How Can Dietary Alterations Affect Cancer Development / Pathogenesis? (Evidence Based Article)

^{How Can Dietary Alterations Affect Cancer Development / Pathogenesis?}

Cancer Pathogenesis

Definition

Tortora and Grabowski (2006) define cancer as ‘a group of diseases characterized by uncontrolled or abnormal cell proliferation. When cells in a part of the body divide without control, the excess tissue that develops is called a tumour or neoplasm.’

According to Stevens and Lowe (2006) cancer is the second most common cause of death (after ischaemic heart disease) in most developed countries, accounting for about 23% of all mortality.

The World Health Organisation (2009) stated cancer was responsible for 7.4 million deaths (or around 13% of all deaths worldwide) in 2004. It further said that above 70% of the cancer deaths occurred in low- and middle-income countries, providing a possible link between lifestyle and cancer risk.

Cancer Development – The Three Stages

The development of cancer is generally divided into three stages; (1) initiation, (2) promotion and (3) progression. In the tumour initiation stage, normal cells are exposed to various types of carcinogens; these might be chemical, physical, or microbial, resulting in genetic changes (Van Poppel and Van Den Berg 1997). The resultant changed genotype cannot be reversed to its normal state, however, the initiated cell phenotype is unable to fully express without the presence of a promoter. The promoters work by enhancing the expression of the initiated phenotype and provide a growth stimulus, thus allowing clonal expansion. This second stage does not involve any genetic changes and is therefore considered reversible. Pryor (1997) stated that the promotion stage always involves free radicals, whereas the progression stage normally does not.

Van Poppel (1997) stated that carcinogenesis is a multistep process, which most likely involves activation of proto-oncogenes and/or inactivation of tumour suppresser genes. Pryor (1997) suggests that free radicals play a part in the initiation stage of carcinogenesis. The study further implies that this occurs either in the oxidative activation of a procarcinogen to its carcinogenic form or when the carcinogenic species bind to the DNA, or both these processes.

Tumour presentation

Tumours vary in presentation in terms of developmental progression and shape. They may be cancerous, in other terms malignant, meaning that they have the ability to undergo metastasis, thus spreading cancerous cells to other parts of the body often with fatal consequences. Metastasis has been linked to gene expression patterns in several clinical trials, in terms of prognosis. In a study published by Park et al (2007) it was concluded that through use of their self-developed mRNA expression-based model, it would be possible to generate a gene expression profiling system which could improve survival prediction in patients with breast cancer. In other words, a model which could give an approximate survivability rating dependant on the genes which are analyzed. This is a good example of exciting innovative research which is being conducted in this pathological area.

Dietary Alterations

Alterations in diet seem to be able to affect environmental factors in carcinogenesis, thus preventing or inhibiting the development of cancer (Hart and Turturro 1997). The study suggests the mechanisms behind this are (1) decreased body weight, which results in decreased carcinogenic cellular proliferation and increased apoptosis of cancer cells, in a number of organs which can be regulated in size by overall body size (2) lowered body temperature, which they claim reduce DNA damage (3) enhancing antioxidant damage defence systems, thus decreasing oxidative damage. A dietary study by Norat el al (2005), including 478 040 european subjects, showed that the risk of colorectal cancer increased with a high consumption of processed and red meat, whereas a high intake of fish was associated with a decreased risk of colorectal cancer.

Mavropoulos et al (2006) demonstrated that diets associatedwith a reduction in insulin level may prove beneficial for prevention of prostate cancer. These results were backed up in an animal study by Venkateswaran et al (2007) which showed that increasing the carbohydrate intake (without altering fat intake or total calories) augmented the growth rate of prostate cancer xenografts. Chan et al (2005) observed inverse associations between consumption of total and specific vegetables and fruits and the risk of pancreatic cancer, and concluded that it may impart some protection against developing pancreatic cancer. These results were backed up by a quantitative systematic review conducted by Bae et al (2009) which showed a decrease in pancreatic cancer risk linked with an increased consumption of citrus fruits.

