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PubMedDate not supplied

A multi-institutional prospective study of lentinan in advanced gastric cancer patients with unresectable and recurrent diseases: effect on prolongation of survival and improvement of quality of life. Kanagawa Lentinan Research Group.

BACKGROUND/AIMS: Lentinan is one of the host-mediated anti-cancer drugs which has been shown to affect host defense immune systems. Although the mechanisms involved in the antitumor effects of lentinan have been reported experimentally, the clinical outcome on prolongation of survival and improvement of quality of life in gastric cancer patients with unresectable or recurrent diseases has yet to be clarified. The aim of the present study was to investigate whether administration of lentinan prolonged survival or improved quality of life in these patients. METHODOLOGY: A multi-institutional randomized prospective protocol, consisting of patients administered tegafur and cisplatin (control group), and patients administered lentinan, tegafur and cisplatin (lentinan group), was performed. Quality of life was investigated using a questionnaire survey. RESULTS: Median survival was significantly longer in the lentinan group than in the control group (297 days vs. 199 days, p = 0.028). One-year survival rate was greater in the lentinan group than in the control group (49.1% vs. 0%). Total QOL score, especially appetite and sleep quality, was significantly improved with the administration of lentinan. CONCLUSIONS: Lentinan is considered to prolong survival and improved quality of life when gastric cancer patients with unresectable or recurrent diseases are treated in combination with other chemotherapeutic agents.

Adjuvants, Immunologic↗
PubMed1980

[Fate of lentinan (antitumor polysaccharide) I : - fate of lentinan in mice, rats, and dogs (author's transl)].

Fate of lentinan, which is one of antitumor polysaccharides, was investigated with 3H-lentinan. 3H-lentinan was prepared by Wilzbach 3H gas exposure labeling, then purified by the gel filtration chromatography. 1) After a single intravenous injection of 3H-lentinan, radioactivity in plasma declined in a biphasic process. 2) There were urinary and fecal excretion, but expiratory excretion was a small proportion. 3) The radioactivity was predominantly incorporated into the liver and spleen, indicating selective retention of the lentinan in reticuloendothelial system cells. On the other hand the level of radioactivity in the lung and kidneys was dropped rapidly. 4) We can not find the selective incorporation of radioactivity into the tumor. 5) There was no species difference on the distribution of lentinan among mouse, rat and dog. 6) These results obtained were similar to other polysaccharides and immunologic antitumor agents.

Animals↗
PubMed1980

[Fate of lentinan (antitumor polysaccharide) II : - fast of methyl lentinan in rats (author's transl)].

3H-labeled lentinan was prepared by methylation with 3H-dimethyl-sulfate. Blood level, distribution and excretion were studied in rats. After intravenous injection of [methyl-3H] -methyl lentinan, radioactivity rapidly disappeared from blood, lung and kidney, distributed mainly in liver, spleen and mesenteric lymph nodes. There was urinary excretion, but expiratory excretion was a small proportion. In the case of multi-injection of [methyl-3H] -methyl lentinan distribution of radioactivity was similar to a single injection, but retention of 3H was less than a single injection. Bile excretion and transport to fetuses and milk were in mere trace amounts. No substantial difference was found between two types of the 3H-labeled lentinan in either the distribution or excretion.

Animals↗
PubMed1986

[Randomized study of lentinan on patients with advanced gastric and colorectal cancer. Tohoku Lentinan Study Group].

A randomized study of mitomycin C (MMC)+5-FU [control group] vs MMC+5-FU+lentinan (LNT) [LNT group] was conducted in order to evaluate the effect of LNT against advanced gastric and colorectal cancers by the envelope method in 166 patients, comprising of 115 cases of gastric cancer and 51 cases of colorectal cancer. Significant increases were observed in the survival rates for the LNT group (p less than 0.05) for both patients with gastric and colorectal cancer. No significant difference was observed in response rates between the aforesaid two groups, though the response rate in the LNT group was slightly higher than the control group. These results suggest that LNT in combination with anticancer drugs prolong the survival time of patients with advanced gastric and colorectal cancer.

