cells at concentrations that harmed neither the bacterium nor the cells, and suppressed the interleukin-8 and oxidative-DNA-damage response.

2. Stage 2

   Atrophy

   Human study existsRefs 3, 4

   Sustained inflammation destroys gastric glands. This is chronic atrophic gastritis, the recognised precancerous stage.

   EP-1, a roughly 3,100-dalton heteroglycan from cultured mycelium, inhibited growth of MNNG-transformed GES-1 cells — a cell model of chronic atrophic gastritis — and induced cell-cycle arrest. A 1985 double-blind human study in chronic atrophic gastritis exists but is indexed as a two-page preliminary report with no retrievable abstract, so its results cannot be checked.

3. Stage 3

   Intestinal metaplasia

   No study—

   Stomach lining cells are replaced by intestine-like cells. Risk rises sharply and regression becomes unlikely.

   No published study has tested any lion’s mane preparation against intestinal metaplasia, in any model.

4. Stage 4

   Dysplasia

   No study—

   Cells become frankly abnormal but stay confined. This is the last stage before invasive cancer.

   No published study has tested any lion’s mane preparation against gastric dysplasia, in any model.

5. Stage 5

   Gastric carcinoma

   Animal modelRefs 1, 2, 5

   Invasive adenocarcinoma.

   Erinacine A reduced viability and invasiveness of TSGH 9201 cells, with no animal arm. Erinacine S triggered apoptosis in AGS cells and inhibited tumour growth in xenograft mice. Culture-broth extracts HTJ5 and HTJ5A were cytotoxic to NCI-87 gastric cells and suppressed NCI-87 xenografts in SCID mice.

“Human study exists” at stage 2 marks that a trial was run, not that it demonstrated benefit — the 1985 report’s results are not retrievable from the public record. No stage of this cascade has a modern human trial of lion’s mane behind it.

Source: Correa’s multistep model for the cascade stages; Xu et al. (1985); Shang et al. (2013); Li et al. (2014); Wang et al. (2015); Kuo et al. (2017); Wang et al. (2019); Tung et al. (2021)

That map is the honest summary of this field, and it is worth sitting with before reading the individual studies. The strongest sections below are all drawn from stages one and five.

Wang 2015: A Cell Model of Atrophic Gastritis

Wang and colleagues (2015) is the only study addressing lion's mane and chronic atrophic gastritis specifically.^[3] It is frequently described as an animal study. It is not.

The researchers screened cultured H. erinaceus mycelium and isolated a polysaccharide they named EP-1, purified through ethanol precipitation, hollow-fibre ultrafiltration and ion-exchange chromatography. EP-1 is a heteroglycan of roughly 3,100 daltons composed of glucose, mannose and galactose, with a backbone of α-D-Glc(1→3) and β-D-Glc(1→3).

The anti-gastritis activity was evaluated in a cell model. The team used MC cells — human gastric mucosa epithelial cells (GES-1) transformed with MNNG, a chemical carcinogen — as a stand-in for chronic atrophic gastritis. EP-1 significantly inhibited the growth of those cells and induced cell-cycle arrest.

The atrophic gastritis study

Wang, Mingxing et al. (2015) · International Journal of Biological Macromolecules

Population

MC cells — human gastric mucosa epithelial (GES-1) cells transformed by MNNG, used as a chronic atrophic gastritis cell model

Intervention

EP-1, a ~3,100 Da heteroglycan of glucose, mannose and galactose isolated from cultured H. erinaceus mycelium

Comparator

Untreated cells

Finding

EP-1 significantly inhibited MC cell growth and interfered with the cells by inducing cell-cycle arrest. The authors concluded EP-1 shows potential for development into functional foods or drugs.

narrow-scope This is a cell-culture experiment. There is no animal arm, no measurement of mucosal thickness or atrophy severity, and no assessment of gastric tissue in a living organism. An anti-proliferative effect on a transformed cell line is not the same as demonstrated mucosal protection.

