Cancer: A single disease with a multitude of manifestions?

Peter Grandics
A-D Research Foundation, 5922 Farnsworth Ct, Carlsbad, CA 92008, USA

Date of Submission	24-Aug-2003
Date of Acceptance	18-Nov-2003
Date of Web Publication	18-Nov-2003

Correspondence Address:

Peter Grandics
A-D Research Foundation, 5922 Farnsworth Ct, Carlsbad, CA 92008
USA.

Source of Support: None, Conflict of Interest: None

DOI: 10.1186/1477-3163-2-9

Abstract

The relationships of critical nutrients such as plant phenolics, vitamins, minerals and lipids are considered with respect to the incidence of a variety of cancers, and analyzed in terms of how these nutrient deficiencies alter immune function, DNA integrity and cell proliferation. With a significant correlation found between cancer and these nutrient deficiencies, the hypothesis is presented here that nutrition could provide a unifying perception of cancer and recast it as a single disease. This further suggests that a coordinated administration of specific, critical nutrients to cancer patients could lead to the reversal of the disease. It is also proposed that the concurrent presence of a variety of nutritional deficiencies in cancer patients requires a multilevel, systemic approach to this disease as opposed to the single active therapeutic agent approach that is the cornerstone of contemporary research and pharmacology.

How to cite this article: Grandics P. Cancer: A single disease with a multitude of manifestions?. J Carcinog 2003;2:9

 

How to cite this URL: Grandics P. Cancer: A single disease with a multitude of manifestions?. J Carcinog [serial online] 2003 [cited 2021 Oct 14];2:9. Available from: https://carcinogenesis.com/text.asp?2003/2/1/9/42438

Introduction
In the 20 ^th century, major structural changes took place in the countries of the developed world. Primarily agrarian societies were transformed into industrial societies with the accompanying migration of the majority of the population into large urban centers. This led to major lifestyle changes with unforeseen consequences. Diet in early 20 ^th century agrarian societies was primarily based on organically produced fresh food. Food production was mainly carried out in relatively small family operations utilizing organic farming methods. By the end of the century, the landscape had completely transformed into large-scale industrial farming, utilizing non-organic production methods along with an industrial processing and distribution system for the majority of essential food items.

Dietary patterns were thoroughly transformed. Data show that per capita energy consumption increased significantly and within that, the fat and animal protein segments more than tripled [1,2]. Although fruit and produce consumption also increased, most of it is not consumed fresh [3]. Due to widespread food processing, the energy density of our foods also increased [1]. The now commonplace refrigeration and freeze storage removed the need for fresh food prepared daily and allowed the distribution of a wide variety of manufactured food products. These changes did not necessarily lead to a quality improvement in our nutrition. Along with these changes, physical activities decreased which may well have contributed to the now-epidemic proportions of obesity in the Western world.

Environmental factors
Although cancer is primarily considered to be genetically linked, it is now well established that diet has a significant effect on cancer incidence [4-6]. In fact, food consumption patterns could provide major insights into cancer risk and prevention despite the fact that their significance is not fully appreciated [7]. The changes in cancer incidence in migrant populations moving from low cancer incidence to high cancer incidence environments clearly demonstrate that environmental factors are more important than genetics [8,9].

Among the developed countries, Japan continues to exhibit the lowest cancer incidence in the major cancers types, including lung, breast and colon carcinomas, although some cancers have increased in incidence due to the introduction of Western dietary practices [10,11]. Notably, immigrant Japanese in California and Hawaii has a much higher incidence of breast and colon cancer [8,9]. In Japan, the consumption of fresh, raw foods continues to remain important even though in all other aspects (industrialization and urbanization) the Japanese have adapted the Western model. In addition, the Japanese have the same risk factors such as smoking, alcohol consumption and sedentary life styles as Westerners. The only notable exception in risk factors is the relative rarity of obesity in Japan, a difference that is also attributable to dietary customs.

Another line of evidence comes from Australia, demonstrating the increase in colon cancer mortality among immigrant populations originating from low-incidence countries [12]. Similar observations were made in some South Pacific Islander groups where the incidence of lung cancer is extremely low despite high rates of smoking [13]. Over the past decades, population-based approaches have identified food classes or nutrients that confer protection from various cancers or enhanced the risk of cancer [14-17]. In fact, there is evidence that dietary manipulations may be protective against 10–70% of all cancers, and may be as high as 50–70% against colon cancer [18,19].

Plant phenolics
Epidemiological studies implicated high-saturated dietary fat and protein as a risk factor for colon cancer and established that high fiber, high fruit and vegetable content are protective [17,18]. The success of the dietary fiber hypothesis [20,21] is particularly intriguing in light of the recognition that the actual protective agent is not the fiber itself, but the cell wall components, phenolic polysaccharides and polyphenols [22-27]. The protective phenolic lignin and hemicellulose components are present in widely different concentrations in the cell walls of various plants and are released by bacterial enzymes in the human colon [23]. Such compounds have been isolated, e.g. from rice bran and green tea, and their cancer protective effects demonstrated [24, 25, 27]. Processed rice bran, however, had no such protective effect [28]. Many of these compounds have antioxidant, anti-mutagenic, anti-carcinogenic and anti-inflammatory effects that may be responsible for their anticancer effects [29].

A readily available source for such phenolic polysaccharides can be located in the nutritional and medical practices of the 19 ^th and early 20 ^th centuries [30,31]. Sugar cane molasses, a widely used nutrient, was served as a sweetener instead of purified sugar, stirred into milk and eaten instead of jam or jelly. It was also a popular medicinal agent:recent analyses demonstrated it to be a rich source of micro- and macronutrients [32]. Blackstrap molasses, its most concentrated form, was used for the therapy of a variety of diseases, including cancer [31]. Anecdotal evidence suggests that cancer was very rare among sugar cane plantation workers who were regularly consuming the raw brown sugar [33]. Blackstrap molasses is rich in a variety of essential minerals including iron, zinc, selenium, magnesium and potassium as well as the majority of the vitamin B complex [33], deficiencies of which confer a major cancer risk [34]. Molasses also contains high concentrations of amino acids and linoleic acid [35], an essential lipid that has a documented anti-tumor effect [36,37].

Cane molasses is fed widely to domestic animals [35]. A feeding study on the phenolic carbohydrate compounds of cane molasses suggested that they are beneficial to both ruminant and non-ruminant animals [38]. The feeding of 8% sugar cane bagasse to broiler chicken demonstrated weight gain and carcass quality as well as elevated immunoglobulin levels [39]. Recent data on cane molasses appear to lend support to historical accounts concerning its effectiveness as both preventative and a possible curative agent for some cancer.