Adult↗
PubMedDate not supplied

Effects of 5'-DFUR and lentinan on cytokines and PyNPase against AH66 ascites hepatoma in rats.

Pyrimidine nucleoside phosphorylase (PyNPase) is an enzyme which converts 5'-deoxy-5-fluorouridine (5'-DFUR) to 5-fluorouracil (5-FU), and is induced by various cytokines in tumor cells. We evaluated a combination of 5'-DFUR and lentinan which is widely used as a biological response modifier (BRM), to verify antitumor effects, the induction of cytokines such as tumor necrosis factor (TNF)-alpha and latent transforming growth factor (TGF)-beta, and PyNPase activity against AH66 ascites hepatoma cells in rats. AH66 ascites hepatoma cells were subcutaneously injected into the backs of Donryu rats. Rats were randomly assigned to a group receiving either 5'-DFUR or lentinan alone, to a group receiving both 5'-DFUR and lentinan, or to a control group. 5'-DFUR was administered orally, and lentinan was administered intraperitoneally. The tumor size, PyNPase activity in the tumor and spleen, and TNF-alpha and TGF-beta in the tumor were examined. The results were as follows. a) Tumor growth was significantly (P < 0.05) inhibited in both the 5'-DFUR group and the 5'-DFUR + Lentinan group when compared to the control group. Tumor growth in the 5'-DFUR + Lentinan group was significantly (P < 0.01) inhibited compared to that in both the 5'-DFUR group and the Lentinan group. b) PyNPase activity in the tumor was significantly (P < 0.01) higher in each group than in the spleen. In the tumor, PyNPase activity was significantly (P < 0.01) higher in the Lentinan group compared to the control group. In the 5'-DFUR + Lentinan group PyNPase activity in the tumor was significantly (P < 0.01) lower compared to the Lentinan group. c) Levels of TNF-alpha and TGF-beta production in the tumor were significantly (P < 0.05) lower in the 5'-DFUR + Lentinan group compared to the control group. These findings suggested that PyNPase activity in the tumor was induced by lentinan but not so in the spleen, and lentinan increased the susceptibility of tumor cells to 5'-DFUR.

Animals↗
PubMed1984

Antitumor activity of lentinan in murine syngeneic and autochthonous hosts and its suppressive effect on 3-methylcholanthrene-induced carcinogenesis.

The antitumor effect of lentinan in syngeneic and autochthonous tumor-host systems and its suppressive effect on 3-methylcholanthrene (MC)-induced carcinogenesis were confirmed using DBA/2 and SWM/Ms hosts. The regressive activity of lentinan against the solid form of Sarcoma 180 was the most effective in DBA/2, SWM/Ms, or A/J mice and less effective in C3H/He or C57BL/6 mice. The growth of a syngeneic MC-induced DBA/2.MC.CS-1 fibrosarcoma (native and trypsinized) was markedly inhibited, and the regression of tumors was detected by the i.p. injection of minute amounts of lentinan into DBA/2 mice, which were the most suitable host in lentinan treatment. When DBA/2 mice were used, lentinan was also effective for even autochthonous primary tumors induced within 15 weeks after MC inoculation, but less effective for tumors induced during the 16 to 36 weeks after MC treatment. Lentinan showed a prominent suppressive effect in MC-induced carcinogenesis using DBA/2 and SWM/Ms mice but not effect when BALB/c, C57BL/6, or C3H/He mice were used. The timing of lentinan administration in the latter result was examined using SWM/Ms mice, and lentinan, when it was given daily for 10 days after the third week of MC inoculation, was strikingly effective (33%), but not so effective (63%) when lentinan was given after the sixth week of MC treatment, compared with tumor-occurrence rate in the control group (88%). The reason why DBA/2, SWM/Ms, or A/J mice were suitable hosts for lentinan treatment is not clear, but the natural killer capability or phagocytic macrophage function in these strains seems to have no relation to lentinan action, because A/J mice are deficient in natural killer function, and in these strains of mice the phagocytic function of macrophages is weak. It may be quite possible that these strains of mice are most sensitive to delayed-type hypersensitivity and/or cytotoxic T-cell response in which T-cells and lentinan play important roles. The tumor-host systems presented here provide a good model in which lentinan retains an inhibitory capacity in syngeneic and autochthonous hosts, and such a model offers the possibility for further study of the host defense mechanism against cancer.