Larsson and Wolk (2007) evaluated four cohort and 5 case-control studies and observed an inverse relation between coffee consumption and risk of liver cancer. Overall an increase in consumption of 2 cups of coffee per day was associated with a 43% reduced risk of liver cancer.

From these findings, it may be stated that the human diet has a significant impact on the risk of developing certain types of cancer and that certain food types seem to have a beneficial effect in decreasing the risk of carcinogenesis.

Hope you have learned something about the development of cancer, the three stages, and also how diet alterations may be associated with beneficial effects in all of these. It has been shown in several studies that antioxidant supplementation may be beneficial in reducing cancer risk.

Live Strong.

^References:

^{Chan, JM., Wang, F., Holly, EA. (2005) Vegetable and fruit intake and pancreatic cancer in a population-based case-control study in the San Francisco bay area. Cancer Epidemiol Biomarkers Prev. 2005 Sep;14 (9):2093-7.}

^{Hart, RW., and Turturro A. (1997). Dietary Restrictions and Cancer. Fundamental Health Perspectives. 105 (4), 989-92.}

^{Larsson, SC., Wolk, A. (2007). "Coffee consumption and risk of liver cancer: a meta-analysis". Gastroenterology 132 (5): 1740–5.}

^{Mavropoulos, JC., Isaacs, WB., Pizzo, SV., Freedland, SJ. Is there a role for a low-carbohydrate ketogenic diet in the management of prostate cancer? Urology (2006) 68:15–8.}

^{Norat, T., Bingham, S., Ferrari, P., Slimani, N., Jenab, M., Mazuir, M., Overvad, K., Olsen, A., Tjønneland, A., Clavel, F., Boutron-Ruault, MC., Kesse, E., Boeing, H., Bergmann, MM., Nieters, A., Linseisen, J., Trichopoulou, A., Trichopoulos, D., Tountas, Y., Berrino, F., Palli, D., Panico, S., Tumino, R., Vineis, P., Bueno-de-Mesquita, HB., Peeters, PH., Engeset, D., Lund, E., Skeie, G., Ardanaz, E., González, C., Navarro, C., Quirós, JR., Sanchez, MJ., Berglund, G., Mattisson, I., Hallmans, G., Palmqvist, R., Day, NE., Khaw, KT., Key, TJ., San Joaquin, M., Hémon, B., Saracci, R., Kaaks, R., Riboli, E. (2005) Meat, fish, and colorectal cancer risk: the European Prospective Investigation into cancer and nutrition. J Natl Cancer Inst. 2005 Jun 15;97(12):906-16.}

^{Park, ES., Lee, JS., Woo, HG., Zhan, F., Shih, JH., Shaughnessy, JD. Jr. Frederic Mushinski, J. (2007) Heterologous tissue culture expression signature predicts human breast cancer prognosis. PLoS One. 2007 Jan 3;2(1):e145.}

^{Pryor, W.A. (1997) Cigarette Smoke Radicals and the Role of Free Radicals in Chemical Carcinogenicity. Environmental Health Perspectives. 105 (4), 875-82.}

^{Stevens, A., Lowe, JS. (2000).Cancer Epidemiology. In: Pathology 2nd edition. Chapter 6: Epidemiology of Neoplastic Disease. PP.101-104 Published by Mosby Elsevier. Edinburgh, London, New York, Philadelphia, St.Louis, Sydney, Toronto.}

^{Tortora, GJ., Grabowski, SR. (2006).Disorders: Homeostatic Imbalances. In: Principles of anatomy and physiology. Chapter 3: The Cellular Level of Organization. PP.99 Published by John Wiley & Sons, Inc. Hoboken, New Jersey.}

^{Van Poppel, G, and Van Den Berg, H. (1997) Vitamins and Cancer. Cancer letters. 114, 195-202.}

^{Venkateswaran, V., Haddad, A., Fleshner, NE., Fan, R., Sugar, RM., Nam, R., Klotz, LH., Pollak, M. (2007) Association of Diet-Induced Hyperinsulinemia With Accelerated Growth of Prostate Cancer (LNCaP) Xenografts. Journal of the National Cancer Institute 2007 99(23):1793-1800.}