Component
Yeast beta-(1->3)/(1->6)-glucan
Yeast beta-(1->3)/(1->6)-glucan. Species, exposure and limitations are retained in each linked claim.
5 recorded relationships. Experimental role, claim status and evidence remain attached to each record.
How nutrients influence it
Every nutrient with a recorded effect on this component, credited to the nutrient that acted rather than the chapter that recorded it. Open a nutrient to see the findings and the conditions they were measured under.
Other things that act on it
Enzymes, hormones, genes, and other components with a recorded effect. These are not nutrients, so they do not count toward the arrows above. Each finding names the chapter that recorded it.
How nutrients reach it in more than one step
Chains of two or more recorded steps that end here, grouped by the nutrient they start from. Each step is a separate finding, so a chain is a route a mechanism could take, not proof that it does.
Tracing routes…
What it does
Every recorded relationship this component is part of, grouped by its role. Plain wording comes first; the technical statement follows.
What it acts on
One patient developed a dose-limiting toxicity of transient self-limiting hepatic transaminase elevation 5 days after starting beta-glucan at 120 milligrams per kilogram per day, overall 1, 3, 12 and 24 evaluable patients had complete response, partial response, stable and progressive disease respectively at the end of treatment, positive human anti-mouse antibody response and dectin-1 rs3901533 polymorphism were associated with better overall survival, and beta-glucan dose level and serum beta-glucan levels did not correlate with response.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/glucan-research/34944886.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "ebbaee1e57b37044ff51d85d98d519101169e09a734d420c8bce53faab1d19f0", "start_char": 0, "end_char": 1471, "text_sha256": "ebbaee1e57b37044ff51d85d98d519101169e09a734d420c8bce53faab1d19f0"}
- experimental_model
- Phase I dose escalation of oral yeast glucan with an anti-GD2 antibody across cohorts of three to six patients
- exposure
- Oral yeast beta-glucan escalated from 10 to 200 milligrams per kilogram per day for 17 days with intravenous 3F8 antibody
- limitations
- A single-arm phase I with no control for the antibody alone, so the glucan contribution to any response cannot be isolated. Forty-four patients completed 141 cycles and forty were evaluable at end of treatment.
- nutrient_topic
- Beta-glucan research collection; topical membership is not evidence of a direct clinical effect, and each preparation is recorded as its own entity with no family link joining any pair. · Beta-glucan
- organism
- Human
- plain_language
- Across a twentyfold range of doses, how much was taken did not predict who responded; a receptor gene variant did.
- primary_references
- [bg-p34944886] Phase I Trial of Oral Yeast-Derived β-Glucan to Enhance Anti-GD2 Immunotherapy of Resistant High-Risk Neuroblastoma. (2021). https://pubmed.ncbi.nlm.nih.gov/34944886/ DOI: 10.3390/cancers13246265
- tissue_or_cell_type
- Relapsed or refractory high-risk neuroblastoma
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Phase I dose escalation of oral yeast glucan with an anti-GD2 antibody across cohorts of three to six patients · source_derived_draft · unverified_draft