Wang M et al., Int J Biol Macromol. 2015;81:656-61. PMID 26314904

The distinction is not pedantic. A great deal of secondary writing about lion's mane converts this result into "protects the stomach lining in animals," complete with mucosal thickness and inflammation endpoints that the study never measured. What EP-1 actually did was slow the growth of a transformed cell line in a dish. That is a legitimate finding at the precancerous stage, and it is the only one anyone has. It is also a long way from the claim it is usually made to support.

The one human data point at this stage is older and weaker still. Xu and colleagues published a double-blind study of H. erinaceus in chronic atrophic gastritis in the Chinese Medical Journal in 1985.^[4] It is a two-page preliminary report. No abstract is retrievable from the indexed record, and sample size, effect size and outcome measures cannot be recovered from it. A trial existing is not the same as a trial reporting a usable result, and in forty years nobody has repeated it. For the full gastritis evidence base, see lion's mane and gastritis.

Erinacine A Against Gastric Cancer: The Kuo 2017 Proteomics Study

Kuo and colleagues (2017) investigated erinacine A — a diterpenoid isolated from the ethanol extract of H. erinaceus mycelium — against gastric cancer cells using a proteomics approach.^[2]

Erinacine A treatment of TSGH 9201 gastric cancer cells increased cytotoxicity and the generation of reactive oxygen species, and decreased invasiveness as measured directly by Boyden chamber migration assay. Caspases were activated and TRAIL — a death-receptor ligand — was expressed at higher levels. Apoptosis was accompanied by sustained phosphorylation of the FAK/AKT/p70S6K and PAK1 pathways.

The proteomic screen surfaced two differentially expressed proteins the authors flagged as candidates: 14-3-3 sigma, and MTUS2, a microtubule-associated tumour suppressor candidate. Their proposal is that erinacine A drives an apoptotic cascade in these cells by activating FAK/AKT/p70S6K/PAK1 and upregulating those two proteins.

Two limits are worth stating plainly. The authors present this as a mechanism they speculate upon from the observed protein changes, not one they proved by blocking it. And the study has no animal arm at all — everything reported happened in cell culture.

Erinacine S: The Epigenetic Mechanism

The most mechanistically specific finding in lion's mane gastric cancer research comes from Tung and colleagues (2021), published in Food & Function.^[1]

Erinacine S is a separate diterpenoid from the more-studied erinacine A, also isolated from the mycelium. Tested against AGS gastric cancer cells, it induced apoptosis with increased reactive oxygen species production — and, importantly, that ROS increase occurred in gastric cancer cells but not in normal cells. Selectivity of that kind is the property that separates a candidate compound from a general cytotoxin.

In AGS cells, erinacine S activated the extrinsic apoptosis pathway — TRAIL, Fas-L, and caspases-8, -9 and -3 — while suppressing the anti-apoptotic molecules Bcl-2 and Bcl-XL in a time-dependent manner. It also caused G1 cell-cycle arrest through inactivation of CDKs and cyclins. The route to the histone mark ran through ROS-derived AKT/FAK/PAK1 signalling, which drove the H3K4 trimethylation on the FasL and TRAIL promoters.

The study did not stop at cells. Erinacine S inhibited tumour growth in an in vivo xenograft mouse model, and immunohistochemistry on the tumour tissue showed the mechanism holding up in the animal: FasL and TRAIL protein raised, and PCNA and cyclin D1 — markers of proliferation — lowered.

Two Compounds · One Pathway, Two Different Reaches

“The Erinacines” Are Two Separate Experiments

Erinacine A and erinacine S are usually described together, as though one body of evidence covered both. In gastric cancer they are two studies, four years apart, on different cell lines. They converge on the same signalling module — and then separate on how far the work was carried.

