-IBIS-1.7.6-
tx
urinary system
bladder cancer
Nutrition

dietary guidelines

eating principles:
• several short-medium length alkaline fasts interspersed by 3 week eating intervals

therapeutic foods:
• burdock root, squash, watercress
• foods rich in Vitamins A, C, E and B-complex

fresh juices:
• carrot (Walker, p. 129)
• carrot and spinach (Walker, p. 129)
• carrot, beet, and cucumber (Walker, p. 129)
• grape juice fast (Brandt)

recommendations for all cancers:
• seaweeds, mushrooms - Chinese black and Shiitake, figs, beets, beet tops, papaya, mung beans, licorice, sea cucumbers, carrot, garlic, walnut, lychee fruit, mulberries, asparagus, pumpkin, burdock, dandelion greens, white fungus, taro roots, pearl barley, grains, fresh fruits and vegetables (Ni, pp. 108-109)

specific remedies:
• soup of black or ling zhi mushrooms and white fungus, three times daily (Ni, pp. 108-109)
• boil together mung beans, pearl barley, adzuki beans, and figs (Ni, pp. 108-109)
• dandelion, burdock, and chrysanthemum flower tea (Ni, pp. 108-109)

avoid:
• meat, chicken, coffee, cinnamon, anise, pepper, dairy products, spicy foods, high fat foods, nitrate-containing foods, smoking, constipation, stress


supplements

• Lactobacillus acidophilus and other probiotc bacterial flora
Megadose vitamins: In a randomized clinical trial involving 65 patients with biopsy confirmed transitional cell carcinoma of the bladders, researchers found decreased bladder tumor recurrence in those given RDA multivitamins plus 40,000 units vitamin A, 100 mg. vitamin B6, 2,000 mg. vitamin C, 400 units vitamin E and 90 mg. zinc along with BCG (bacillus Calmette-Guerin) immunotherapy. (Lamm DL, et al. J Urol 1994 Jan;151(1):21-26.)
• Vitamin C to tolerance
• Vitamin A
• Vitamin B-complex
• Vitamin B6
• Vitamin E
• Lecithin
• Zinc (Bastyr)
• Shark cartilage: 2 g per kg body weight, per day, to inhibit angiogenesis (growth of new blood vessels) in and to tumors. While anecdotal claims of efficacy are widespread no large scale, well-designed clinical research on the efficacy of cartilage for the treatment of cancer have been conducted so no conclusive evidence is available.
(Lane, 1992)
• Vitamins C and E for patients using adriamycin: antioxidants, specifically reduces cardiac toxicity of adriamycin (Doxorubicin) (Fujita, et al., 1982, 42: p. 309-316; Ellison, 1985; 37 (3): 112-113; Am Heart J, 1986; 111: p. 95)

» drug interactions:
• Vitamins B1, B2, B3, Vitamin K and folic acid can become deficient in patients using chemotherapy due to consequent anorexia, damage to the digestive tract, and malabsorption (Dreizen, et al., 1990; 87 (1): 163-170)
• Vitamin K has been found to potentiate various chemotherapeutic drugs in animals (Taper, et al., 1987; 40: 575-579)
• Vitamin A and cancer chemotherapy, esp. fluorouracil (5-FU): vitamin A enhances antitumor effect in animals (Nakagawa, et al., 1985; 76: 887-894)


footnotes

Akaza H. New strategy of biochemoprevention on recurrence of superficial bladder cancer based on a hypothesis of the mechanism of recurrence. Gan To Kagaku Ryoho 1997;24 Suppl 1:253-256.

Aso, Y, Akazan H. Prophylactic effect of a Lactobacillus casei preparation on the recurrence of superficial bladder cancer. BLP Study Group. Urol Int 1992;49:125-129.

Aso, Y, Akaza H, Kotake T, et al. Preventive effect of a Lactobacillus casei preparation on the recurrence of superficial bladder cancer in a double-blind trial. The BLP Study Group. Eur Urol 1995;27:104-109.

Folkman J, Klagsburn M. Angiogenic factors. Science. 1987;235:442-447.