### bg-dose-did-not-track-response One patient developed a dose-limiting toxicity of transient self-limiting hepatic transaminase elevation 5 days after starting beta-glucan at 120 milligrams per kilogram per day, overall 1, 3, 12 and 24 evaluable patients had complete response, partial response, stable and progressive disease respectively at the end of treatment, positive human anti-mouse antibody response and dectin-1 rs3901533 polymorphism were associated with better overall survival, and beta-glucan dose level and serum beta-glucan levels did not correlate with response. Condition category: normal nutrient_topic: Beta-glucan research collection; topical membership is not evidence of a direct clinical effect, and each preparation is recorded as its own entity with no family link joining any pair. plain_language: Across a twentyfold range of doses, how much was taken did not predict who responded; a receptor gene variant did. organism: Human tissue_or_cell_type: Relapsed or refractory high-risk neuroblastoma experimental_model: Phase I dose escalation of oral yeast glucan with an anti-GD2 antibody across cohorts of three to six patients limitations: A single-arm phase I with no control for the antibody alone, so the glucan contribution to any response cannot be isolated. Forty-four patients completed 141 cycles and forty were evaluable at end of treatment. exposure: Oral yeast beta-glucan escalated from 10 to 200 milligrams per kilogram per day for 17 days with intravenous 3F8 antibody evidence_span: {"source_cache": "artifacts/glucan-research/34944886.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "ebbaee1e57b37044ff51d85d98d519101169e09a734d420c8bce53faab1d19f0", "start_char": 0, "end_char": 1471, "text_sha256": "ebbaee1e57b37044ff51d85d98d519101169e09a734d420c8bce53faab1d19f0"} [bg-p34944886] Phase I Trial of Oral Yeast-Derived β-Glucan to Enhance Anti-GD2 Immunotherapy of Resistant High-Risk Neuroblastoma. (2021). https://pubmed.ncbi.nlm.nih.gov/34944886/ DOI: 10.3390/cancers13246265
Complete structured claim and evidenceEligible patients receiving GD2/GD3 vaccine were randomly assigned to group 1 with 54 patients to receive no beta-glucan or group 2 with 53 patients to receive an oral beta-glucan regimen during the first 5 weeks of vaccine priming, and from week 6 onwards all 107 patients received oral beta-glucan during vaccine boost, adding oral beta-glucan during the first 5 weeks of vaccine priming elicited a higher anti-GD2 IgG1 antibody response in group 2 at 1.80 with 90% CI 0.12 to 3.39 and P = .08 against a planned type I error of 0.10, antibody titre correlated significantly with dectin-1 single nucleotide polymorphism, and the genotype frequency, seroconversion rates and vaccine-related toxic effects were similar in the 2 groups.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/glucan-research/36547975.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "156766d12dba66e36fba78a5ca31f9c41f50f88f74817ba4d545a7a3ed5e23f2", "start_char": 0, "end_char": 2766, "text_sha256": "156766d12dba66e36fba78a5ca31f9c41f50f88f74817ba4d545a7a3ed5e23f2"}
- experimental_model
- Phase 2 randomised clinical trial isolating the adjuvant effect during the vaccine priming phase
- exposure
- Oral beta-glucan during the first 5 weeks of GD2/GD3 vaccine priming against none, with all patients receiving glucan from week 6 onward
- limitations
- A randomised design that isolates one adjuvant window, with a prespecified type I error of 0.10 rather than the conventional 0.05. The endpoint is an antibody titre, not survival.
- nutrient_topic
- Beta-glucan research collection; topical membership is not evidence of a direct clinical effect, and each preparation is recorded as its own entity with no family link joining any pair. · Beta-glucan
- organism
- Human
- plain_language
- Starting the glucan earlier raised the antibody the vaccine was meant to raise, at a significance bar the trial had set in advance at one in ten.