Shared spine — reported in both studies

• →Reactive oxygen species generated in the cancer cell
• →The AKT / FAK / PAK1 signalling module engaged
• →TRAIL, a death-receptor ligand, expressed at higher levels
• →Caspases activated, ending in apoptosis

Erinacine A

Ref 2

Kuo 2017 · proteomics screen

Tested in: TSGH 9201 gastric cancer cells

Cells only — no animal arm

Only in this study

• ·Invasiveness measured directly, by Boyden chamber migration assay, and reduced.
• ·Discovery proteomics surfaced two differentially expressed proteins: 14-3-3 sigma and the tumour-suppressor candidate MTUS2.
• ·Mechanism proposed from the observed protein changes rather than tested against a pre-chosen target.

Erinacine S

Ref 1

Tung 2021 · mechanism study

Tested in: AGS gastric cancer cells + xenograft mice

Cells and live animals

Only in this study

• ·Apoptosis was selective: reactive oxygen species rose in gastric cancer cells but not in normal cells.
• ·The epigenetic step was identified — H3K4 trimethylation on the FasL and TRAIL promoters — not merely inferred.
• ·Tumour growth was inhibited in xenograft mice, with FasL and TRAIL raised and PCNA and cyclin D1 lowered in the tumour tissue.

Neither compound has been given to a person with gastric cancer. The difference above is a difference between two preclinical studies, not between two levels of clinical proof.

Source: Kuo et al., Cellular Physiology and Biochemistry (2017); Tung et al., Food & Function (2021)

That reach difference is the reason it is misleading to talk about "the erinacines" as a single evidence base in gastric cancer. Erinacine S was carried into an animal and the mechanism was confirmed there. Erinacine A was not.

Li 2014: Cell Lines, Xenografts, and a Ranking Worth Reading

Li and colleagues (2014), in the Journal of Ethnopharmacology, tested two extracts from H. erinaceus culture broth — designated HTJ5 and HTJ5A — against liver, colon and gastric cancer, in vitro and in vivo.^[5] Twenty-two compounds were isolated and characterised from the extract fractions.

Both extracts showed concentration-dependent cytotoxicity against all four cell lines tested, including the NCI-87 gastric line. In the in vivo work, SCID mice bearing subcutaneous xenografts of all four tumour types were given HTJ5 or HTJ5A orally at 500 and 1,000 mg/kg/day, compared against 5-fluorouracil given intraperitoneally at its maximum tolerated dose. Both extracts showed significant antitumour efficacy against all four xenograft models without toxicity to the host, and the authors report them as more effective than 5-FU with less toxicity.

That last result is the one most often quoted, and it is usually quoted imprecisely. The 5-FU comparison was made in the xenograft models, not in the cell line assays. And the study contains an internal ranking that the citation almost never carries.

Inside One Study · Li 2014

The Gastric Line Was the Least Sensitive of the Four Tested

Li 2014 screened two culture-broth extracts against four gastrointestinal cancer cell lines. It is routinely cited as gastric cancer evidence, and it is. But within the study the gastric line needed the highest concentration of all four to halve cell viability — about six times more extract than the most sensitive liver line.

IC50 in mg/mL — shorter bar means more sensitive

Huh-7Liver

HTJ5

0.80

HTJ5A

1.50

HT-29Colon

HTJ5

1.25

HTJ5A

1.25

HepG2Liver

HTJ5

2.50

HTJ5A

2.00

NCI-87Gastric

Least sensitive

HTJ5

5.00

HTJ5A

4.50

This does not cancel the finding — both extracts still suppressed NCI-87 xenograft tumours in mice, and did so with less toxicity than 5-fluorouracil. It qualifies it. The gastric result is the weakest of the four the study reports, and a claim that lion’s mane is particularly active against stomach cancer does not follow from this study’s own numbers.

Source: Li et al., Journal of Ethnopharmacology (2014). IC50 values by MTT assay, mean ± SD.

Both things are true at once: lion's mane extracts outperformed a standard chemotherapy agent in these mouse models, and the gastric line was the least responsive of the four the study screened. A reader told only the first half comes away with a distorted picture.