Folate, vitamin B12 and other micronutrients
In the past decade it became apparent that low normal levels of certain vitamins may cause diseases in at-risk populations, such as middle to elderly age groups and pregnant women, and that such abnormalities might be overcome by ensuring high normal plasma levels of the respective vitamins [40-42]. Metabolic defects of folate are associated with circulatory diseases [43,44] as well as neural and cognitive disorders [45]. Folate deficiency has recently been associated with pathogenesis in a variety of malignancies [46-50]. The most understood functions of folate and vitamin B12 are in the area of synthesis of purines and pyrimidines, as well as the maintenance of the methylation process that is essential for regulated cell division [51].

Several lines of evidence, both in vitro and in vivo , suggest that folate deficiency has pro-neoplastic effects. Deoxynucletide pool imbalance and uracil misincorporation into DNA in folate deficient cell lines has been described [52,53]. Enhanced development of colonic neoplasia was observed in a folate-deficient rat model [54,55]. Several human studies demonstrate that folate deficiency may potentiate neoplastic processes and that high dietary folate intake is protective [46-50,56]. It is well established that folate deficiency leads to nucleotide pool imbalance (uracil misincorporation), DNA strand breaks [57,58], hypomethylation of DNA [59-61], increased gene expression [62-64], altered chromatin conformation [63,64], as well as altered cellular proliferation [62,67]. All these phenomena have been associated with carcinogenesis and tumorigenesis.

It has been recommended that patients undergoing chronic methotrexate or other antifolate therapy increase folate intake [68]. In such cases, high dose of folic acid (5 mg/day) have reduced therapy-associated toxicity with apparent preservation of antitumor activity [69]. This supports the view that antifolates act through a direct cytotoxic mechanism [70].

There is a close interrelationship between folate and vitamin B12 in the synthesis, repair and methylation of DNA. In a human clinical trial, a three-month-long supplementation with 3.5 times the Australian Recommended Daily Allowance (RDA) for folic acid and vitamin B12 was found to reduce micronuclei frequency, a DNA damage marker, in healthy young adults by 25% [71]. This study emphasized that supplementation levels higher than the RDA may be required in large populations to minimize DNA damage. Our RDAs were based on information on acute effects, because optimum amounts for long-term health is unknown. However, these data suggest that RDA levels may need to be reevaluated to make sure that adequate levels of these nutrients are available for genomic stability.

Supplementation with folic acid and vitamin B12 has reduced the severity of smoking-induced bronchial metaplasia in humans [72,73], underscoring the importance of these vitamins. Folate and vitamin B12 deficiencies that lead to chromosome breaks affect a significant 10–14% of the U.S. population [74-77]. The two deficiencies may act synergistically. Vitamin B6, which also participates in DNA methylation, was also found to be deficient in about 10% of the U.S. population [76].

Besides the above micronutrients, niacin, iron, selenium and zinc deficiencies that also affect DNA integrity are common in the United States [76,78]. All these data suggest that micronutrient deficiencies, which can mimic radiation or chemical damage to DNA, are affecting a considerable proportion of the U.S. population, and the correction of these deficiencies will be a major public health concern in the coming decades.

Iodine
Iodine is another critical micronutrient, and iodine deficiency has a profound effect on human health [79,80]. Mild to moderate iodine deficiency has been associated with an extraordinarily high occurrence of hyperthyroidism in at-risk populations [81]. Epidemiological studies have established that the incidence of goiter runs parallel to that of thyroid cancer [82-84]. In a rat model, iodine deficiency has been found to be a more efficient tumor promoter than the carcinogen itself [85].

The relationship between thyroid function and breast physiology was strengthened by observations that reproducible breast dysplasia and neoplasia were obtained in iodine deficiency that was reversible with iodine replacement [86,87]. Breast cancer patients as a group were found to have a lower thyroid function than women having conditions unrelated to breast cancer [88].

It has been pointed out that in the U.S., breast cancer tends to occur in geographical areas associated with iodine deficiency [89]. In contrast, in Japan, where iodine intake levels are higher, a much lower breast cancer incidence is observed [90]. Fibrocystic breast disease, a known risk factor for breast cancer, can largely be prevented by iodine supplementation [91]. In this study, molecular iodine was found to be more effective than iodide, the currently favored form of iodine supplementation. In iodine supplementation studies unrelated to cancer, molecular iodine complexed to lipids was also found to be more effective than iodide [92]. It was also reported that iodolipids formed from iodine in the thyroid gland may play a role in providing proliferative control in breast tissue [93]. Another observation is that in old Pharmacopoeias, for oral iodine administration the molecular form was prescribed [94].

While breast cancer rates in Japan have been comparatively low, they have been increasing recently: this has been associated with the “Westernization” of the country’s diet [11]. A study from Spain also established a link between regions of iodine deficiency and breast cancer mortality rates [95]. Traditional Eastern Asian medicine has long used iodine-rich seaweed for cancer treatment [96]. This observation is interesting in light of the fact that in malignant thyroid nodules, the iodine concentration was found to be 15 times lower than in benign nodules [97], demonstrating severe iodine deficiency in the tumor tissue. Recent studies with animal models support the anti-cancer effect of iodine [98,99].

Iodine deficiency has a profound negative effect on the immune system [100]. A significant immune deficiency has been reported among patients with gastric cancer, thyroid cancer and goiter [101]. Iodine was also found to increase immunoglobulin G synthesis in vitro in human lymphocytes [102]. Impaired capacity of immunoglobulin production in active cancer patients has been observed [103], which might be modulated by iodine supplementation. These observations indicate that iodine has a direct effect on the immune system and anticancer defenses.

In 1990, statistics showed that iodine deficiency affected about one-third of the world’s population, and despite efforts to correct this problem, it persists. A recent study from South Africa indicated a significant iodine deficiency country-wide [84]. Another study from Switzerland reported that despite more than 80 years of a national iodine supplementation program, only 24% of the participants in the healthy volunteer group reached the WHO recommended level for dietary iodine intake, indicating a significant iodine deficiency among the Swiss [104]. This result was attributed to the growing consumption of manufactured food products deficient in iodine. Although similar data is not available for the United States, a comparable level of development and the high popularity of manufactured foods suggest that the US situation is likely not much different from that in Switzerland.