- primary_references
- [bg-p36547975] Effect of Oral β-Glucan on Antibody Response to Ganglioside Vaccine in Patients With High-Risk Neuroblastoma: A Phase 2 Randomized Clinical Trial. (2023). https://pubmed.ncbi.nlm.nih.gov/36547975/ DOI: 10.1001/jamaoncol.2022.5999
- tissue_or_cell_type
- High-risk neuroblastoma
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Phase 2 randomised clinical trial isolating the adjuvant effect during the vaccine priming phase · source_derived_draft · unverified_draft
### bg-immunogenicity-in-genetic-responders Eligible patients receiving GD2/GD3 vaccine were randomly assigned to group 1 with 54 patients to receive no beta-glucan or group 2 with 53 patients to receive an oral beta-glucan regimen during the first 5 weeks of vaccine priming, and from week 6 onwards all 107 patients received oral beta-glucan during vaccine boost, adding oral beta-glucan during the first 5 weeks of vaccine priming elicited a higher anti-GD2 IgG1 antibody response in group 2 at 1.80 with 90% CI 0.12 to 3.39 and P = .08 against a planned type I error of 0.10, antibody titre correlated significantly with dectin-1 single nucleotide polymorphism, and the genotype frequency, seroconversion rates and vaccine-related toxic effects were similar in the 2 groups. Condition category: normal nutrient_topic: Beta-glucan research collection; topical membership is not evidence of a direct clinical effect, and each preparation is recorded as its own entity with no family link joining any pair. plain_language: Starting the glucan earlier raised the antibody the vaccine was meant to raise, at a significance bar the trial had set in advance at one in ten. organism: Human tissue_or_cell_type: High-risk neuroblastoma experimental_model: Phase 2 randomised clinical trial isolating the adjuvant effect during the vaccine priming phase limitations: A randomised design that isolates one adjuvant window, with a prespecified type I error of 0.10 rather than the conventional 0.05. The endpoint is an antibody titre, not survival. exposure: Oral beta-glucan during the first 5 weeks of GD2/GD3 vaccine priming against none, with all patients receiving glucan from week 6 onward evidence_span: {"source_cache": "artifacts/glucan-research/36547975.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "156766d12dba66e36fba78a5ca31f9c41f50f88f74817ba4d545a7a3ed5e23f2", "start_char": 0, "end_char": 2766, "text_sha256": "156766d12dba66e36fba78a5ca31f9c41f50f88f74817ba4d545a7a3ed5e23f2"} [bg-p36547975] Effect of Oral β-Glucan on Antibody Response to Ganglioside Vaccine in Patients With High-Risk Neuroblastoma: A Phase 2 Randomized Clinical Trial. (2023). https://pubmed.ncbi.nlm.nih.gov/36547975/ DOI: 10.1001/jamaoncol.2022.5999
Complete structured claim and evidence
What acts on it
Recent data indicated that barley beta-1,3;1,4-glucan given orally potentiated the activity of antitumour monoclonal antibody leading to enhanced tumour regression and survival, and this investigation showed that orally administered yeast beta-1,3;1,6-glucan functioned similarly to barley beta-1,3;1,4-glucan with antitumour monoclonal antibody, with both oral beta-1,3-glucans a requirement for iC3b on tumours and CR3 on granulocytes being confirmed by demonstrating therapeutic failures in mice deficient in C3 or CR3.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_span
- {"source_cache": "artifacts/glucan-research/15240666.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "eaff7297fa40df19ef82e5e1de433ec0cf34590a7e3fda6aa6061e0922666781", "start_char": 0, "end_char": 1454, "text_sha256": "eaff7297fa40df19ef82e5e1de433ec0cf34590a7e3fda6aa6061e0922666781"}
- experimental_model
- Fluorescein-labelled oral glucans tracked through macrophages to marrow, with therapy in C3-deficient and CR3-deficient mice
- exposure
- Orally administered barley beta-1,3;1,4-glucan and orally administered yeast beta-1,3;1,6-glucan, each with antitumour monoclonal antibody
- limitations
- The single experiment in this collection that tested a cereal mixed-linkage glucan and a yeast branched glucan side by side in the same protocol. It is a mouse tumour model, and oral uptake in mice does not establish the same uptake in people.
- nutrient_topic
- Beta-glucan research collection; topical membership is not evidence of a direct clinical effect, and each preparation is recorded as its own entity with no family link joining any pair. · Beta-glucan
- organism
- Mouse
- plain_language
- A cereal glucan and a yeast glucan did the same job by the same route, which is the result that refuses to let the two be filed apart.
