On the basis of standard laboratory tests and animal models used to screen anticancer drugs, there is little evidence to support a specific cancer -killing ability for laetrile. These investigations used numerous cultured cell lines and tumor models, and they explored the following issues: (1) whether laetrile, given alone or in combination with other substances, exhibits anticancer activity of any kind; (2) the toxic effects associated with laetrile treatment; (3) the location of laetrile breakdown in the body and how this breakdown occurs; and (4) the route(s) of excretion for laetrile and its breakdown products.
Animal studies of laetrile have used rodents,[1,2,3,4,5,6,7,8,9,10,11,12] dogs,[13,14,15] rabbits, and a cat. Early work led to the hypothesis that enzymes were necessary to release cyanide from amygdalin. When high levels of these enzymes were present, symptoms of cyanide poisoning were more pronounced.[1,15] In two studies sponsored by the National Cancer Institute and published in 1975, various rodent cancers (osteogenic sarcoma, melanoma, carcinosarcoma, lung carcinoma, and leukemia) were transplanted into rats and mice.[2,3] In both studies, the animals were treated with intraperitoneal injections of amygdalin, with or without the enzyme beta-glucosidase. None of the solid tumors or leukemias that were investigated responded to amygdalin at any dose that was tested. No statistically significant increase in animal survival was observed in any of the treatment groups. Similar results were obtained in another study using human breast and colon cancer cells implanted into mice (xenograft models). Amygdalin at every dose level tested produced no response either as a single agent or in combination with beta-glucosidase. It was discovered that animals experienced more side effects when beta-glucosidase was given concurrently (at the same time) with amygdalin, compared with amygdalin alone.[2,3]
Melanoma is a malignant tumor of melanocytes, which are the cells that make the pigment melanin and are derived from the neural crest. Although most melanomas arise in the skin, they may also arise from mucosal surfaces or at other sites to which neural crest cells migrate, including the uveal tract. Uveal melanomas differ significantly from cutaneous melanoma in incidence, prognostic factors, molecular characteristics, and treatment. (Refer to the PDQ summary on Intraocular (Uveal) Melanoma Treatment...
Additional cell culture and animal studies involving more than a dozen other tumor models have been published.[1,4,5,7,8,10,11,16,17,18,19,20] In one study, preliminary findings by one of the principal investigators that amygdalin inhibited the growth of primary tumors and the incidence of lung metastases in mice bearing spontaneous (not treatment-induced) mammary adenocarcinomas could not be confirmed. However, positive results were obtained in four studies.[11,17,18,20]