Maitake D-Fraction enhances antitumor effects and reduces immunosuppression by mitomycin-C in tumor-bearing mice

Nutrition ◽  
2005 ◽  
Vol 21 (5) ◽  
pp. 624-629 ◽  
Author(s):  
Noriko Kodama ◽  
Yukihito Murata ◽  
Akihiro Asakawa ◽  
Akio Inui ◽  
Masahiko Hayashi ◽  
...  
Keyword(s):  
Mitomycin C ◽  
Antitumor Effects ◽  
Tumor Bearing

scholarly journals Ganoderma formosanum Exopolysaccharides Inhibit Tumor Growth via Immunomodulation

2021 ◽  
Vol 22 (20) ◽  
pp. 11251
Author(s):  
Hsing-Chun Kuo ◽  
Yen-Wenn Liu ◽  
Chi-Chin Lum ◽  
Kai-Di Hsu ◽  
Shin-Ping Lin ◽  
...  
Keyword(s):  
Tumor Growth ◽  
Carcinoma Cell ◽  
Culture Conditions ◽  
Lymphocyte Subpopulation ◽  
Mice Model ◽  
Cytokine Mrna ◽  
Antitumor Effects ◽  
Tumor Bearing ◽  
Therapeutic Model ◽  
Ganoderma Formosanum

Ganoderma formosanum (GF) is a medicinal mushroom endemic to Taiwan. Previous research established the optimal culture conditions to produce exopolysaccharide rich in β-glucan (GF-EPS) from submerged fermentation of GF. The present study investigated the antitumor effects of GF-EPS in a Lewis lung carcinoma cell (LLC1) tumor-bearing mice model. In the preventive model, GF-EPS was orally administered to mice before LLC1 injection. In the therapeutic model, GF-EPS oral administration was initiated five days after tumor cell injection. The tumor size and body weight of the mice were recorded. After sacrifice, the lymphocyte subpopulation was analyzed using flow cytometry. Spleen tissues were used to analyze cytokine mRNA expression. The results showed that GF-EPS (80 mg/kg) effectively suppressed LLC1 tumor growth in both the preventive and therapeutic models. GF-EPS administration increased the proportion of natural killer cells in the spleen and activated gene expression of several cytokines. Our results provide evidence that GF-EPS promotes tumor inhibition through immunomodulation in tumor-bearing mice.

scholarly journals Antitumor effects of melanin fromLachnumYM226 and its derivative in H22 tumor-bearing mice

MedChemComm ◽  
2018 ◽  
Vol 9 (6) ◽  
pp. 1059-1068 ◽  
Author(s):  
Fang Shi ◽  
Jinglei Li ◽  
Ziyang Ye ◽  
Liuqing Yang ◽  
Tingting Chen ◽  
...  
Keyword(s):  
Antitumor Effect ◽  
Antitumor Effects ◽  
Tumor Bearing

LM and ALM showed notable antitumor effect in H22 tumor-bearing mice and ALM was more effective.

The antitumor effects of Qigong-emitted external Qi and its influence on the immunologic functions of tumor-bearing mice

1991 ◽  
Vol 11 (4) ◽  
pp. 253-256 ◽  
Author(s):  
Lei Xue-feng ◽  
Bi Ai-hua ◽  
Zhang Zhi-xiang ◽  
Cheng Zheng-yao
Keyword(s):  
Antitumor Effects ◽  
Tumor Bearing

scholarly journals Antitumor effects of ethanol extracts from Hyptis Rhomboidea in H22 tumor-bearing mice

2017 ◽  
Vol 13 (52) ◽  
pp. 571 ◽  
Author(s):  
Fang-Rong Cheng ◽  
Hong-Xin Cui ◽  
Lu Tang ◽  
Ke Yuan
Keyword(s):  
Antitumor Effects ◽  
Tumor Bearing ◽  
Ethanol Extracts

scholarly journals In vivo induction of terminal differentiation of malignant myelopoietic progenitor cells by CSF-inducing biological response modifiers

Blood ◽  
1986 ◽  
Vol 67 (4) ◽  
pp. 980-987
Author(s):  
E Schlick ◽  
FW Ruscetti
Keyword(s):  
Bone Marrow ◽  
Tumor Cells ◽  
Tumor Therapy ◽  
Terminal Differentiation ◽  
Biological Response ◽  
Biological Response Modifiers ◽  
Therapeutic Effects ◽  
Antitumor Effects ◽  
Tumor Bearing

We have investigated the mechanisms by which colony-stimulating factor (CSF)-inducing biological response modifiers (BRM) may have beneficial effects on tumor-bearing hosts undergoing anti-tumor therapy. First, we have documented that treatment of mice with the chemically defined BRM maleic anhydride divinyl ether copolymer (MVE-2), which induces CSF secretion by macrophages (M phi) and bone marrow cells (BMC), significantly increased growth and differentiation of normal myelopoietic cells and counteracted the myelosuppressive effects of cyclophosphamide (CY). Second, we established that MVE-2 may exert CSF- mediated antitumor effects on certain leukemic tumor cells. Serum from mice pretreated in vivo with MVE-2, which contained CSF, induced terminal differentiation of cloned tumor cells from the CSF responsive WEHI-3B D+ subline in vitro, but not from the WEHI-3B D- subline, which is unresponsive to CSF. In vivo experiments showed that treatment of mice bearing the WEHI-3B D+ tumor first with CY and three days later with the CSF inducer MVE-2, significantly increased their survival time and rendered 20% to 50% of the tumor-bearing mice disease free. No such effects were obtained in mice bearing the WEHI-3B D- tumor. Thus, the induction of CSF or other differentiation factors by some BRMs may result in therapeutic effects against certain leukemias based on at least two distinct mechanisms: In addition to their restorative effects on normal bone marrow functions, CSF-inducing BRMs may also prevent further leukemogenesis by induction of terminal differentiation of leukemic cells.

scholarly journals Passive immunization against tumor necrosis factor partially abrogates interleukin 2 toxicity.

1989 ◽  
Vol 170 (3) ◽  
pp. 1015-1020 ◽  
Author(s):  
D L Fraker ◽  
H N Langstein ◽  
J A Norton
Keyword(s):  
Neutralizing Antibodies ◽  
Tumor Necrosis ◽  
Pulmonary Metastases ◽  
Interleukin 2 ◽  
Passive Immunization ◽  
Therapeutic Index ◽  
Antitumor Effects ◽  
Tumor Bearing ◽  
And Control ◽  
Necrosis Factor

Passive immunization against TNF allowed non-tumor-bearing C3H/HEN mice and tumor-bearing C57BL/6 mice to tolerate significantly more doses of IL-2 before death (p less than 0.005 and p less than 0.001, respectively). The antitumor effect of IL-2 against both 3-d and 10-d pulmonary metastases was maintained in mice treated concurrently with neutralizing antibodies to TNF. In one experiment with 10-d pulmonary metastases, increased administration of IL-2 made possible by passive immunization against TNF significantly improved the antitumor response compared to equitoxic doses of IL-2 and control antibody. The results indicate that TNF is a mediator of IL-2 toxicity but contributes minimally to the antitumor effects of IL-2. Strategies to inhibit TNF may improve the therapeutic index of IL-2 as a neoplastic agent.

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