What Human Data Exists — and What It Is About

There is human evidence connecting mushrooms to gastric cancer, but it is not about lion's mane.

Ba and colleagues (2023) pooled 3,900 gastric cancer cases and 7,792 controls from 11 studies within the Stomach Cancer Pooling (StoP) Project.^[9] Higher mushroom consumption was associated with lower gastric cancer risk: relative risk 0.82 for the highest versus lowest consumption categories, with a 95% confidence interval of 0.71 to 0.95. Combining all 15 studies gave a relative risk of 0.77 (95% CI 0.63–0.95). The association was stronger in Western Pacific countries, at 0.59 (95% CI 0.40–0.87) across six studies.

Fact check

Does this mean lion's mane lowers stomach cancer risk?

The claim

“Studies show mushrooms reduce gastric cancer risk, so lion's mane reduces gastric cancer risk.”

Conflating pooled epidemiology on culinary mushroom intake with the preclinical literature on a specific medicinal species.

What research shows

Misleading

The StoP pooled analysis measured mushroom consumption via food frequency questionnaires. It captured the mushrooms people actually eat — button, shiitake, oyster and similar culinary species — and did not isolate Hericium erinaceus, which is rarely a dietary staple in the cohorts studied.

The finding is observational and cannot establish causation; people who eat more mushrooms differ from those who eat fewer in many ways. It is a real signal about mushroom-rich diets, and it is genuinely encouraging for the field. It is simply not a finding about lion's mane, and no amount of restating it makes it one.

Ba DM et al., Eur J Cancer Prev. 2023;32(3):222-228. PMID 36912187

For the upstream antimicrobial evidence, which sits at stage one of the cascade, see Hericium erinaceus and H. pylori. Shang and colleagues (2013) found ethyl acetate fractions of the fruiting body inhibited nine clinical H. pylori isolates at 62.5–250 µg/mL,^[7] and Wang and colleagues (2019) found an ethanolic extract inhibited six strains at about 2 mg/mL while blocking bacterial adhesion to gastric epithelial cells and suppressing their interleukin-8 and oxidative DNA damage response.^[8]

Lion's mane for gastric cancer

1. Cell studiescompleted

   Gastric cancer lines TSGH 9201, AGS and NCI-87; a chronic atrophic gastritis cell model; H. pylori isolates (Kuo 2017; Tung 2021; Li 2014; Wang 2015; Shang 2013)

2. Animal studiescurrent

   Xenograft mice bearing gastric tumours, for erinacine S and for the culture-broth extracts (Tung 2021; Li 2014)

3. Case reportsmissing

   No published case reports of lion's mane use in gastric cancer

4. Small human trialmissing

   None in gastric cancer. The only human study in any gastric condition is the 1985 atrophic gastritis report, which has no retrievable results (Xu 1985)

5. Large RCTmissing

   No randomized controlled trial has tested lion's mane in gastric cancer patients

6. Meta-analysismissing

   No trials exist to pool. The only human meta-analytic data concerns mushroom consumption generally, not lion's mane (Ba 2023)

The evidence tops out at xenograft mice. That is a real rung — a compound that shrinks an established tumour in a living animal has cleared a bar most natural products never reach — but the three rungs above it are all empty, and xenograft models are among the least predictive of eventual human benefit in oncology.

Wang 2015; Shang 2013; Li 2014; Kuo 2017; Wang 2019; Tung 2021; Xu 1985; Ba 2023

Important

Critical

Gastric cancer is not a condition to self-treat

Concern

Gastric cancer outcomes depend heavily on how early treatment begins. Substituting or delaying oncological care in favour of a supplement — or adding a supplement without telling the treating team — can cost survival time. Nothing in this literature supports lion's mane as a treatment, and none of it was generated in human patients.

What the research says

Treat this evidence as what it is: preclinical mechanism research that may or may not one day inform a therapy. Persistent stomach symptoms, unexplained weight loss, difficulty swallowing or blood in stool need medical assessment, not a supplement.