Animals↗
PubMed1985

Effect of lentinan on the chemiluminescence produced by human neutrophils and the murine macrophage cell line C4M phi.

Lentinan, an immunopotentiating polysaccharide, stimulates the production of chemiluminescence (CL) by human neutrophils and the murine macrophage cell line C4M phi. The CL enhancing effect of lentinan opsonized in human serum is greater than that of lentinan itself. Lentinan's stimulation of neutrophil CL was increased by 1/2 when opsonized in human serum inactivated at 56 degrees C to remove complement, while the CL was increased two fold by lentinan opsonized in whole serum. This indicates that C3b and immunoglobulin contribute separate signals in the activation process mediated by opsonized lentinan. The distinct roles of the C3b and Fc receptors was further illuminated by the finding that an Fc receptor-negative cell line was unresponsive to lentinan opsonized in heat inactivated serum (56 degrees C), whereas it exhibited a five fold increase in CL in response to lentinan opsonized in serum containing complement. Lentinan in an opsonized form can stimulate the production of CL via C3b and Fc receptors. This mechanism may be considered as one mode of action of lentinan and other similar immunopotentiating and antitumour glucan-type polysaccharides.

Animals↗
PubMed1994

Reconstitution of anti-tumor effects of lentinan in nude mice: roles of delayed-type hypersensitivity reaction triggered by CD4-positive T cell clone in the infiltration of effector cells into tumor.

Lentinan, an antitumor polysaccharide used clinically in Japan, requires the intact T cell compartment to manifest its antitumor effects. The aim of the current study was to clarify the mechanisms playing crucial roles in the T cell requirement in the expression of antitumor effects of lentinan. Lentinan treatment of BDF1 mice transplanted intradermally with FBL-3 induced complete tumor regression and a marked increase in survival time. The antitumor action of lentinan was abolished in mice treated simultaneously with antibodies to CD4 and CD8 antigens, whereas antibody to CD4, CD8 or NK1.1 alone was ineffective. The natural killer, cytotoxic T lymphocyte, and helper T cell activities were already augmented in this FBL-3/BDF1 system and thus further augmentation of these activities by lentinan was not observed. These activities did not correlate with the antitumor activity of lentinan, as was confirmed in lymphocyte subset depletion experiments. On the contrary, the delayed-type hypersensitivity (DTH) response against tumor-associated antigens was triggered by lentinan and was abrogated only in mice treated simultaneously with antibodies to CD4 and CD8 antigens. Furthermore, a non-cytolytic tumor-associated antigen-specific CD4+ T cell clone able to induce the DTH response in concert with lentinan reconstituted the antitumor effects in B6 nude mice when administered with lentinan. These results suggest that, in addition to the augmentation of immune effector cell activity against tumors, infiltration of these cells into the tumor burden initiated by the DTH responses at tumor sites may be involved in eradication of tumors by lentinan.

Animals↗
PubMed1984

Immunotherapy of Madison 109 lung carcinoma and other murine tumors using lentinan.