Lipids
It has been previously discussed that the essential lipid linoleic acid present in cane molasses has antitumor effects. Such lipids are also found at high concentrations in rose oil [105], which has a history of medicinal use dating back at least 5,000 years. The traditional Indian Ayurvedic medical practice uses oral rose oil for the treatment of a variety of inflammatory conditions, as well as emotional stress [106]. Anti-anxiety effects of rose oil have recently been confirmed [107]. Rose oil is a potent inhibitor of the growth of Helicobacter pylori [108], implicated in the etiology of gastric cancer. Therefore, rose oil may exert a “sanitizing” effect in the gut. It has also been suggested that rose oil may be valuable for human consumption because of its high unsaturated lipid content [105].

The gastrointestinal link
The general processing capacity of the digestive tract plays a critical role in both health and disease. Traditional Indian Ayurvedic medicine states that health requires robust digestion [109]. Under conditions of prolonged stress, the secretion of digestive juices is diminished, reducing the digestive capacity in the gut.

Impaired digestion has been implicated in the pathomechanism of cancer for nearly a century: in 1906, pancreatic proteolytic enzymes were demonstrated to defend the body against cancer [110]. This finding was followed up during the first decade of the century, with the publication of tumor regression as well as remission in terminal cancer patients [111-114]. With the advent of formal science-based medicine in the early 1900s, this approach slipped into oblivion.

Animal studies performed in the 1960s demonstrated the effectiveness of pancreatin therapy for tumors [115,116]. It was also demonstrated that orally ingested pancreatic enzymes pass intact into the intestine, and are re-adsorbed into the circulation during the enteropancreatic recycling process [117,118]. In the 1960s, an alternative physician in Texas developed a pancreatin-based cancer therapy [119] and demonstrated cases of pancreatic cancer patients who survived in excess of 5 years. This was followed up in the late 1990s by a pilot prospective case study with patients having inoperable stage II-IV pancreatic adenocarcinoma [120]. The results suggested a significantly increased survival for patients who received large doses of pancreatic enzymes, vitamins and minerals followed by the detoxification of the intestines. Many medical practitioners in the past included intestinal cleansing as part of their procedures because they recognized the importance of the gut function in health and disease [121-123].

The resident bacterial flora in the digestive tract plays an important role in metabolic activities, nutrient adsorption, immune function, trophic effects on the intestinal epithelia, and protection against alien microbes [124]. A substantial portion of these bacterial populations remains to be described. Diet has a significant effect on the human intestinal flora [125,126], and the promoting effects of the large bowel contents in colonic carcinogenesis are documented both in animal models and man [127]. The activity of colonic bacteria in the release of essential phenolic polysaccharides from plant cell walls has been discussed. Opportunistic bacterial and parasitic infections also occur in cancer [128-131] that amplify the downward spiral of diminishing nutrient processing capacity of the gut. It is therefore critical to cleanse the digestive and excretory system in cancer patients.

Again, if we research the medical practices of the 19 ^th and early 20 ^th centuries, we find that oral sulfur was widely used to “clean out the system” [31]. Sulfur is safe to consume [132] and has a wide spectrum of antibacterial and antiparasitic effects [133]. It is also a potent scavenging agent for toxic heavy metals such as mercury, cobalt or silver that have been reported to concentrate in malignant tissue [97]. Oral sulfur was listed in the Pharmacopoiea [133], but in the second half of the 20 ^th century its medical use was abandoned. Another sanitizing agent both for the gut and the urinary system is apple cider vinegar (ACV). Such use of ACV has a historical record dating back over 3,000 years [134]. In addition, ACV has been used for the treatment of a number of specific conditions [134], which suggests that it has a beneficial systemic effect, much of it remains to be re-discovered by methods of modern medical science.

Subtle energetic properties of nutrients
A subtle energetic aspect of nutrients is a concept that is largely missing from modern nutritional sciences. We are all familiar with the different feeling experienced when consuming a freshly picked fruit versus a stale one that has been sitting for weeks on the shelves of a food distribution outlet. Some Asian cultures attribute such subtle energetic characters to nutrients, e.g., the yin and yang that is related to chi, the life energy believed to animate every living thing. With our food we consume this energy, which enhances its nutritional value. Freshness of food is emphasized in these cultures, as the life energy is gradually lost after harvest. The consumption of raw, fresh foods in Japan has already been correlated with a low incidence of the major forms of cancer.

This concept was impossible to subject to modern scientific analysis until Wilhelm Reich proved experimentally the existence of a life energy field that is not electromagnetic in nature, but can produce thermal and electric effects in a well reproducible and quantifiable manner [135]. A recent academic study has confirmed Reich’s basic findings [136,137]. The incorporation of his methodologies into our working knowledge base could add an exciting new dimension to nutritional science, as we may finally be able to quantify “what health is” and definitively establish what kind of nutrient intake is required for long term health.

Reich also made fundamental contributions to understanding the emotional aspects of the disease process and in particular cancer that he determined to be a manifestation of subtle energetic processes in the body [138]. We are now aware that emotional stress down-regulates the immune system and makes people more prone to cancer [139-142]. Reich’s analysis of the subtle energetic processes in cancer patients and their relationship to those emotional blocks makes his research perhaps the most original and intriguing area of study in the history of 20 ^th century medical science.

Although Reich was occasionally skeptical about a possible unification of his subtle energy-based approach to cancer versus our mechanistic, physico-chemical approach, there seems to be no conflict between these methodologies, and instead I suggest that they merely represent different observational levels of the same reality. The unification of a subtle energetic description of disease processes with our current mechanistic, physico-chemical approach is both inevitable and necessary to solving the mysteries of degenerative diseases such as cancer, which claim so many lives today.

Overcoming tumor adaptation
Acquired drug resistance is a common problem with metastatic cancers, contributing to the deaths of more than 450,000 patients annually in the US [143]. A tumor may respond initially to therapy but recur later with acquired drug resistance, or exhibit an intrinsic resistance from the outset. Multidrug-resistance (MDR) manifests through an ATP-dependent drug efflux pump, the P–170 glycoprotein or MDR pump [144]. Quinine has been found to reverse MDR in a variety of tumor cell lines and has been safely used in combination with chemotherapy with leukemias, myelomas and lymphomas [145-147]. Very little information is available on direct cytotoxic effects of quinine [148].

