Cancer cells’ most important biological characteristic is to divide and proliferate in an uncontrolled fashion, thus contributing to the invasive progression of tumors. Interestingly, all cells of the same tumor are not clones. This is known as cancer cell heterogeneity.

The long-debated theory of cancer stem cells argues that there is a small group of cells within the tumor that are exclusively responsible for cancer fueling and regrowth after therapy. These deadly “mother cells”, which have been pinpointed for the first time last August in three independent studies on different cancers (1-3), show a similar behavior as other normal stem cells in healthy tissues. They can self-renew, give rise to all tumor cell types of the tumor bulk and, more importantly, are largely unaffected by standard therapies such as chemotherapy or radiation.

If the cancer stem cell story is further established by future studies, and in particular by human studies, it will then enable researchers to design new treatments able to reach the very heart of the disease, and thus prevent its recurrence. In this context, food components will be expected to play a very important regulatory role.

Indeed, mounting evidence suggests that bioactive food components car modify the self-renewal capabilities of cancer stem cells (4). This is the case for vitamin A from liver (5), two components found in tea (epigallocatechin-3-gallate (EGCG) and theanine) (6), vitamin D in fish (7, 8), genistein in soy (9) , choline in eggs (10), and curcumin in curry spices (11). These bioactive components can modulate various steps in the process of self-renewal (for details on pathway see (4)).

Thus, adequate consumption of specific food items, including the above-mentioned micronutrients and possibly many others, may help prevent tumor initiation, and possibly impact propagation and regrowth by interfering with the anarchic property of cancer cells to self-renew. However, for cancer patients, nutritional interventions cannot replace proper medical surveillance and treatment, but may be recommended as accompanying measures by the medical profession.

1.    Driessens, G., et al. (2012). Defining the mode of tumour growth by clonal analysis. Nature 488, 527-30
2.    Chen, J., et al. (2012). A restricted cell population propagates glioblastoma growth after chemotherapy. Nature 488, 522-6
3.    Schepers, A. G., et al. (2012). Lineage tracing reveals Lgr5+ stem cell activity in mouse intestinal adenomas. Science 337, 730-5
4.    Kim, Y. S., Farrar, W., Colburn, N. H. and Milner, J. A. (2012). Cancer stem cells: potential target for bioactive food components. The Journal of nutritional biochemistry 23, 691-8
5.    Ginestier, C., et al. (2009). Retinoid signaling regulates breast cancer stem cell differentiation. Cell cycle 8, 3297-302
6.    Balasubramanian, S., Adhikary, G. and Eckert, R. L. (2010). The Bmi-1 polycomb protein antagonizes the (-)-epigallocatechin-3-gallate-dependent suppression of skin cancer cell survival. Carcinogenesis 31, 496-503
7.    Aguilera, O., et al. (2007). The Wnt antagonist DICKKOPF-1 gene is induced by 1alpha,25-dihydroxyvitamin D3 associated to the differentiation of human colon cancer cells. Carcinogenesis 28, 1877-84
8.    Pendas-Franco, N., et al. (2008). DICKKOPF-4 is induced by TCF/beta-catenin and upregulated in human colon cancer, promotes tumour cell invasion and angiogenesis and is repressed by 1alpha,25-dihydroxyvitamin D3. Oncogene 27, 4467-77
9.    Carlo-Stella, C., et al. (1996). Selection of myeloid progenitors lacking BCR/ABL mRNA in chronic myelogenous leukemia patients after in vitro treatment with the tyrosine kinase inhibitor genistein. Blood 88, 3091-100
10.    Mehedint, M. G., Niculescu, M. D., Craciunescu, C. N. and Zeisel, S. H. (2010). Choline deficiency alters global histone methylation and epigenetic marking at the Re1 site of the calbindin 1 gene. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 24, 184-95
11.    Kakarala, M., et al. (2010). Targeting breast stem cells with the cancer preventive compounds curcumin and piperine. Breast cancer research and treatment 122, 777-85