Lentinan was evaluated initially against the Lewis (LL) and Madison 109 (M109) lung carcinomas implanted in the footpads of syngeneic mice. Activity in these tumor models was assessed by both reduction in early tumor growth rates and increases in life span and cures, relative to untreated control mice with tumors. Lentinan given i.p. to mice bearing LL footpad tumors caused a reduction in tumor growth rate in only one of three experiments and an increase in life span of 48% at one dose level on another occasion. In contrast, lentinan given i.p. to mice bearing M109 footpad tumors was consistently curative (50 to 70%) in three experiments despite the lack of an effect upon early tumor growth rate. In subsequent experiments, syngeneic mice were implanted s.c. with M109 or LL and treated with lentinan. Although lentinan had no substantial effect upon LL, 25 to 75% of mice bearing s.c. M109 tumors were cured in three separate experiments following early treatment initiation. Delayed lentinan therapy, initiated when s.c. M109 tumors were greater than 100 mg, also resulted in complete tumor regression and cure of 29 to 63% of the mice in three experiments. Surgical adjuvant immunotherapy of s.c. M109 using lentinan also improved survival rates over those obtained using surgery alone. Mice cured of s.c.-implanted M109 using lentinan, or surgery plus lentinan, but not surgery alone, survived a rechallenge with M109. The therapeutic effects of lentinan in mice implanted s.c. with B16 melanoma were inconsistent.

Animals↗
PubMed1992

In vitro generation of activated natural killer cells and cytotoxic macrophages with lentinan.

The in vitro effect of lentinan in inducing activation of killer cells and cytotoxic macrophages has been examined. Human peripheral blood mononuclear cells were cultured with lentinan for 2, 4 and 8 days. After 4 days cytotoxicity was increased 4% by lentinan less than 1,000 ng/ml. After 8 days, it was increased 12% by 25 and 1,000 ng/ml lentinan. The phenotype of the killer cells induced by lentinan was CD2+, CD16+ and CD56+, suggesting that they were natural killer cells. Macrophages separated from the spleens of 6 patients with gastric cancer were cultured with lentinan for 7 days, and their cytotoxicity increased 19%. The optimal concentration of lentinan was from 25 to 100 ng/ml. The findings suggest that the antitumour effect of lentinan is due to the activation of killer cells in vivo, because the optimal concentration of lentinan for the induction of killer cells in vitro was equivalent to the plasma concentration obtained after clinical doses of this agent.

Antigens, Surface↗
PubMed1989

Effect of lentinan and mannan on phagocytosis of fluorescent latex microbeads by mouse peritoneal macrophages: a flow cytometric study.

Lentinan, an immunopotentiating beta-1,3-glucan polysaccharide stimulated the in vitro phagocytosis of BSA-coated, C3b- or monoclonal immunoglobulin (IgG2b)-coated fluorescent microspheres by resident or thioglycollate-elicited mouse macrophages in a dose-dependent manner. Analysis of flow cytometric data has shown that microbead phagocytosis of resident macrophages, which exhibit a lower basic phagocytic activity than the thioglycollate elicited ones, has been augmented by up to 900% due to lentinan. The percent ratio of phagocytes among peritoneal exudate cells, however, remained unchanged after short-term lentinan stimulation. Preincubation of the cells with lentinan resulted in increased ingestion of the microbeads. Activation of phagocytosis by lentinan is therefore due in part to the direct stimulation of the cells, however, lentinan also serves as supplementary opsonin for C3b-coated beads. Mannan inhibited the ingestion of C3b-coated microspheres by 75%, which was abolished in part when lentinan was also added to the cells. Mannan did not influence the phagocytosis of BSA-coated or IgG-coated beads. Our data, based solely on in vitro studies, suggest a beta-glucan receptor mediated activation of phagocytes by lentinan. These receptors are different from the C3b, Fc or mannose receptors. It is very likely that stimulation of phagocytic activity of macrophages by lentinan may contribute to the antitumor action of this immunopotentiating polysaccharide.

Animals↗
PubMed1995

Lentinan augments skin reaction induced by bradykinin: its correlation with vascular dilatation and hemorrhage responses and antitumor activities.