Quinine has a history in medicine besides its use as an anti-malarial. Quinine was used to treat inflammations and fevers [149] and was prescribed as a body tonic to strengthen the system [149,150]. The beverage Tonic Water has preserved in its name the long-forgotten medicinal origins of quinine. However, the concentration of quinine in Tonic Water today is too low for any beneficial systemic effect. Therefore, the use of quinine in cancer may be warranted both for its anti-inflammatory properties as well as its inhibitory effect on tumor adaptation to therapies.

Discussion
This review has considered several critical nutrient deficiencies that may contribute to the manifestation of a number of cancers, as well as nutrients that have been found deficient in cancer cells. It is also observed that traditional nutritional and medicinal agents used in the past provided a rich supply of these critical nutrients and assisted in the restoration of digestive and excretory functions. Again, blackstrap molasses is a source of plant phenolic compounds, the majority of the vitamin B complex, critical minerals such as iron, zinc, selenium, magnesium and potassium, as well as essential unsaturated lipids.

Rose oil is another historically proven source of essential lipids. Our current understanding on the vital role of folate and vitamin B12 in maintaining DNA integrity and function should prompt us to reevaluate dietary requirements for these essential vitamins. Iodine deficiency, which has been demonstrated in cancer, was also shown to impair the immune system and increase the incidence of several cancers. The disinfecting effects of oral sulfur and apple cider vinegar in the gut and the urinary system help restore digestive and excretory functions, a cornerstone of early medical practice.

A large number of studies demonstrate the inadequacy of Western dietary habits for supplying adequate amounts of critical nutrients and also demonstrate the fundamental role of nutrition in disease prevention and control. Hippocrates, the father of modern medicine stated, “Your food shall be your medicine and your medicine shall be your food.” Currently, both in the public and the scientific community are lacking in their attention to the effects of multiple nutritional deficiencies on the human organism.

It seems reasonable to conclude that a number of coincidental critical nutritional deficiencies can lead to and co-exist in the state of cancer. Disregulation of numerous regulatory and metabolic pathways may occur at multiple levels, eventually leading to the disintegration of metabolic and regulatory networks in terminal cancer. This suggests that cancer is a systemic disease, and that a tumor is likely a late-stage effect rather than the cause of the disease itself. It also explains why cancer typically recurs after the eradication of individual tumors. Therefore, focusing on the cancer cell cannot lead us to understanding the fundamentals of the disease. Here, the results speak for themselves.

It appears unrealistic that we can successfully intervene into this vast out-of-balance network of physiological processes with single active agent therapies and restore balance and health. The time has arrived to abandon one-dimensional thinking and consider the human organism more like a matrix or interconnected system, instead. The large body of available data on metabolic and regulatory processes coupled with methods of information technology should allow us to establish correlations between apparently distant molecular, cellular and physiological events. This would bring a true paradigm shift in our approach to understanding and treating diseases.

The old-time medicinal use of blackstrap molasses, apple cider vinegar, oral sulfur and molecular iodine, rose oil and quinine testifies to a remarkable understanding of human physiology by our ancestors. Such nutritional approach allows a unifying perception of cancer that could recast it as a single disease. This would also suggest that all cancers may arise out of a common cellular/physiological event and, in fact, new evidence points into this direction.

Cancer stem cells for leukemias [151], brain cancer [152] and breast cancer [153] have been described lending support to the 40 years old idea that all cancers may originate from a common progenitor. Thus, evidence is accumulating in support of the view that cancer may actually be a single disease and, as such could be treated by a single therapy.

Our working hypothesis was that by re-supplying critical nutrients to cancer patients in an oral nutritional supplement cocktail and simultaneously cleansing the digestive and excretory systems by using the described methods of past centuries of medicine, we might cure a wide range of or perhaps all types cancers. Essential ingredients of the supplement include blackstrap molasses, apple cider vinegar, sulfur, quinine, rose oil, folic acid, vitamin B12 and molecular iodine [patent pending]. This supplement is currently being tested in a variety of stage III-IV cancer patients refractory to current therapies.

In conclusion, this paper presents the case that multiple, concurrent nutritional deficiencies may play a fundamental role in tumorigenesis and suggests that the disease process could be reversed by re-supplying the required nutrients in adequate amounts. In addition, a new approach to cancer is advocated that would unify our traditional mechanistic, physico-chemical methodologies with subtle energy-based concepts, under the umbrella of contemporary rigorous scientific testing methods.