- primary_references
- [bg-p15240666] Mechanism by which orally administered beta-1,3-glucans enhance the tumoricidal activity of antitumor monoclonal antibodies in murine tumor models. (2004). https://pubmed.ncbi.nlm.nih.gov/15240666/ DOI: 10.4049/jimmunol.173.2.797
- tissue_or_cell_type
- Gut, spleen, lymph node, bone marrow and tumour
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Fluorescein-labelled oral glucans tracked through macrophages to marrow, with therapy in C3-deficient and CR3-deficient mice · source_derived_draft · unverified_draft
### bg-barley-and-yeast-converge Recent data indicated that barley beta-1,3;1,4-glucan given orally potentiated the activity of antitumour monoclonal antibody leading to enhanced tumour regression and survival, and this investigation showed that orally administered yeast beta-1,3;1,6-glucan functioned similarly to barley beta-1,3;1,4-glucan with antitumour monoclonal antibody, with both oral beta-1,3-glucans a requirement for iC3b on tumours and CR3 on granulocytes being confirmed by demonstrating therapeutic failures in mice deficient in C3 or CR3. Condition category: machinery_impairment nutrient_topic: Beta-glucan research collection; topical membership is not evidence of a direct clinical effect, and each preparation is recorded as its own entity with no family link joining any pair. plain_language: A cereal glucan and a yeast glucan did the same job by the same route, which is the result that refuses to let the two be filed apart. organism: Mouse tissue_or_cell_type: Gut, spleen, lymph node, bone marrow and tumour experimental_model: Fluorescein-labelled oral glucans tracked through macrophages to marrow, with therapy in C3-deficient and CR3-deficient mice limitations: The single experiment in this collection that tested a cereal mixed-linkage glucan and a yeast branched glucan side by side in the same protocol. It is a mouse tumour model, and oral uptake in mice does not establish the same uptake in people. exposure: Orally administered barley beta-1,3;1,4-glucan and orally administered yeast beta-1,3;1,6-glucan, each with antitumour monoclonal antibody evidence_span: {"source_cache": "artifacts/glucan-research/15240666.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "eaff7297fa40df19ef82e5e1de433ec0cf34590a7e3fda6aa6061e0922666781", "start_char": 0, "end_char": 1454, "text_sha256": "eaff7297fa40df19ef82e5e1de433ec0cf34590a7e3fda6aa6061e0922666781"} [bg-p15240666] Mechanism by which orally administered beta-1,3-glucans enhance the tumoricidal activity of antitumor monoclonal antibodies in murine tumor models. (2004). https://pubmed.ncbi.nlm.nih.gov/15240666/ DOI: 10.4049/jimmunol.173.2.797
Complete structured claim and evidence
Where it participates (unsigned role)
CR3 serves as the leukocyte beta-glucan receptor through a cation-independent lectin site located C-terminal to the I-domain of CD11b that contains the binding sites for iC3b, ICAM-1 and fibrinogen, a 10-kilodalton soluble zymosan polysaccharide consisting largely of mannose and approximately 5% glucose bound with high affinity of 6.7 x 10(-8) M, binding was blocked not only by pure beta-glucans from yeast, mushroom, seaweed or barley but also by N-acetyl-D-glucosamine and alpha- or beta-methylmannoside and alpha- or beta-methylglucoside, and its sugar specificity is broader than originally appreciated.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/glucan-research/8558003.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "00a0fef65e91375066fe9920200032466aec1c0d85bf548d53f64c3d384106b7", "start_char": 0, "end_char": 1936, "text_sha256": "00a0fef65e91375066fe9920200032466aec1c0d85bf548d53f64c3d384106b7"}
- experimental_model
- Flow cytometry with labelled soluble polysaccharides, CR3 and CR4 chimeras, and a panel of domain-specific antibodies
- exposure
- Labelled beta-glucans from yeast, mushroom, seaweed and barley, and a 10-kilodalton soluble zymosan polysaccharide
- limitations
- Binding and inhibition rather than function. The highest-affinity ligand measured was not a pure beta-glucan but a mannose-rich zymosan polysaccharide, and the sugar specificity proved broader than beta-glucan alone.