The effects of lentinan, an antitumor polysaccharide, on vascular reactions against vasoactive mediators were investigated in murine systems. Lentinan augmented intradermal reactions against bradykinin. Induction of acute phase proteins (APP) and the vascular dilatation hemorrhage (VDH) reaction on the ears have been reported to reflect the host responses to lentinan. The strain difference in the intensity of skin reactions coincided with those observed in VDH responses and with lentinan-induced antitumor effects against Sarcoma 180. Augmentation of skin reactions was not observed in T-cell-deficient mice. Inhibitors of lipoxygenase, thrombin and plasmin which reduced skin reactions also decreased the incidence of tumor necrosis positive mice among FBL-3-bearing mice treated with lentinan. Furthermore, B10D2 mice treated with fluorouracl (5-FU) and lentinan 10 days after S908.D2 transplantation showed complete tumor regression and augmented skin reactions, whereas augmentation of skin reactions and tumor regression were not observed in mice treated with 5-FU and lentinan 32 days after tumor inoculation. Taken together, these results suggest that these vascular reactions might play crucial roles in antitumor effects of lentinan and that the skin reaction, the convenient method for investigating vascular reactions, is a promising tool to monitor host sensitivity to lentinan in antitumor responses.

Adjuvants, Immunologic↗
PubMed2002

Inhibition of human colon carcinoma development by lentinan from shiitake mushrooms (Lentinus edodes).

OBJECTIVES: Lentinan was extracted from shiitake mushrooms (Lentinus edodes) via a new cost-effective procedure that resulted in high purity (88%) and yield. Unlike previous reports whereby the lentinan was given parenterally, in this study the emphasis was on the oral administration of lentinan. The goal is to document whether the efficacy of the antitumor property is still expressed through this route of administration. DESIGN: Initial study on the action of lentinan was conducted using murine lymphoma (K36) cells in a AKR mouse model. Further investigation on the effectiveness of the extracted lentinan was then performed using human colon-carcinoma cell lines in mice. Six established human colon-carcinoma cell lines segregated into three groups of different degrees of differentiation were used in this study. One group was not fed (control) and the second group was prefed with lentinan for 7 days prior to inoculations with the cancer cells. The size of the tumors that developed was rated after 1 month. RESULTS: Significant regression in tumor formation was observed in prefed mice compared to control (unfed) mice when K36 or human colon-carcinoma cells were used. Significant reductions in the size of the tumors were observed in mice prefed with lentinan. Follow-up investigation proceeded with the use of nude mice (athymic). Lymphocytes extracted from AKR mice prefed with lentinan for 7 days were inoculated into the nude mice. This was then followed by inoculation of the human colon-carcinoma cell lines into these mice. Much smaller tumors were formed in nude mice inoculated with lymphocytes, in contrast to the larger tumor formed in nude mice without lymphocytes inoculation. CONCLUSION: This study showed that the antitumor property of lentinan was maintained with oral administration. In addition, "primed" lymphocytes, when given passively to immunodeficient mice, were able to retard the development of tumors in these mice.

Adjuvants, Immunologic↗
PubMed1996

Lentinan enhances sensitivity of mouse colon 26 tumor to cis-diamminedichloroplatinum (II) and decreases glutathione transferase expression.