 References

1.	von Koerber K, Mannle Th, Leitzmann C: Vollwert-Ernahrung. Haug Verlag, Heidelberg; 1993:S37-43.
2.	Weisburger JH, Wynder EL: Dietary fat intake and cancer. Hema­tol Oncol Clin North Am 1991, 5(1):7-23.
3.	Committee on Diet, Nutrition and Cancer: Diet, Nutrition and Cancer, The relationship between nutrients and cancer. Washington DC: National Academy Press 1982:51-66.
4.	Feldman EB: Dietary intervention and chemoprevention-1992 perspective. Prev Med 1993, 22:661-666.
5.	Bowen PE: Dietary intervention strategies: Validity, execution and interpretation of outcomes in Nutrition and Cancer Pre­vention. Edited under the auspices of AICR New York: Kluyver Academic/ Plenum Publishers; 2000.
6.	Rodler I, Zajkas G: Hungarian cancer mortality data and food availability in the last four decades of the 20th century. Nutr Metabol 2002, 46:49-56.
7.	Kune S, Kune GA, Watson LF: Case-control study of dietary eti­ological factors: the Melbourne colorectal cancer study. Nutr Cancer 1987, 9:1-29.
8.	Buell P: Changing incidence of breast cancer in Japanese­American woman. J Natl Cancer Inst 1973, 51:1479-1483.
9.	Kolonel LN, Hankin JH, Lee J, Chu SY, Nomura AM, Hinds MW: Nutrient intakes in relation to cancer incidence in Hawaii. Br J Cancer 1981, 44:332-339.
10.	Parkin DM, Pisani P, Ferlay J: Global cancer statistics. CA Cancer J Clin 1999, 49:33-64.
11.	Tominaga S, Kuroishi T: An ecological study on diet/nutrition and cancer in Japan. Int J Cancer 1997, 10(suppl):2-6.
12.	McMichael AJ, McCall MG, Hartshorne JM, Woodings TL: Patterns of gastrointestinal cancer in European migrants to Australia: the role of dietary change. Int J Cancer 1980, 25:431-437.
13.	Le Marchand L, Hankin JH, Bach F, Kolonel LN, Stacewicz-Sapuntzakis M, Bowen PE, Beecher GR, Laudon F, Baque P, Daniel R, Seruvatu L, Henderson B: An ecological study of diet and lung cancer in the South Pacific. Int J Cancer 1995, 63:18-23.
14.	Block G, Patterson B, Subar A: Fruit, vegetables and cancer pre­vention: a review of the epidemiological evidence. Nutr Cancer 1986, 18:1-29.
15.	Schapira DV: Diet, obesity, fat distribution and cancer in women. J Am Med Wom Assoc 1991, 46:126-130.
16.	Carroll KK, Khor HT: Dietary fat in relation to tumorigenesis. Progr Biochem Pharmacol 1975, 10:308-353.
17.	Negri E, D’Avanzo B, Tavani A: The role of vegetables and fruit in cancer risk. In Epidemiology of Diet and Cancer Edited by: Hill MJ, Giacosa A, Caygill CP. London: Ellis Horwood; 1994:327-334.
18.	Doll R, Peto R: The cause of cancer: quantitative estimates of avoidable risks of cancer in the United States today. J Natl Cancer Inst 1981, 66:1191-1308.
19.	Kim YI: AGA technical review: impact of dietary fiber on colon cancer occurrence. Gastroenterology 2000, 118:1235-1257.
20.	Burkin DS: Related disease-related cause? Lancet 1969, 2:1229-1231.
21.	Department of Health (New Zeeland): Food for health. The report of the Nutrition Task Force to the Department of Health Wellington, NZ Department of Health; 1991.
22.	Bacic A, Harris PJ, Stone BA: Structure and function of plant cell walls. In The Biochemistry of Plants, Carbohydrates Volume 14. Edited by: Preiss J. San Diego, CA: Academic; 1988:297-371.
23.	Kroon PA, Faulds CB, Ryden P, Robertson JS, Williamson H: Release of covalently bound ferulic acid from fiber in the human colon. J Agric Food Chem 1996, 45:661-667.
24.	Hudson EA, Dinh PA, Kokubun T, Simmonds MS, Gescher A: Char­acterization of potentially chemopreventive phenols in extracts of brown rice that inhibit the growth of human breast and colon cancer cells. Cancer Epidemiol Biomarkers Prev 2000, 9:1163-1170.
25.	Ferguson LR, Harris PJ: Protection against cancer by wheat bran: role of dietary fibre and phytochemicals. Eur J Cancer Prev 1999, 8:17-25.
26.	Ferguson LR: Role of plant polyphenols in genomic stability. Mutat Res 2001, 475:89-111.
27.	Graham HN: Green tea composition, consumption and polyphenol chemistry. Prev Med 1992, 21:334-350.
28.	Alberts DS, Martinez ME, Roe DJ, Guillen-Rodriguez JM, Marshall JR: Lack of effect high fiber cereal supplement on the recur­rence of colorectal adenomas. Phoenix Colon Cancer Pre­vention Physician’s Network. N Engl J Med 2000, 342:1156-1162.
29.	Surh Y-J, Choo K-S, Cha H-H, Han SS, Keum YS: Molecular mech­anism underlying chemopreventative activities of anti­inflammatory phytochemicals: downregulation of COX-2 and iNOS through suppression of NF-kB activation. Mutat Res 2001, 480-481:243-268.
30.	Chase AW: Practical Recipes Ann Arbor: Michigan; 1864:142.
31.	Scott C: Crude black molasses New York: Benedict Lust Publications; 1980:23-63.
32.	USDA Nutrient Database for Standard Reference. Release 13 Composition of Foods. Blackstrap molasses .
33.	Scott C: Crude black molasses New York: Benedict Lust Publications; 1980:89.
34.	Ames BA: DNA damage from micronutrient deficiencies is likely to be a major cause of cancer. Mutat Res 2001, 475:7-20.
35.	Mee JML, Coy C, Stanley RW: Amino acid and fatty acid compo­sition of cane molasses. J Food Sci Agric 1979, 30:429-432.
36.	Serrano M, Thompson LU: The effect of flaxseed supplementa­tion on early risk markers for mammary carcinogenesis. Can­ cer Lett 1991, 60:135.
37.	Thompson LU, Rickard SE, Orcheson LJ, Seidl MM: Flaxseed and its lignan and oil components reduce mammary tumor growth at a late stage of carcinogenesis. Carcinogenesis 1996, 17:1373-1376.
38.	Fahey GC, Williams JE, McLaren GA: Influence of molasses lignin­hemicellulose fractions in rat nutrition. J Nutr 1976, 106:1447-1451.
39.	Hegazy RA, El-Faramawy AA: Substitution of sugar cane bagasse in the chicken diet and immune response. Nahrung/Food 2001, 45:364-367.
40.	MRC Vitamin Study Research Group: Prevention of neural tube defects results of the Medical Research Council Vitamin Study. Lancet 1991, 338:131-137.
