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¡¡Eradication of Cancer Cells via Regeneration

1. Killing of Cancer and Transformed Cells in vitro
2. Selective Killing of Cancer Cells Co-Cultured with Normal Cells
3. Promoting Growth of Normal Cells in vitro
4. Differential Metabolism of MEBO Regenerative Nutrients in Cancer and Normal Cells
5. Killing of Cancer Cells in Tumor Tissue in vitro
6. Suppression of Ascites Tumor Growth in Animal Tumor Models
7. Eradication of Skin Cancer in Patients
8. Eradication of Leukemia in Patients
9. Regeneration of internal organs of cancer patients
10. Ongoing Clinical Studies of End-Stage Cancer Patients

4. Differential Metabolism of MEBO Regenerative Nutrients in Cancer and Normal Cells

To explore the mechanism of dual functions of the MEBO regenerative nutrients, examination of the cancer cells and normal cells under ultra-fine electron microscope was carried out.  A549 lung cancer cells and MRC5 normal lung fibroblasts were cultured in the presence of the MEBO regenerative nutrients for 48 hours and then fixed for microscopic examination.

As shown in Figure 10.4.1 below, under a scanning electron microscope there is a dramatic difference in the cell surface morphology of the cancer before and after exposure to the MEBO regenerative nutrients.  The rich microvilli extending from the surface of the cancer cell and attached to the culture plate (Figure 10.4.1a) virtually disappeared and detached (Figure 10.4.1b).  In comparison, cell surface morphology in the normal cell appeared to be normal after the treatment with the MEBO regenerative nutrients (Figures 10.4.1c-d). 

The intracellular components of the cancer and normal cells were examined under a transmission electron microscopy.  Dramatic differences were also observed in the response of the cancer and normal cells to the MEBO regenerative nutrients.  As shown in Figure 10.4.2, both types of cells readily absorbed the MEBO nutrients that are lipophilic, as shown by the dark dots of oil droplets inside the cells (Figure 10.4.2a).  Surprisingly, in the cancer cell, upon uptake of the nutrients into the cytoplasm, it can be observed that mitochondria of the cancer cell were enlarged and swollen while the nucleus stopped dividing (Figure 10.4.2b). The nutrient droplets stayed in the cytoplasm and did not get metabolized before the growth arrest which was then followed by cell death (Figure 10.4.2c). 

In contrast, in the normal cell the MEBO nutrient droplets were taken into the cytoplasm and gradually metabolized by the cell (Figures 10.4.2d-e).  The normal cells not only did not die but also underwent vigorous proliferation as shown by active cell division and increase of cell numbers in the culture.  Mitochondria of the normal cell appeared to be normal after uptake of the MEBO regenerative nutrients. 

These results demonstrate distinctly differential metabolism of the MEBO regenerative nutrients in cancer and normal cells.  The cancer cells absorb the nutrients, which causes enlargement and swelling of mitochondria, the power plants of a cell.  As observed under the microscope, the cancer cells subsequently undergo growth arrest which is followed by cell death.  It is conceivable that the substantial modification of the structure of mitochondria leads to disruption of their function, leading to a shutdown of the cellular activity and release of pro-apoptotic factors, causing cell death.  Importantly, the growth of the normal cells is not negatively affected but instead promoted to more vigorous levels.  Such dual functions of the MEBO regenerative nutrients could explain why the MEBO regenerative nutrients exhibit little toxicity yet possess efficacy in suppressing tumor growth in animal models and clinically.


The results obtained are quite intriguing and exciting in that the MEBO regenerative nutrients exhibit a dual function: promoting normal cell growth while killing transformed or cancer cells.  Such a differential response of normal vs. cancer cells appears to be related to differential reactions in mitochondria, to say the least. 

