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ANTI-MALIGNANCY FORMULA


Ingredients
Astragalus membranaceous-Huang Qi
Ganoderma Lucidum-Ling Zhi
Angelica sinensis-Dang Gui
Rehmannia glutinosa-Shu Di
Lycium chinensis-Gou Qi Zi
Ligustrum lucidum-Nu Zhen Zi
Oldenlandia diffusa-Bai Hua She She Cao
Salvia chinensis-Shi Jian Chuan
Scutellaria barbata-Ban Zhi Lian
Lobelia chinensis-Ban Bian Lian
Solanum nigrum-Long Kui
Duchesnea indica-She Mei
Ranunculus ternatus-Mao Zhua Cao
Polygonum bistorta-Quan Shen
Polygonum orientale-Shui Hong Hua Zi
Polygonum cuspidatum-Hu Zhang

Other Ingredients
Starch (rice)



Comments


A1 Anti Malignancy Formula is designed to be compatible with Western medical interventions such as chemotherapy, surgery and radiotherapy. Therefore, for patients with malignant tumours, especially patients especially in middle and late periods during chemotherapy, A1 Anti Malignancy Formula is an effective method in treatment or an adjuvant treatment for promoting rehabilitation.
Professor Zhang, once a student of the famous TCM doctor Shi Jinmo, and now over eighty years old, has explored methods of treating cancers with TCM for over 50 years. In the last ten years, Doctor Zhang has consulted diagnosed, treated 120,000 patients with various cancers, and has developed A1 Anti Malignancy Formula, based on his experiences of supporting the Vital-qi and anti-cancer. His total effective rate was 88.7%. This Chinese herbal medicine, increases immunity, kills cancer cells, restores haematogenous function, remits the disease first and thus gradually cures it, Professor Zhang Renji further modified and improved his formula and worked out the prescription for A1 Anti Malignancy Granules.
The famous text "Huang Di Nei Jin¡¤Su Wen" (Inner Cannon of Yellow Emperor¡¤Plain Questions) says: "The Vital-qi will be impaired where pathogenic factors gather together". The occurrence of tumour, most of all, is closely related to the weakness of Vital-qi. Tumours, obviously an excess syndrome of pathogenic factors, are usually manifested as accumulation of Heat and Toxin and the stagnation of qi and Blood, Phlegm and lumps. Weak Vital-qi and inability to resist the pathogenic factors will cause the lingering of pathogenic factors, and pathogenic factors will impair Vital-qi, and exhaust Essence and Blood so that Vital-qi will be even weaker.
In this formula, Astragalus (huang qi) and Ganoderma (ling zhi, Reishi) are combined to invigorate the Vital-qi, reinforce the Spleen, and strengthen the body. Dang Gui and Rehmannia (shu di huang) are used to nourish Blood and yin. Lycium Fruit (gou qi zi) and Ligustri Fruit (nu zhen zi) can tonify the Liver and Kidney. Above medicines have the Vital-qi-supporting effect of invigorating qi; nourishing Blood, tonifying the Liver and Kidney, supplementing Essence and Marrow, they're the main drugs of this formula. The main drugs are assisted with Oldenlandia (bai hua she she cao), shi jian chua, Herba Scutelleria (ban zhi lian), Herba Lobelia (ban bian lian), Herba Solani (long kui), Fragaria indica (she mei) and Rhizoma Polygoni bistorta (quan shen) etc. to clear Heat, remove Toxin, and remove accumulation of pathogenic Heat and cancer toxin of the tumours.
Adjuvant drugs include Flos Imperata (mao zhua cao), Rhizoma Polygoni cuspidati (hu zhang), Polygonum orientale (shui hong hua zi) that can activate Blood, remove Blood stasis, and dissolve lumps to remove or alleviate the Blood stasis and lumps in cancers and tumours. Thus, the assistant and adjuvant drugs have the effect of removing pathogenic factors and anticancer. The whole formula is a medicine that can support the Vital-qi, remove pathogenic factors, consolidate the constitution, resist cancers and remove lumps. It has the characteristics of combination of expectant and causal treatment, supporting the Vital-qi without causing Evil-lingering and removing pathogenic factors without impairing the Vital-qi.