Folkman J, Cotran R. Relation of vascular proliferation to tumor growth. Int Rev Exp Pathol. 1976;16:207-248. (Review)

Folkman J. The vascularization of tumors. Sci Am. 1976 May;234(5):58-64, 70-73.

Horsman MR, Alsner J, Overgaard J. The effect of shark cartilage extracts on the growth and metastatic spread of the SCCVII carcinoma. Acta Oncol 1998;37(5):441-445.
Abstract: This study was designed to investigate the potential of shark cartilage extracts to inhibit the growth and metastatic spread of a murine solid tumour. The SCCVII carcinoma, implanted in the right rear foot of C3H mice, was used. Following tumour implantation, two different commercially available extracts of shark cartilage (Sharkilage and MIA Shark Powder) were dissolved in water and orally administered to the mice at doses that ranged from 5 to 100 mg per mouse. These injections were repeated on a daily basis for up to 25 days post-implantation of the primary tumour. Compared to non-drug-treated animals, daily administration of the shark cartilage extracts did not show any adverse toxicity (as measured by changes in body weight and lethality). More importantly, none of the shark cartilage doses tested had any retarding effect on the growth of the primary tumour, nor did they inhibit the development of metastases seen in the lungs of the tumour-bearing mice at autopsy. In conclusion, our results offer no support for the proposed use of shark cartilage extracts as an anti-cancer therapy.

Hunt TJ, Connelly JF. Shark cartilage for cancer treatment. Am J Health-System Pharm 1995 August 15;52:1756,1760.

Lamm DL, Riggs DR, Shriver JS, vanGilder PF, Rach JF, DeHaven JI. Megadose vitamins in bladder cancer: a double-blind clinical trial. J Urol 1994 Jan;151(1):21-26.
Abstract: Epidemiological and laboratory studies suggest that vitamin supplements may be helpful in the prevention of some cancers but clinical trials to date have failed to demonstrate protection with naturally occurring vitamins. Without substantiation of the highly touted benefits of vitamins, few physicians who care for cancer patients have recommended their use. A total of 65 patients with biopsy confirmed transitional cell carcinoma of the bladder enrolled in a randomized comparison of intravesical bacillus Calmette-Guerin (BCG) with or without percutaneous administration was also randomized by closed envelope to therapy with multiple vitamins in the recommended daily allowance (RDA) versus RDA multivitamins plus 40,000 units vitamin A, 100 mg. vitamin B6, 2,000 mg. vitamin C, 400 units vitamin E and 90 mg. zinc. The addition of percutaneous BCG did not significantly lessen tumor recurrence but recurrence after 10 months was markedly reduced in patients receiving megadose vitamins. The 5-year estimates of tumor recurrence are 91% in the RDA arm and 41% in the megadose arm (p = 0.0014, Mantel-Cox). Overall recurrence was 24 of 30 patients (80%) in the RDA arm and 14 of 35 (40%) in the high dose arm (p = 0.0011, 2-tailed Fisher's exact test). Megadose vitamins A, B6, C and E plus zinc decrease bladder tumor recurrence in patients receiving BCG immunotherapy. Further research will be required to identify which ingredient(s) provide this protection.

Lane AW, Contreras E Jr. High rate of bioactivity (reduction in gross tumor size) observed in advanced cancer patients treated with shark cartilage material. J Naturopathic Med 1992;3:86-88.

Lane IW, Comac L. Sharks Don't Get Cancer: How Sharks Cartilage Could Save Your Life. Avery, 1992.

Lane IW. 60 Minutes. July 11, 1993 transcript.

Langer R, Conn H, Vacanti J, Haudenschild C, Folkman J. Control of tumor growth in animals by infusion of an angiogenesis inhibitor. Proc Natl Acad Sci U S A. 1980 Jul;77(7):4331-4335.
Abstract: Angiogenesis and tumor growth were inhibited in two different animal models by regional infusion of a partially purified cartilage extract. In rabbits bearing corneal implants of V2 carcinoma and receiving the inhibitor, vascular growth rates were < 3% of those in control animals receiving either Ringer's solution or bovine trypsin inhibitor (Trasylol). Subconjunctival B16 melanoma implants in mice receiving the inhibitor weight < 2.5% of implants in mice receiving Ringer's solution, Trasylol, or albumin. Histologic study of major organs and standard blood tests revealed no toxic effects in any of the animals. The inhibitor did not retard the growth of either tumor cell type in tissue culture at concentrations as high as 1 mg/ml. These results suggest that the cartilage factor does not interfere with the growth of the tumor cell population directly but that it prevents tumor growth by inhibiting angiogenesis.