- nutrient_topic
- Beta-glucan research collection; topical membership is not evidence of a direct clinical effect, and each preparation is recorded as its own entity with no family link joining any pair. · Beta-glucan
- organism
- Human
- plain_language
- The complement receptor grips sugars at a second site, separate from the one that grips the complement fragment.
- primary_references
- [bg-p8558003] Analysis of the sugar specificity and molecular location of the beta-glucan-binding lectin site of complement receptor type 3 (CD11b/CD18). (1996). https://pubmed.ncbi.nlm.nih.gov/8558003/ DOI: 10.4049/jimmunol.156.3.1235
- tissue_or_cell_type
- Leukocytes
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Flow cytometry with labelled soluble polysaccharides, CR3 and CR4 chimeras, and a panel of domain-specific antibodies · source_derived_draft · unverified_draft
### bg-cr3-has-a-lectin-site CR3 serves as the leukocyte beta-glucan receptor through a cation-independent lectin site located C-terminal to the I-domain of CD11b that contains the binding sites for iC3b, ICAM-1 and fibrinogen, a 10-kilodalton soluble zymosan polysaccharide consisting largely of mannose and approximately 5% glucose bound with high affinity of 6.7 x 10(-8) M, binding was blocked not only by pure beta-glucans from yeast, mushroom, seaweed or barley but also by N-acetyl-D-glucosamine and alpha- or beta-methylmannoside and alpha- or beta-methylglucoside, and its sugar specificity is broader than originally appreciated. Condition category: normal nutrient_topic: Beta-glucan research collection; topical membership is not evidence of a direct clinical effect, and each preparation is recorded as its own entity with no family link joining any pair. plain_language: The complement receptor grips sugars at a second site, separate from the one that grips the complement fragment. organism: Human tissue_or_cell_type: Leukocytes experimental_model: Flow cytometry with labelled soluble polysaccharides, CR3 and CR4 chimeras, and a panel of domain-specific antibodies limitations: Binding and inhibition rather than function. The highest-affinity ligand measured was not a pure beta-glucan but a mannose-rich zymosan polysaccharide, and the sugar specificity proved broader than beta-glucan alone. exposure: Labelled beta-glucans from yeast, mushroom, seaweed and barley, and a 10-kilodalton soluble zymosan polysaccharide evidence_span: {"source_cache": "artifacts/glucan-research/8558003.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "00a0fef65e91375066fe9920200032466aec1c0d85bf548d53f64c3d384106b7", "start_char": 0, "end_char": 1936, "text_sha256": "00a0fef65e91375066fe9920200032466aec1c0d85bf548d53f64c3d384106b7"} [bg-p8558003] Analysis of the sugar specificity and molecular location of the beta-glucan-binding lectin site of complement receptor type 3 (CD11b/CD18). (1996). https://pubmed.ncbi.nlm.nih.gov/8558003/ DOI: 10.4049/jimmunol.156.3.1235
Complete structured claim and evidenceDectin-1 lacks residues involved in calcium ligation that mediates carbohydrate-binding by classical C-type lectins, and among 187 diverse sequence-defined oligosaccharide probes together with designer microarrays from a neutral soluble glucan from S. cerevisiae, curdlan from Alcaligenes faecalis and pustulan from Umbilicaria papullosa, Dectin-1 binding is detected exclusively to 1,3-linked glucose oligomers, the minimum length required for detectable binding being a 10- or 11-mer, and 11-13 gluco-oligomers in clustered form displayed on liposomes mimic the macromolecular beta-glucans and compete with zymosan binding and triggering of tumour necrosis factor alpha secretion.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/glucan-research/16371356.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "dd98941694dedd8e3e85766c0c299b54fbc29ca8cce7c61a333efceee796867f", "start_char": 0, "end_char": 1911, "text_sha256": "dd98941694dedd8e3e85766c0c299b54fbc29ca8cce7c61a333efceee796867f"}
- experimental_model
- Neoglycolipid oligosaccharide microarrays built from three glucan polysaccharides and screened against 187 sequence-defined probes
- exposure
- Dectin-1 binding to oligosaccharide probes generated from a soluble yeast glucan, curdlan and pustulan
- limitations
- A binding assignment on arrayed probes rather than on a cell surface. The clustered-ligand test uses liposomes and a Dectin-1-expressing cell line.