41.	Daly LE, Kirke PN, Molloy A, Weir DG, Scott JM: Folate levels and neural tube defects. Implications for prevention. JAMA 1995, 274:1698-1702.
42.	Kirke PN, Molloy A, Daly LE, Burke H, Weir DG, Scott JM: Maternal plasma folate and vitamin B12 are independent risk factors for neural tube defects. Q J Med 1993, 86:703-708.
43.	Scott JM, Weir DG: Homocysteine and cardiovascular disease. Q J Med 1996, 89:561-563.
44.	Selhub J, D’Angelo A: Relationship between homocysteine and thrombotic disease. Am J Med Sci 1998, 316:129-141.
45.	Clarke R, Smith AD, Jobst KA, Refsum H, Sutton L, Ueland PM: Folate, vitamin B12 and total homocysteine levels in con­firmed Alzheimer disease. Arch Neurol 1998, 55:1449-1455.
46.	Weir DG, Scott JM: Colonic mucosal folate concentrations and their association with colorectal cancer. Am J Clin Nutr 1998, 68:763-764.
47.	Giovannucci E, Stampfer MJ, Colditz GA, Hunter DJ, Fuchs C, Rosner BA, Speizer FE, Willett WC: Multivitamin use, folate and colon cancer in women in the Nurse’s health study. Ann Intern Med 1998, 129:517-524.
48.	Almadori G, Bussu F, Galli J, Cadoni G, Zappacosta B, Persichilli S, Minucci A, Giardina B: Serum folate and homocysteine levels in head and neck squamous cell carcinoma. Cancer 2002, 94:1006-1011.
49.	Murr C, Berchtold J, Norer B, Waldhart E, Wachter H, Fuchs D: Neopterin as a prognostic parameter in patients with squa­mous cell carcinomas of the oral cavity. Int J Cancer 1998, 79:476-480.
50.	Shrubsole MJ, Jin F, Dai Q, Shu X-O, Potter JD, Herbert JR, Gao Y-T, Zheng W: Dietary folate intake and breast cancer risk: Results from the Shanghai Breast Cancer Study. Cancer Res 2001, 61:7136-7141.
51.	Scott JM, Weir DG: Folic acid, homocysteine and one-carbon metabolism: a review of essential biochemistry. J Cardiovas Risk 1998, 5:223-227.
52.	Wickramashinge SN, Fida S: Misincorporation of uracil into the DNA of folate- and B12 deficient HL60 cells. Eur J Hematol 1993, 50:127-132.
53.	James SJ, Basnakian AG, Miller BJ: In vitro folate deficiency induces deoxynucleotide pool imbalance, apoptosis and mutagenesis in Chinese hamster ovary cells. Cancer Res 1994, 54:5075-5080.
54.	Paspatis GA, Kalafatis E, Oros L, Xourgias V, Koutsioumpa P, Kara­manolis DG: Folate status and adenomatous colonic polyps: a colonoscopically controlled study. Dis Colon Rectum 1995, 38:64-68.
55.	Bird CL, Swendseid ME, Witte JS, Shikany JM, Hunt IF, Frankl HD, Lee ER, Longnecker MP, Haile RW: Red cell and plasma folate, folate consumption, and the risk of colorectal adenomatous pol­yps. Cancer Epidemiol Biomarkers Prev 1995, 4:709-714.
56.	Cravo M, Fidalgo P, Pereira AD, Gouveia-Oliveira A, Chaves P, Selhub J, Mason JB, Mira FC, Leitao CN: DNA methylations as an inter­mediary biomarker in colorectal cancer: modulation by folic acid supplementation. Eur J Cancer Prev 1994, 3:473-479.
57.	Kim Y-I, Pogribny IP, Basnakian AG, Miller JW, Selhub J, James SJ, Mason JB: Folate deficiency in rats induces DNA strand breaks and hypomethylation within p53 tumor suppressor gene. Am J Clin Nutr 1997, 65:45-52.
58.	Kim Y-I, Shirwadkar S, Choi S-W, Puchyr M, Wang Y, Mason JB: Effects of dietary folate on DNA strand breaks within muta­tion-prone exons of the p53 gene in the rat colon. Gastroenter­ ology 2000, 119:151-161.
59.	Cheah MS, Wallace CD, Hoffman RM: Hypomethylation of DNA in human cancer cells: a site specific change in the c-myc oncogene. J Natl Cancer Inst 1984, 73:1057-1061.
60.	Goelz SE, Vogelstein B, Hamilton SR, Feinberg AP: Hypomethyla­tion of DNA from benign and malignant human colon neo­plasms. Science 1985, 228:187-190.
61.	Adany R, Iozzo R: Hypomethylation of the decorin proteogly­can gene in human colon cancer. Biochem J 1991, 276:301-306.
62.	Baylin SB, Herman JG: DNA hypermethylation in tumorigene­sis: epigenetics joins genetics. Trends Genet 2000, 16:168-174.
63.	Feinberg AP, Vogelstein B: Hypomethylation of the ras onco­genes in primary human cancers. Biochem Biophys Res Commun 1983, 111:47-54.
64.	Sharrard RM, Royds JA, Rogers S, Shorthouse AJ: Patterns of meth­ylation of the c-myc gene in human colorectal cancer pro­gression. Br J Cancer 1992, 65:667-672.
65.	Keshet I, Lieman-Hurwitz J, Cedar H: DNA methylation affects the formation of active chromatin. Cell 1986, 44:535-543.
66.	Lewis J, Bird A: DNA methylation and chromatin structure. FEBS Lett 1991, 285:155-159.
67.	Jones PA, Laird PW: Cancer epigenetics coming of age. Nat Genet 1999, 21:163-167.
68.	Morgan SL, Baggott JE, Vaughn WH, Austin JS, Veitch TA, Lee JY, Koopman WJ, Krumdieck CL, Alarcon GS: Supplementation with folic acid during methotrexate therapy for rheumatoid arthritis. A double-blind, placebo-controlled trial. Ann Intern Med 1994, 121:833-841.
69.	Calvert H: Folate status and the safety of antifolates. Semin Oncol 2002, 29(suppl 5):3-7.
70.	Barnard RD, Freeman MD: Reversal of aminopterin toxicity by water soluble cuprodihydroporphirins (chloresium). Am J Digest Dis 1954, 21:163-169.
71.	Fenech M: Recommended dietary allowances for genomic sta­bility. Mutat Res 2001, 480-481:51-54.
72.	Heimburger DC, Alexander CB, Birch R, Butterworth CE Jr, Bailey WC, Krumdieck CL: Improvement in bronchial squamous cell metaplasia in smokers treated with folic acid and vitamin B­12. Report of a preliminary randomized, double-blind inter­vention trial. JAMA 1988, 259:1525-1530.
73.	Saito M, Kato H, Tsuchida T, Konaka C: Chemoprevention effects on bronchial squamous metaplasia by folate and vitamin B­12. Chest 1994, 106:496-499.
74.	Senti FR, Pilch SM: Analysis of folate data from the second national Health and Nutrition Examination Survey (NHANES II). J Nutr 1985, 115:1398-1402.