Particularly relevant for: Anyone with diagnosed gastric cancer, a precancerous gastric lesion, H. pylori infection, or unexplained upper gastrointestinal symptoms

What to do

Discuss any mushroom supplement with your oncology or gastroenterology team, particularly alongside chemotherapy or H. pylori eradication therapy.

This article is educational and is not medical advice. Evidence base: Xu 1985; Li 2014; Wang 2015; Kuo 2017; Tung 2021; Gravina 2023

The Bottom Line

Lion's mane has preclinical evidence at three of the five stages of the H. pylori-to-cancer progression, and none at intestinal metaplasia or dysplasia. At the start of the cascade, extracts inhibit H. pylori in culture and block its adhesion to gastric cells (Shang 2013, Wang 2019). At the end, erinacine A reduced viability and invasiveness of TSGH 9201 cells with no animal arm (Kuo 2017); erinacine S induced selective apoptosis in AGS cells via H3K4 trimethylation on the FasL and TRAIL promoters and inhibited xenograft tumour growth (Tung 2021); and culture-broth extracts HTJ5 and HTJ5A suppressed NCI-87 tumours in SCID mice more effectively than 5-fluorouracil, though the gastric line was the least sensitive of four screened (Li 2014). At the precancerous stage, the mycelial polysaccharide EP-1 inhibited growth of MNNG-transformed gastric epithelial cells in a cell model — not, as often reported, in rats (Wang 2015). Intestinal metaplasia and dysplasia have never been tested. The only human study in any gastric condition is a 1985 preliminary report with no retrievable results (Xu 1985), and the human evidence linking mushrooms to lower gastric cancer risk concerns mushroom consumption generally rather than lion's mane (Ba 2023). No trial has tested lion's mane against gastric cancer in people.

Frequently Asked Questions

Is lion's mane good for stomach cancer?

Nobody knows, because it has never been tested in people with stomach cancer. In cell and animal studies, lion's mane compounds inhibit gastric cancer cells through identified mechanisms: erinacine S induces apoptosis via H3K4 trimethylation on the FasL and TRAIL promoters and shrank tumours in xenograft mice (Tung 2021); erinacine A reduced viability and invasiveness of TSGH 9201 cells in culture (Kuo 2017); and culture-broth extracts suppressed NCI-87 gastric tumours in mice (Li 2014). All of it is preclinical. Gastric cancer requires oncological treatment, and this research does not support using lion's mane in place of it.

Did lion's mane really beat chemotherapy in a study?

In one animal study, in a specific sense. Li 2014 gave SCID mice bearing human tumour xenografts either lion's mane culture-broth extract orally or 5-fluorouracil intraperitoneally at its maximum tolerated dose, and reported the extracts as more effective with less toxicity across all four tumour models. That is a real result, but it is a mouse xenograft comparison, not a clinical trial, and xenograft models routinely fail to predict human outcomes. Within that same study, the gastric cell line was the least sensitive of the four tested.

Does lion's mane help with atrophic gastritis or gastric ulcers?

The evidence is thinner than it is usually presented. Wang 2015 tested a mycelial polysaccharide called EP-1 against MNNG-transformed gastric epithelial cells used as a cell model of chronic atrophic gastritis, where it inhibited growth and caused cell-cycle arrest — this was a cell-culture experiment, not an animal study. A double-blind human trial in chronic atrophic gastritis was published in 1985, but it is a two-page preliminary report whose results cannot be retrieved, and it has never been repeated (Xu 1985). Lion's mane's effect on ulcer healing specifically has little direct study evidence.

Can lion's mane treat H. pylori?

Lion's mane extracts inhibit H. pylori in laboratory studies — ethyl acetate fractions inhibited nine clinical isolates at 62.5–250 µg/mL (Shang 2013), and an ethanolic extract inhibited six strains at around 2 mg/mL while blocking the bacterium's adhesion to gastric cells (Wang 2019). Since H. pylori infection drives the gastric cancer progression, this sits upstream of the cancer question. But no human eradication data exists, and H. pylori is treated with a proven antibiotic regimen that should not be substituted or delayed.