Langer R, Brem H, Falterman K, Klein M, Folkman J. Isolations of a cartilage factor that inhibits tumor neovascularization. Science. 1976 Jul 2;193(4247):70-72.
Abstract: A cartilage fraction isolated by guanidine extraction and purified by affinity chromatography inhibits tumor-induced vascular proliferation and consequently restricts tumor growth. This fraction contains several different proteins; the major one has a molecular weight of about 16,000. The fraction strongly inhibits protease activity.

Lee A, Langer R. Shark cartilage contains inhibitors of tumor angiogenesis. Science 1983 Sep 16;221(4616):1185-1187.
Abstract: Shark cartilage contains a substance that strongly inhibits the growth of new blood vessels toward solid tumors, thereby restricting tumor growth. The abundance of this factor in shark cartilage, in contrast to cartilage from mammalian sources, may make sharks an ideal source of the inhibitor and may help to explain the rarity of neoplasms in these animals.

Mathews J. Media feeds frenzy over shark cartilage as cancer treatment. J National Cancer Institute 1993 Aug 4;85(15):1190-1191.

Mathews J. Sharks still intrigue cancer researchers. J National Cancer Institute 1992 July 1;84(13):1000-1002.

McGuire TR, Kazakoff PW, Hoie EB, Fienhold MA. Antiproliferative activity of shark cartilage with and without tumor necrosis factor-alpha in human umbilical vein endothelium. Pharmacotherapy. 1996 Mar-Apr;16(2):237-244.

Miller DR, Anderson GT, Stark JJ, Granick JL, Richardson D. Phase I/II trial of the safety and efficacy of shark cartilage in the treatment of advanced cancer. J Clin Oncol 1998 Nov;16(11):3649-3655.
Abstract: PURPOSE: Patients with cancer and chronic inflammatory disorders have used shark cartilage (SC) preparations for many years. Preclinical studies that support their beneficial effects are scanty, and reports of clinical trials have been anecdotal. The proposed mechanisms of antitumor action include direct or indirect inhibition of angiogenesis. Because of the emerging use of SC as an alternative to conventional cancer therapy, this trial was launched to evaluate the safety and efficacy of SC. PATIENTS AND METHODS: Sixty adult patients with advanced previously treated cancer (breast, 16 patients; colorectal, 16 patients; lung, 14 patients; prostate, eight patients; non-Hodgkin lymphoma, three patients; brain, one patient; and unknown primary tumor, two patients) were enrolled. Eligibility criteria included confirmation of diagnosis, resistance to conventional therapy, objective measurable disease, life expectancy of 12 weeks or greater, Eastern Cooperative Oncology Group (ECOG) performance status of 0 to 2, no recent or concomitant anticancer therapy, no prior SC, and informed consent. Patients underwent evaluation of the extent of disease, quality-of-life score (Functional Assessment of Cancer Therapy-General [FACT-G] scale), and hematologic, biochemical, and selected immune function studies at baseline and after 6 and 12 weeks of SC therapy. The dose of SC was 1 g/kg daily orally in three divided doses. Standard criteria were used to evaluate adverse events and response. RESULTS: Ten of 60 patients were lost to follow-up(LTFU) or refused further treatment (RFT) before the 6-week evaluation and were not assessable for toxicity and response. Three patients with stable disease at 6 weeks were LTFU or RFT thereafter. Of the 47 fully assessable patients, five were taken off study because of gastrointestinal toxicity or intolerance to SC. Progressive disease (PD) at 6 or 12 weeks occurred in 22 and five patients, respectively. Five patients died of PD while undergoing SC therapy. No complete (CRs) or partial responses (PRs) were noted. Median time to tumor progression in the entire study population was 7+/-9.7 weeks (mean, 11.4 weeks; range, 3.7 to 45.7 weeks). Ten (20%) of 50 assessable patients, or 16.7% of the 60 intent-to-treat patients, had stable disease (SD) for 12 weeks or more. The median time to tumor progression was 27 weeks, the mean was 28.8+/-9.9 weeks, and the range was 18.6 to 45.7 weeks. In this subset, FACT-G scores improved in four patients, were unchanged in four patients, and declined in two patients. Twenty-one adverse events (grade 1, eight events; grade 2, seven events; and grade 3, six events) were recorded, 14 of which were gastroenterologic (nausea, vomiting, constipation). CONCLUSION: Under the specific conditions of this study, SC as a single agent was inactive in patients with advanced-stage cancer and had no salutary effect on quality of life. The 16.7% rate of SD was similar to results in patients with advanced cancer treated with supportive care alone.