75.	Subar AF, Block G, James LD: Folate intake and food sources in the US population. Am J Clin Nutr 1989, 50:508-516.
76.	Wilson JW, Enns CW, Goldman JD, Tippett KS, Mickle SJ, Cleveland LE, Chahil PS: Data tables: Combined results from USDA’s 1994 and 1995 continuing survey of food intakes by individu­als and 1994 and 1995 diet and healthy knowledge survey. USDA/ARS Food Survey Research Group, Beltsville Human Nutrition Research Center, Riverdale, MD. .
77.	van Asselt DZ, de Groot LC, van Staveren WA, Blom HJ, Wevers RA, Biemond I, Hoefnagels WH: Role of cobalamine intake and atrophic gastritis in mild cobalamine deficiency in older Dutch subjects. Am J Clin Nutr 1998, 68:328-334.
78.	Levander OA, Burk RF: Selenium. in Present Knowledge in Nutrition. Edited by: Ziegler EE, Filer LJ. Washington DC: ILSI Press; 1996:320-328.
79.	Foster HD: Disease family trees: the possible roles of iodine in goiter, cretinism, multiple sclerosis, amyothropic lateral sclerosis, Alzheimer’s and Parkinson’s diseases and cancer of the thyroid, nervous system and skin. Med Hypothesis 1987, 24:249-263.
80.	Boyages SC, Collins JK, Maberly GF, Jupp JJ, Morris J, Eastman CJ: Iodine deficiency impairs intellectual and neuromotor devel­opment in apparently-normal person: a study of rural inhab­itants of North-central China. Med J Australia 1989, 150:676-682.
81.	Laurberg P, Pedersen KM, Hreidarsson A, Sigfusson N, Iversen E, Knudsen PR: Iodine intake and the pattern of thyroid disor­ders: A comparative epidemiological study of thyroid abnor­malities in the elderly in Iceland and Jutland, Denmark. J Clin Endocrinol Metab 1998, 83:765-769.
82.	Galanti MR, Sparen P, Karlsson A, Grimelius L, Ekbom A: Is resi­dence in areas of endemic goitre a risk factor for thyroid can­cer? Int J Cancer 1995, 61:615-621.
83.	Franchesci S: Iodine intake and thyroid carcinoma-A potential risk factor. Exp Clin Endocrinol Diabetes 1997, 106(Suppl 3):S38-S44.
84.	Kalk WJ, Sitas F, Patterson AC: Thyroid cancer in South Africa­an indicator of regional iodine deficiency. S Afr Med J 1997, 87:731-733.
85.	Ohshima M, Ward JM: Dietary iodine deficiency as a tumor pro­moter and carcinogen in F334/Ncr male rats. Cancer Res 1986, 46:877-883.
86.	Eskin BA: Iodine and mammary cancer. Adv Exp Med Biol 1977, 91:293-304.
87.	Eskin BA: Iodine metabolism and breast cancer. NY Acad Sci 1970, 32:911-947.
88.	Mittra I, Hayward JL: Hypothalamic-pituitary-thyroid axis in breast cancer. Lancet 1(7863):885-889. 1974 May 11
89.	Spencer JM: Geological influences on regional health prob­lems. Texas J Sci 1970, 21:459-469.
90.	Parker SL, Tong T, Bolden S, Wingo PA: Cancer statistics. CA Can­ cer J Clin 1997, 47:5-27.
91.	Ghent WR, Eskin BA, Low DA, Hill LP: Iodine replacement in fibrocystic disease. Can J Surg 1993, 36:453-460.
92.	Phillips DI, Lusty TD, Osmond C, Church D: Iodine supplementa­tion: Comparison of oral or intramuscular iodized oil vs oral potassium iodide. A controlled trial in Zaire. Int J Epidemiol 1988 17:142-147
93.	Dugrillon A: Iodolactones and iodoaldehydes-mediators of iodine in thyroid autoregulation. Exp Clin Endocrinol Diabetes 1996, 104(suppl 4):41-45.
94.	Pharmacopoiea of the United States, Eight Decennial Revision 1905:250.
95.	Serra-Majem LL, Tresserras R, Canela J, Salleras L: Dietary iodine deficiency and breast cancer mortality: an ecological study. Int J Epidemiol 1988, 17:686-687.
96.	Zhang D-Z: The treatment of cancer by integrated Chinese­ Western medicine. Boulder CO: Blue Poppy Press; 1989:21-43.
97.	Zaichick VY, Tsyb A, Vtyurin BM: Trace elements and thyroid cancer. Analyst 1995, 120:817-821.
98.	Kato N, Funahashi H, Ando K, Takagi H: Suppressive effects of iodine preparations on proliferation of DMBA-induced breast cancer in rat. J Jpn Soc Cancer Ther 1994, 29:582-588.
99.	Funahashi H, Imai T, Tanaka Y, Tobinaga J, Wada M, Morita T, Yamada F, Tsukamura K, Oiwa M, Kikumori T, Narita T, Takagi H: Suppres­sive effect of iodine on DMBA-induced breast tumor growth in the rat. J Surgical Oncol 1996, 61:209-213.
100.	Lofti M, Mason JB: The prevention and control of iodine defi­ciency disorders. ACC/SCN Nutrition Policy Discussion Paper No. 3, 7: United Nations. .
101.	Marani L, Venturi S, Masala R: Role of iodine in delayed immune response. Isr J Med Sci 1985, 21:864.
102.	Weetman AP, McGregor AM, Campbell H, Lazarus JH, Ibberson HK, Hall R: Iodine enhances IgG synthesis by human peripheral blood lymphocytes in vitro. Acta Endocr (Copenh) 1983, 103:210-215.
103.	Lee AKY, Rowley M, Mackay IR: Antibody-producing capacity in human cancer. Br J Cancer 1970, 24:454-63.
104.	Als C, Lauber K, Brander L, Luscher D, Rosler H: The instability of dietary iodine supply over time in an affluent society. Experi­ entia 1995, 51:623-633.
105.	Ozcan M: Nutrient composition of rose (Rosa canina L.) seed and oils. J Med Food 2002, 5:137-140.
106.	Discover Ayurveda Health Goals, The Ayurvedic view on roses and health [http://www.discoverayurveda.com/health/ health_roses.html]
107.	Umezu T: Behavioral effects of plant-derived essential oils in the Geller type conflict test in mice. Jpn J Pharmacol 2000, 83:150-153.
108.	Boyanova L, Neshev G: Inhibitory effect of rose oil products on Helicobacter pylori growth in vitro: preliminary report. J Med Microbiol 1999, 48:705-706.
109.	Lad V: The complete book of Ayurvedic home remedies New York: Three Rivers Press; 1998:209-211.
110.	Beard J: The action of trypsin upon the living cells of Jensen’s mouse tumor. Br Med J 1906, 4:140-141.
111.	Wiggin PH: Case of multiple fibrosarcoma of the tongue, with remarks on the use of trypsin and amylopsin in the treat­ment of malignant disease. JAMA 1906, 47:2003-2008.
112.	Cutfield A: Trypsin treatment of malignant disease. Br Med J 1907, 5:525.