Recently, it has been recognized that mitochondria play new critical roles in cell metabolism ¨D regulation of cell death pathways.  Gogvadze et al. (2008) ¡°Mitochondria in cancer cells: what is so special about them?¡± Trends in Cell Biol. 18:165-173. Wang (2008) ¡°The expanding role of mitochondria in apoptosis¡± Genes & Dev. 15:2922-2933.  It has been reported that several mitochondrial proteins that reside in the intermemebrane space of mitochondria, in response to a variety of apoptotic stimuli, are released to the cytosol and/or the nucleus, thereby directly activating cellular apoptotic program and causing apoptosis of the cell.  Liu et al. (1996) ¡° Induction of apoptosis program in cell-free extracts: requirement for dATP and cytochrome c¡± Cell 86:147-157.  Verhagen et al. ¡°Identification of DIABLO, a mammalian protein that promotes apoptosis by binding to and antagonizing IAP proteins¡± Cell 102:43-53. Based on our EM data obtained, the cancer cell death induced by the MEBO nutrients can be attributed to activation through disruption of mitochondrial membrane and subsequent releasing of the apoptotic proteins.  In contrast, normal cells in the presence of the MEBO nutrients not only survive but also grow rigorously. 

A number of agents, including chemotherapeutic drugs (e.g., cisplatin and arsenic oxide) and compounds isolated from natural sources (e.g., epigallocatechin gallate (EGCG) and beta-carotene) are shown to be able directly or indirectly target mitochondria, the ¡°power plants¡± of the cell.  Pederson (2007) ¡°The cancer cell¡¯s ¡°power plants¡± as promising therapeutic targets: An overview¡± J. Bioenerg. Biomembr. 39: 1-12. However, there has been no report of these agents having a dual function of killing cancer cells while promoting normal cell growth and regeneration, as demonstrated by the MEBO nutrients.  It is well known that virtually all of anti-cancer chemotherapeutic agents can cause the side effects of suppressing the growth of normal, fast dividing cells, such as epithelial cells in the skin, hair follicles and mucosa, as well as that of the hematological cells.

It is plausible that the intrinsic differences in the metabolism of normal and cancer cells may contribute to the differential response to the MEBO nutrients.  It has been observed that cancer cells produce most of their ATP through glycolysis, even under aerobic conditions, and there is a correlation between glycolytic ATP production and aggressiveness of the tumor cells.  Warburg (1930) ¡°The metabolism of tumors¡± London: Arnold Constable.  Simonnet et al. (2002) ¡°Low mitochondrial respiratory chain content correlates with tumor aggressiveness in renal cell carcinoma¡± Carcinogenesis 23:759-768.  When rapidly growing tumors shift their ATP production to glycolysis, mitochondrial activity slows down.  Gogvadze et al. (2008), supra.  By absorbing the highly lipophilic MEBO nutrients, the cancer cells seem to be unable to metabolize them; instead, the undigested lipid droplets stayed inside the cytoplasm, which caused swelling of mitochondria, leading to cell death (Figure 10.4.2c).  In contrast, in the normal cell the nutrient droplets were taken into the cytoplasm and gradually metabolized by the cell (Figures 10.4.2d-e); mitochondria in the normal cells did not appear to be damaged by the uptake of the nutrients and continued to function normally, if not more vigorously. As demonstrated in the skin and mucosal tissue regeneration of wound and ulcer patients, the MEBO nutrients consistently promote physiological repair and regeneration of normal cells in humans, including fully developed adult humans.

The unique ability of the MEBO nutrients to promote normal cell growth without damaging the cellular power plants¨Dmitochondria (as demonstrated in their clinical efficacy in promoting tissue and organ regeneration and in in vitro cellular studies) and their surprising ability to induce apoptosis of transformed and cancer cells are extremely desirable in the development of safe and efficacious products for cancer treatment and prevention.  As MEBO nutrients are formulated using natural botanicals safely used for human consumption for thousands of years, these products have superior safety profiles and can be safely used a nutritional support for cancer patients, which forms the scientific foundation for MEBO¡¯s ongoing large population human studies of end-stage cancer patients.  See Section 10.10 below.  This innovative approach to cancer treatment and prevention will open a new fertile field for basic and clinical applications.

 
   
¡¡ACHIEVEMENTS
Introduction
Core Science & Technology of MEBO
Exploration of Fundamental Mechanisms of Adult Human Body Regeneration
Eradication of Cancer Cells via Regeneration
 









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