What mushroom has the strongest gastric cancer research?

Lentinan, from shiitake, by a wide margin. It is an injectable preparation used as an adjunct to chemotherapy for gastric cancer in Japan, with multiple clinical studies and meta-analyses examining survival when combined with chemotherapy. Lion's mane has mechanistically specific work — the erinacine studies are among the more detailed natural-product mechanism papers in this area — but it remains entirely preclinical for gastric cancer. Mechanistic sophistication and clinical evidence are different things, and lentinan has the second while lion's mane has the first.

Could lion's mane prevent stomach cancer?

It is an open question that the existing research does not answer. Prevention would have to be demonstrated somewhere along the precancerous part of the cascade — atrophy, intestinal metaplasia, dysplasia. Lion's mane has one cell-model study at the atrophy stage (Wang 2015) and nothing at all at metaplasia or dysplasia. The human data showing lower gastric cancer risk with higher mushroom intake is about mushroom consumption in general, not lion's mane (Ba 2023). Anyone concerned about gastric cancer risk should ask their doctor about H. pylori testing, which has an established evidence base behind it.

Sources & References

1. 1RTHM-01448·Tung, Shui-Yi et al. (2021). “Apoptotic mechanisms of gastric cancer cells induced by isolated erinacine S through epigenetic histone H3 methylation of FasL and TRAIL..” Food & function.Study breakdown →PubMed →↩
2. 2RTHM-00884·Kuo, Hsing-Chun et al. (2017). “A Comparative Proteomic Analysis of Erinacine A's Inhibition of Gastric Cancer Cell Viability and Invasiveness..” Cellular physiology and biochemistry : international journal of experimental cellular physiology.Study breakdown →PubMed →↩
3. 3RTHM-00408·Wang, Mingxing et al. (2015). “A polysaccharide from cultured mycelium of Hericium erinaceus and its anti-chronic atrophic gastritis activity..” International journal of biological macromolecules.Study breakdown →PubMed →↩
4. 4RTHM-00005·Xu, C P et al. (1985). “A double-blind study of effectiveness of hericium erinaceus pers therapy on chronic atrophic gastritis. A preliminary report..” Chinese medical journal.Study breakdown →PubMed →↩
5. 5RTHM-00614·Li, Guang et al. (2014). “Anticancer potential of Hericium erinaceus extracts against human gastrointestinal cancers..” Journal of ethnopharmacology.Study breakdown →PubMed →↩
6. 6RTHM-01700·Gravina, Antonietta Gerarda et al. (2023). “Hericium erinaceus, a medicinal fungus with a centuries-old history: Evidence in gastrointestinal diseases..” World journal of gastroenterology.Study breakdown →PubMed →↩
7. 7RTHM-00304·Shang, Xiaodong et al. (2013). “In vitro anti-Helicobacter pylori effects of medicinal mushroom extracts, with special emphasis on the Lion's Mane mushroom, Hericium erinaceus (higher Basidiomycetes)..” International journal of medicinal mushrooms.Study breakdown →PubMed →↩
8. 8RTHM-00592·Wang, Ge et al. (2019). “In Vitro and In Vivo Inhibition of Helicobacter pylori by Ethanolic Extracts of Lion's Mane Medicinal Mushroom, Hericium erinaceus (Agaricomycetes)..” International journal of medicinal mushrooms.Study breakdown →PubMed →↩
9. 9RTHM-00815·Ba, Djibril M et al. (2023). “Mushroom consumption and risk of gastric cancer: a pooled analysis within the stomach cancer pooling project and a combined meta-analysis with other observational studies..” European journal of cancer prevention : the official journal of the European Cancer Prevention Organisation (ECP).Study breakdown →PubMed →↩