113.	Campbell JT: Trypsin treatment of a case of malignant disease. JAMA 1907, 48:225-226.
114.	Little WL: A case of malignant tumor, with treatment. JAMA 1908, 50:1724.
115.	King LS: Prevention of virus-induced mammary tumors by an orally active pancreas factor. Exp Med Surg 1965, 23:345-347.
116.	King LS: A novel method of enhancing antibody production. Southwest Med 1965, 46:222-224.
117.	Gotze H, Rothman SS: Enteropancreatic circulation of digestive enzymes as a conservative mechanism. Nature 1975, 257:607-609.
118.	Liebow C, Rothman SS: Enteropancreatic circulation of diges­tive enzymes. Science 1975, 189:472-474.
119.	Kelley WD: One answer to cancer: An ecological approach to the success­ ful treatment of malignancy Pomeroy WA: Health Research Books;967.
120.	Gonzalez NJ, Isaacs LL: Evaluation of pancreatic proteolytic enzyme treatment of adenocarcinoma of the pancreas, with nutrition and detoxification support. Nutr Cancer 1999, 33:117-124.
121.	Bastedo WA: Colon irrigation. JAMA 1932, 98:734-736.
122.	Friedenwald J, Morrison S: Value, indications, limitations and technic of colonic irrigations. Med Clin North Am 1935:1611-1629.
123.	Snyder RG: The value of colonic irrigation in counteracting auto-intoxication of intestinal origin. Med Clin North Am 1939:781-788.
124.	Malagelada GF Jr: Gut flora in health and disease. Lancet 2003, 361(9356):512-519.
125.	Hill MJ: Diet and the human intestinal bacterial flora. Cancer Res 1981, 41(9 Pt2):3778-3780.
126.	Mallett AK, Rowland IR: Factors affecting the gut microflora. In Role of the Gut Flora in Toxicity and Cancer Edited by: Rowland IR. London: Academic; 1988:347-382.
127.	van der Werf SD, Nagengast FM, van Berge Henegouwen GP, Huij­bregts AW, van Tonergen JH: Intracolonic environment and the presence of colonic adenomas in man. Gut 1983, 24:876-880.
128.	Vargo D, Moskovitz M, Floch MH: Faecal bacterial flora in cancer of the colon. Gut 1980, 21:701-705.
129.	Noureldin MS, Shaltout AA, El Hamshary EM, Ali ME: Opportunistic intestinal protozoal infections in immunocompromised chil­dren. J Egypt Soc Parasitol 1999, 29:951-961.
130.	Adel-Rahim AY: Parasitic infections and hepatic neoplasia. Dig Dis 2001, 19:288-291.
131.	Fiorini M, Messina MF, Barrachia A: Peripherial intramonocytic and intraneutrophil leishmanias observed in chronic myelo­monocytic leukemia (CMMoL) patient. Hematologica 2002, 87:EIM21.
132.	Goodman LS, Gilman A: The Pharmacological Basis of Therapeutics New York: Macmillan Publishing Co; 1970:1057-1058.
133.	Council of the Pharmaceutical Society of Great Britain: British Pharma­ceutical Codex The Pharmaceutical Press; 1968:813.
134.	Bragg PC, Bragg P: Apple Cider Vinegar Health Science; 1997.
135.	Reich W: The Orgone accumulator. The Cancer Biopathy Volume 2. New York: Farrah, Strauss and Giroux; 1973:108-150.
136.	136.Muschenic S, Gerbauer R: The (Psycho-)Physiological effects of the Reich orgone energy accumulator. Dissertation University of Marburg, West Germany; 1985.
137.	Lassek H: Vegeto-Orgontherapie nach Wilhelm Reich. Natural Healing Methods for the European Community, Doc. Reg. V.5, Min. of Tech., Niedersachen, Univ. Lueneburg, Germany 1991.
138.	Reich W: The carcinomatous shrinking biopathy. The Cancer Biopathy Volume 2. New York: Farrah Strauss and Giroux;; 1973:151-212.
139.	Scurry MT, Levin EM: Psychosocial factors related to the inci­dence of cancer. Int J Psychiatry Med 1979, 9:159-177.
140.	Baltrusch HJ, Waltz M: Cancer from a biobehavioural and social epidemiological perspective. Soc Sci Med 1985, 20:789-794.
141.	Irwin M, Daniels M, Risch SC, Bloom E, Weiner H: Plasma cortisol and natural killer cell activity during bereavement. Biol Psychi­atry 1988, 24:173-178.
142.	Lissoni P, Cangemi P, Pirato D, Roselli MG, Rovelli F, Brivio F, Malu­gani F, Maestroni GJ, Conti A, Laudon M, Malysheva O, Giani L: A review on cancer-psychospiritual status interactions. Neu­ roendocrinol Lett 2001, 22:175-180.
143.	Gottesman MM, Pastan I: Biochemistry of multidrug resistance mediated by the multidrug transporter. Ann Rev Biochem 1993, 62:385-427.
144.	Shapiro AB, Ling V: Using purified P-glycoprotein to under­stand multidrug resistance. J Bioeng Biomembr 1995, 27:7-13.
145.	Solary E, Velay I, Chauffert B, Bidan JM, Caillot D, Dumas M, Guy H: Sufficient levels of quinine in serum circumvent the multid­rug resistance of leukemic cell line K562/ADM. Cancer 1991, 68:1714-1719.
146.	Gala JL, Noel H, Rodhain J, Ma DFF, Ferrant A: P-glycoprotein pos­itive, drug resistant invasive lymphoepithelial thymoma: treatment response to chemotherapy with cyclosporin and quinine. J Clin Pathol 1995, 48:679-681.
147.	Solary E, Caillot D, Chauffert B, Casanovas RO, Dumas M, Maynadie M, Guyt H: Feasibility of using quinine, a potential multidrug resistance-reversing agent, in combination with mitox­antrone and cytarabine for the treatment of acute leukemia. J Clin Oncol 1992, 11:1730-1736.
148.	Gold EF, Ben-Efraim S: Selective killing of mitogen-induced transformed cells by quinine sulfate in vitro. Int Arch Allergy Appl Immunol 1978, 57:177-182.
149.	Chase AW: Practical Recipes Ann Arbor: Michigan; 1864:85-86.
150.	Tate K: Old-Time Home Remedies. In house of the White Birches. Berne IN; 1998:128-129.
151.	Passegue E, Jamieson CH, Ailles LE, Weissman IL: Normal and leukemic hematopoiesis: are leukemias a stem cell disorder or a reacquisition of stem cell characteristics? Proc Natl Acad Sci USA 2003, 100(Suppl 1):11842-11849.
152.	Singh SK, Clarke ID, Terasaki M, Bonn VE, Hawkins C, Squire J, Dirks PB: Identification of a cancer stem cell in human brain tumors. Cancer Res 2003, 63:5821-5828.
153.	Dick JE: Breast cancer stem cells revealed. Proc Natl Acad Sci USA 2003, 100:3547-3549.