Research


Astragalus (huang qi)
The in vitro potentiation of LAK cell cytotoxicity in cancer and aids patients induced by F3—a fractionated extract of Astragalus membranaceus
The in vitro induction of LAK cell activity was studied in cancer and AIDS patients. F3, an immuno-regulatory component of Astragalus membranaceus was shown capable of potentiating the LAK cell inducing activity of rIL-2. The killing activity against Hs294T melanoma cell line of LAK cells induced by 50 U/ml rIL-2 in the presence of F3 (55 micrograms/ml) reached 64% which was comparable to that (60%) induced by 500 u/ml of rIL-2 alone. With F3 plus rIL-2, the effector to target cell ratio could be reduced to one-half in order to obtain an equivalent level of cytotoxicity when rIL-2 was used alone. In some patients, whose peripheral blood lymphocytes were relatively inert to rIL-2, F3 could make them responsive to rIL-2. These results imply that F3 may be useful to potentiate LAK cell activity, reduce the amount of rIL-2 and thus minimize the later's toxic side effects when used in vivo.
—Chu DT, Lin JR, Wong W. Zhonghua Zhong Liu Za Zhi. 1994 May;16(3):167-71.

Suppressive effect of Astragalus membranaceus Bunge on chemical hepatocarcinogenesis in rats.
Astragalus membranaceus (AM) has been widely used for treating liver diseases in traditional Chinese medicine. Experimental evidence indicates that it has antitumor potential. In this study, the effect of AM on hepatocarcinogenesis induced by diethylnitrosamine (DEN), two-thirds partial hepatectomy, and 2-acetylaminofluorene (2-AAF) (DEN-PH-AAF) was evaluated using glutathione S-transferase placenta form (GST-P) as marker. First, rats were injected intraperitoneally (i.p.) with DEN (200 mg/kg in saline), a two-thirds partial hepatectomy was carried out 2 weeks later, and the rats were then placed on a basal diet containing 0.02% AAF from week 3 to week 8 to induce hepatocarcinogenesis. The rats were given AM (90 mg/kg or 180 mg/kg body weight) by gavage from week 3 to week 8 (treatment groups). The formation of GST-P-positive foci and the expression of GST-P protein and mRNA caused by DEN-PH-AAF were reduced in the treatment groups, which clearly suggests that AM is effective in delaying DEN-PH-AAF-induced hepatocarcinogenesis.
—Cui R, He J, Wang B, Zhang F, Chen G, Yin S, Shen H. Cancer Chemother Pharmacol. 2003 Jan;51(1):75-80. Epub 2002 Nov 26.

3. Effect of Astragalan on secretion of tumor necrosis factors in human peripheral blood mononuclear cells
The extracts of Astragalus membranaceus have been further isolated by liquid chromatography. One of the fractions (Astragalan, M.W. 20, 000-25, 000) could enhance the secretion of tumor necrosis factor (TNF) from human peripheral blood mononuclear cells (PBMC) in vitro. After isolation of adherent and nonadherent mononuclear cells from PBMC, Astragalan increased the secretion of TNF-alpha and TNF-beta respectively. These results suggest further study of Astragalan would promote the application of Astragalan in cancer immunotherapy.
—Zhao KW, Kong HY. Zhongguo Zhong Xi Yi Jie He Za Zhi. 1993 May;13(5):263-5, 259.

Ganoderma (ling zhi, Reishi)
Prevention of Triterpenoids Isolated from Ganoderma Lucidum on Oral Carcinoma and Its Effects on Cells.
Objective: To discuss the inhibition mechanism of ganoderma triterpenoids in the development and progression of oral cancer. Methods: We established two hamster cheek pouch dynamic cancer animal models and examined the expression of caspase -3 by immunohistochemistry technology. The data was analyzed with jmtjrj 10.34. Results: In the whole dynamic carcinogenesis observation period, the occurrence of two groups’histological difference was significant (P<0.01). The severity in group A was always lower than that in group B. Immunohistoehemical study of caspase-3 showed that its expression gradually strengthened with the development of epithelial lesions. In different lesions from normal, simple hyperplasia, dyspiasia to carcinoma, the positive stainings of group A were slightly lower than those of group B. There was no significant difference in the normal and simple hyperplasia between group A and B by rank sum test. However, there was a significant difference in dysplasia and carcinoma between group A and B(P<0.05). Conclusion: Ganoderma triterpenoids can inhibit carcinoma of the oral mucosa. Ganoderma triterpenes might not play a role in apoptosis, conversely, it might exhibit directly a cytotoxic effect..
—ZHANG Juan, GAO Wen -xin, WANG Xiang, Wei Xiufeng, Cai Yan, Wang Jiafeng. Kou Qiang Yi Xue Yan Jiu. 2008; 24(5): 487-490.