We investigated the influence of a combination of lentinan, a biological response modifier, and cis-diamminedichloroplatinum(II) (CDDP) on the growth and glutathione S-transferase (GST) content of colon 26 tumor to examine whether lentinan represses GST expression and enhances the therapeutic effects of CDDP. Female CDF1 mice inoculated subcutaneously with transplantable colon 26 adenocarcinoma cells (1 X 10(6)/mouse) received intraperitoneal administrations of lentinan, CDDP, or the two drugs in combination, on days 10, 14, 17 and 21 after the inoculation. On day 24, tumor weights (estimated from their length and width) were significantly lower in the CDDP+ lentinan group (2.7+/-1.3 g) than in the CDDP alone group (4.3+/-0.7 g, P<0.05), both values being less than in the nontreated control group (7.2+/-1.5 g). The major GST form of colon 26 tumor was identified as GST-II, the Pi class form, and a minor form as GST-III belonging to the Mu class. Both GST-II and GST-III values on day 24 were significantly decreased in the lentinan alone (0.90+/-0.29 and 0.26 +/-0.11 microg/mg protein, respectively) and lentinan + CDDP groups (0.98+/-0.22 and 0.29+/-0.07 microg/mg protein), as compared with the control levels (1.39+/-0.20 and 0.52+/-0.11 microg/mg protein). However, these values were not different between the CDDP alone and lentinan + CDDP groups. Neither tissue interleukin (IL)-6, glutathione nor platinum values were different between the two groups. IL-6 values were elevated in about half of the samples treated with lentinan or CDDP and exhibited a modest inverse correlation with GST-II levels (r= -0.46). A GST inhibitor, ethacrynic acid, enhanced the sensitivity of cultured colon 26 cells to CDDP, suggesting the possible involvement of GST in modulating the cytotoxicity of CDDP to this cell line. These results indicated that lentinan administration decreases tissue GST-II and GST-III contents and enhances the sensitivity of colon 26 tumor to CDDP.

Adenocarcinoma↗
PubMed1982

Antitumor effect of polysaccharide lentinan on MH-134 ascites hepatoma in C3H/He mice.

Lentinan inhibited the proliferation of MH-134 ascites hepatoma transplanted subcutaneously. The best result occurred when 1 mg-2 mg/kg of lentinan was administered for 10 consecutive days from the eighth day after tumor transplantation. Tumor proliferation was 33% inhibited as measured by the average tumor diameter. The average survival (days) when chemotherapy with mitomycin-C (MMC), 5-FU and Ara-C in combination with lentinan, was administered concurrently in the second week of the tumor transplantation was 29.2 days as compared to 20.5 days in the untreated group, 25.1 days in the group given lentinan alone, and 22.0 days in the group receiving chemotherapy alone. When lentinan was administered in combination with bacterial lipopolysaccharide (LPS), the group given lentinan for 5 consecutive days from the third day after tumor transplantation and 30 micrograms LPS i.p. on the thirteenth day, had 70% inhibition of tumor as measured by the average tumor weight. The antitumor activity of lentinan was studied by following changes in macrophage migration inhibition activity (MI). In the untreated group, MI activity disappeared on the 14th day after tumor transplantation. In the group treated with lentinan, spleen cells had positive activity suggesting a restorative action of lentinan on the immune suppression accompanying tumor growth.

Animals↗
PubMed1998

A placebo-controlled trial of the immune modulator, lentinan, in HIV-positive patients: a phase I/II trial.

Lentinan is a beta 1-->3 glucan isolated from Lentinus edodes (Shiitake mushroom) which has immune modulating properties. We have conducted two phase I/II placebo-controlled trials on a total of 98 patients. In one study at the San Francisco General Hospital (SFGH), ten patients each were administered 2, 5, or 10 mg of lentinan or placebo i.v. once a week for eight weeks. In the second study at the Community Research Initiative in New York (CRI), two groups of 20 patients each were administered 1 or 5 mg of lentinan i.v. twice a week for 12 weeks, and ten patients were administered placebo (vehicle containing mannitol plus dextran 40) i.v. twice a week. Entry criteria were an HIV positive test, CD4 levels of 200-500 cells, age 18-60 years, and without current opportunistic infections. This study confirms, in Caucasian subjects also, the good tolerability of lentinan observed in Japanese cancer patients. Side effects were mainly mild, especially when infusion was carried out over a 30-minute period. In the SFGH study, where administration was over a ten minute period, there were nine side effects severe enough to be reported to the FDA (one case each of anaphylactoid reaction, back pain, leg pain, depression, rigor, fever, chills, granulocytopenia and elevated liver enzymes) and there were four patients who discontinued therapy because of side effects. In the CRI study, where infusion was over a 30-minute period, there were no side effects reportable to the FDA and there were four dropouts due to side effects or personal preference. Most side effects resolved promptly after the discontinuation of medication, and all of them were relieved within 24 hours. Patients in the study have shown a trend toward increases in CD4 cells and in some patients neutrophil activity. Because of the small numbers, these values do not have statistical significance. Inasmuch as no side effects such as anemia, leukopenia, pancreatitis or neuropathy were seen, and in view of the positive effects of lentinan on certain surrogate markers (recognizing that these were small studies), we recommended a long-term clinical trial of lentinan in combination with didanosine (ddI) or zidovudine in HIV positive patients. Most patients in these trials did not have measurable p24 levels. In the CRI trials of ten patients with elevated p24 levels, eight on lentinan and two on placebo had decreased p24 levels. Of these decreases, those with lentinan and one with placebo were marked. These results were provocative and needed confirmation. Subsequent to this study, a trial of lentinan in combination with didanosine (ddI) showed a mean increase of 142 CD4 cells/mm3 over a twelve month period, in contrast to a decrease in CD4 cells in patients on ddI alone (Gordon et al. 1995).