Moses MA. A cartilage-derived inhibitor of neovascularization and metalloproteinases. Clin Exp Rheumatol. 1993 Mar-Apr;11 Suppl 8:S67-69. (Review)

Oikawa T, Ashino-Fuse H, Shimamura M, Koide U, Iwaguchi T. A novel angiogenic inhibitor derived from Japanese shark cartilage (I). Extraction and estimation of inhibitory activities toward tumor and embryonic angiogenesis. Cancer Lett. 1990 Jun 15;51(3):181-186.

Ono M, Izumi H, Yoshida S, Goto D, Jimi S, Kawahara N, Shono T, Ushiro S, Ryuto M, Kohno K, Sato Y, Kuwano M. Angiogenesis as a new target for cancer treatment. Cancer Chemother Pharmacol. 1996;38 Suppl:S78-82. (Review)
Abstract: Neovascularization is often required for rapid growth of solid tumors and also limits vascular metastasis of tumor cells. Neovascularization-targeting agents are a recent innovation that may be a novel means of anticancer therapy. These antiangiogenic drugs have been developed by targeting cell proliferation of vascular endothelial cells, basement-membrane-degrading enzymes, angiogenic factors/receptors, extracellular matrix, angiogenesis signaling, and cell-cell/cell-matrix interactions. In this report, we describe how tumor angiogenesis occurs and how antiangiogenic agents are developed.

Pauli BU, Memoli VA, Kuettner KE. Regulation of tumor invasion by cartilage-derived anti-invasion factor in vitro. J Natl Cancer Inst. 1981 Jul;67(1):65-73.

Sheu JR, Fu CC, Tsai ML, Chung WJ. Effect of U-995, a potent shark cartilage-derived angiogenesis inhibitor, on anti-angiogenesis and anti-tumor activities. Anticancer Res 1998 Nov-Dec;18(6A):4435-4441.
Abstract: BACKGROUND: A potent angiogenesis inhibitor, U-995, has been purified from the cartilage of the blue shark (Prionace glauca). U-995 is composed of two single peptides with molecular mass of 10 and 14 kDa, respectively. MATERIALS AND METHODS: U-995 was designed to study human umbilical vein endothelial cell (HUVEC) migration and proliferation in vitro and angiogenesis induced by TNF alpha in chicken chorioallantoic membrane (CAM). Furthermore, we determined the ability of U-995 to inhibiting tumor cell growth and metastasis. RESULTS: U-995 (15 and 30 micrograms/ml) markedly inhibited HUVEC migration and, at 15-50 micrograms/ml produced a dose-dependent decline in [3H]-thymidine incorporation. 30 and 50 micrograms/ml of U-995, when added to TNF alpha-induced angiogenesis caused discontinuous and disrupted blood vessels. Moreover, U-995 (30 micrograms/ml) markedly prevented collagenase-induced collagenolysis. In addition, when 200 micrograms U-995 was injected i.p. into mice it suppressed sarcoma-180 cell growth and B16-F10 mouse melanoma cell metastasis in vivo. CONCLUSIONS: These results suggest that the anti-angiogenic effects of U-995 may be be due to interference with the proliferation and migration of HUVECs as well as inhibition of collagenolysis, thereby leading to inhibition of both angiogenesis and tumor cell growth.