Literatus: Normal but deadly mechanisms

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Tuesday, February 18, 2014

THE beginning of 2014 would not be complete without bringing some hard scientific terms in our discussion of health and well-being, considering that groundbreaking findings in health sciences come to us often in spellbinding words.

Recent breakthroughs in understanding the effects of anti-cancer dietary compounds against cancer forms came in the review that Julian Raffoul, Ahmad Heydari and Gilda Hillman wrote for the Journal of Oncology (2012). Raffoul is professor of Medicine at Emory University School of Medicine (Atlanta, Georgia). Heydari and Hillman perform studies in nutrition and food science, and radiation oncology respectively at Barbara Ann Karmanos Cancer Institute (Detroit, Michigan).

Cancer researchers nowadays focus their energies in three areas: improve cancer cell deaths, reduce residual toxicity from chemotherapy and radiotherapy, and inhibit DNA repair mechanisms present in cancer cells. These involve at least three critical factors essential in normal cell repair and survival. These are apurinic/endonuclease 1 (APE1), an enzyme; nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kB), a protein complex; and hypoxia-inducible factor 1-alpha (HIF-1a), a protein.


The APE1 is a multifunctional protein involved in maintaining genomic integrity and regulating of gene expression. It recognizes and cuts off specific noncoding sites (AP sites) in the genes. In normal physiological conditions, AP sites arise at the rate of 50,000 to 200,000 per cell per day.

Stressful conditions, such as in chemotherapy and radiotherapy, enormously multiply this rate. If unrepaired, AP sites promote cell death as they block gene replication and transcription as well as promote double-strand breaks in genetic materials. APE1 recognizes these sites, and initiates the genetic base excision repair pathway that repairs these damaged sites.

The NF-kB, the first responder to harmful cellular stimuli, promotes cell proliferation and survival by inhibiting stoppage of cell developmental cycle and apoptosis. When APE1 activity increases, NF-kB binding activity that heightens cell survival also increases. On the other hand, the HIF-1a binds genetic materials in order to maintain normal cell proliferation.

Unfortunately, these same mechanisms also exist in cancer cells. It protects the cancer cells against the toxic effects of chemotherapy and radiotherapy, prolonging treatment and at times frustrating it.

Fortunately for us, anti-cancer compounds in plants, particularly soy isoflavones (found in soybean products), experimentally inhibit these genetic repair mechanisms in cancer cells while remaining intact those in normal cells.


Published in the Sun.Star Cebu newspaper on February 19, 2014.


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