Adjuvants, Immunologic↗
PubMed1988

Denaturation and renaturation of a beta-1,6;1,3-glucan, lentinan, associated with expression of T-cell-mediated responses.

Correlation between the higher structure and biological functions of lentinan, a beta-1,6;1,3-glucan capable of potentiating T- and non-T-cell-mediated responses, were investigated by measurements of optical rotation and some biological responses. The addition of urea or dimethyl sulfoxide decreased specific rotation at 589 nm, [alpha]D, of lentinan in a concentration-dependent manner and the removal of these denaturants resulted in the recovery of [alpha]D values. Measurements of optical rotatory dispersion in the spectral region between 600 and 200 nm showed the change in the higher structure of lentinan more clearly. Denaturation and renaturation of lentinan using urea and dimethyl sulfoxide were associated with the decrease and the recovery of antitumor activity against P-815 mastocytoma and vascular dilation and hemorrhage-inducing activity, found to be T-cell-mediated responses. Lentinan was also denatured by NaOH and the transition of [alpha]D values and optical rotatory dispersion curves were seen in the manner of two concentration-dependent phases. Removal of NaOH led to the recovery of optical rotation of lentinan and its antitumor and vascular dilation and hemorrhage-inducing activity. However, recovery of these bioactivities was more difficult in the case of the higher concentrations of NaOH above 2% than the lower ones. During the process of renaturation of lentinan, random aggregation may take place. An increase of serum acute phase proteins, a non-T-cell-mediated response caused by lentinan, was not affected by the change of the higher structure of lentinan.

Acute-Phase Proteins↗
PubMed1987

Antitumor and metastasis-inhibitory activities of lentinan as an immunomodulator: an overview.

The antitumor and metastasis-inhibitory activities, mode of action, and clinical application of lentinan, a strictly purified beta-1,6:beta-1,3-glucan, are reviewed. Lentinan exerts a prominent antitumor effect and prevents chemical and viral oncogenesis. The antitumor action of lentinan is host-mediated. Compared to other well-known immunostimulants, such as bacille Calmette Guérin (BCG), Corynebacterium parvum, and lipopolysaccharide (LPS), lentinan appears to represent a unique class of immunopotentiator, a T cell-oriented adjuvant. Lentinan triggers the increased production of various kinds of bioactive serum factors associated with immunity and inflammation, such as IL-1, CSF, IL-3, vascular dilation inducer, and acute-phase protein inducer, by the direct impact of macrophages or indirectly via lentinan-stimulated T cells, which results in the induction of many immunobiological changes in the host. Augmented IL-1 production amplifies the maturation of immature effector cells to mature cells capable of responding to lymphokines such as IL-2 and T cell-replacing factors. Because of this mode of action, intact T cell compartments for antitumor activity of lentinan are required. Lentinan has little toxic side effects. Excellent results were obtained in a 4 year follow-up of the randomized control study of lentinan in phase III on patients with advanced and recurrent stomach and colorectal cancer.

Adjuvants, Immunologic↗