Experimental study of the inhibition of triterpenoids isolated from ganoderma lucidum on the development of oral squamous cell carcinoma
Objective: To discuss the inhibition mechanism of Ganoderma triterpenoids on the development and progression of oral cancer. Methods : 60 hamster cheek pouch dynamic cancer animal models were established and divided into two groups. A group was treated with Ganoderma triterpenoids, B group was as control. The expression of VEGF were detected with immunohistochemistry method. The data was analyzed with CS10.34. Results : The pathological results showed that the normal epithelial cases of group A (Ganoderma triterpenoids group) were more than those of group B(the control group)and the epithelial dysplasia rate was significantly lower than group B(P<0.01) on 6th week. On 9th week the rates of moderate and severe epithelial dysplasia and carcinoma were lower in group A than in group B(P<0.05). On 12th week the cancer rate was significantly lower in group A than that in group B(P<0.01). In the whole dynamic carcinogenesis observation period, the occurrence of two groups’histological difference was significant(P<0.01). The severity in group A was still lower than that in group B and the grade of cancer induced was lower. Immunohistochemical study showed that the expression of VEGF gradually strengthened with the development of squamous cell carcinoma from normal mucosa. There were significant differences on the three grades, the simple hyperplasia, dysplasia and carcinoma information, of group A and B by rank sum test (P<0.05). Conclusion: Ganoderma triterpenoids can inhibit carcinoma of the oral mueosa and showed significant inhibition of angiogenesis. It can be used for oral squamous cell carcinoma treatment..
—ZHANG Juan, GAO Wenxin, WANG Xiang, WEI Xiufeng, CAI Yan, WANG Jiafeng. Shi Yong Kou Qiang Yi Xue Za Zhi. 2008; 24(6): 784-788.

The Inhibition Effect on Mouse Melanoma Cells Train by Ganoderma Lucidum Polysaccharides in Vitro
Objective: To investigate the inhibition effect of Ganoderma lucidum polysaecharides on mouse melanoma cells of B16F10 in vitro. Method: Proliferation effects of Ganoderma lucidum polysaccharides on B16F10 cells, one of mouse melanoma cell lines, were tested by MTT assay, and the cytotoxicity on these cells was detected by flow cytometry. Result: The proliferation of B16F10 cells were inhibited after co-cultured with ganoderrna lucidum polysaccharides, and the death proportion of B16F10 cells was increased. Conclusion: Ganoderma lucidum polysaccharides maybe inhibit the proliferation of B16F10 cells by inducing cell death..
—QI Man, Shao Xuezhai, Song Youxing, Sun Lixin, Song Ji, Xing Enhong. He Bei Yi Xue. 2009; 15(4): 400-402.

Effects of polysaccharides from ferment liquid of bioconverted Chlorella pyrenoidosa by Ganoderma lucidum on immunological function of tumor-beard mice
Ganoderma lucidum could break cell wall of Chlorella pyrenoidosa and produce bioconverted-polysaccharides when C. pyrenoidosa powder was appended in basic medium of G. lucidum. Effects on immunological function of tumor-beard mice were studied though comparing the polysaccharides from basic media with bioconverted-polysaccharides. The result showed the bioconverted polysaccharides could significantly increase the number of white blood cell, the proliferation of lymphocytes, and the phagocytic function by macrophages at the optimum dose. Therefore, the anti-tumor effect was enhanced significantly..
—YANG Congfa, DING Zhongyang, ZHANG Kechang. Zhong Guo Niang Zao. 2009; (6): 54-57.



 
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