- nutrient_topic
- Beta-glucan research collection; topical membership is not evidence of a direct clinical effect, and each preparation is recorded as its own entity with no family link joining any pair. · Beta-glucan
- organism
- Recombinant protein and a macrophage cell line
- plain_language
- The receptor reads only one linkage, needs a run of about ten sugars to grip at all, and needs them clustered to fire.
- primary_references
- [bg-p16371356] Ligands for the beta-glucan receptor, Dectin-1, assigned using "designer" microarrays of oligosaccharide probes (neoglycolipids) generated from glucan polysaccharides. (2006). https://pubmed.ncbi.nlm.nih.gov/16371356/ DOI: 10.1074/jbc.m511461200
- tissue_or_cell_type
- Cell-free microarray and cultured cells
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Neoglycolipid oligosaccharide microarrays built from three glucan polysaccharides and screened against 187 sequence-defined probes · source_derived_draft · unverified_draft
### bg-only-beta-1-3-oligomers-bind Dectin-1 lacks residues involved in calcium ligation that mediates carbohydrate-binding by classical C-type lectins, and among 187 diverse sequence-defined oligosaccharide probes together with designer microarrays from a neutral soluble glucan from S. cerevisiae, curdlan from Alcaligenes faecalis and pustulan from Umbilicaria papullosa, Dectin-1 binding is detected exclusively to 1,3-linked glucose oligomers, the minimum length required for detectable binding being a 10- or 11-mer, and 11-13 gluco-oligomers in clustered form displayed on liposomes mimic the macromolecular beta-glucans and compete with zymosan binding and triggering of tumour necrosis factor alpha secretion. Condition category: normal nutrient_topic: Beta-glucan research collection; topical membership is not evidence of a direct clinical effect, and each preparation is recorded as its own entity with no family link joining any pair. plain_language: The receptor reads only one linkage, needs a run of about ten sugars to grip at all, and needs them clustered to fire. organism: Recombinant protein and a macrophage cell line tissue_or_cell_type: Cell-free microarray and cultured cells experimental_model: Neoglycolipid oligosaccharide microarrays built from three glucan polysaccharides and screened against 187 sequence-defined probes limitations: A binding assignment on arrayed probes rather than on a cell surface. The clustered-ligand test uses liposomes and a Dectin-1-expressing cell line. exposure: Dectin-1 binding to oligosaccharide probes generated from a soluble yeast glucan, curdlan and pustulan evidence_span: {"source_cache": "artifacts/glucan-research/16371356.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "dd98941694dedd8e3e85766c0c299b54fbc29ca8cce7c61a333efceee796867f", "start_char": 0, "end_char": 1911, "text_sha256": "dd98941694dedd8e3e85766c0c299b54fbc29ca8cce7c61a333efceee796867f"} [bg-p16371356] Ligands for the beta-glucan receptor, Dectin-1, assigned using "designer" microarrays of oligosaccharide probes (neoglycolipids) generated from glucan polysaccharides. (2006). https://pubmed.ncbi.nlm.nih.gov/16371356/ DOI: 10.1074/jbc.m511461200
Complete structured claim and evidence
The events it takes part in
A mechanism often involves more than two components. These are the full events, with every participant and its role.
Situations it appears in
Low-supply and faulty-machinery situations recorded in the chapters where this component plays a part.
In the sources
Preserved passages that mention this component, quoted exactly. Open one to read it in context.
Open hypotheses
Proposed ideas that involve this component. They are labeled as hypotheses and do not change any recorded statement.
This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.