Abstract

The traditional ways of detecting cancer are palpation, X-rays, nuclear medicine, MRI, CT (PET), traditional clinical laboratory procedures, and biopsies. All of these methods are characterized by the necessity of a certain tumor mass, ie, millions of cancer cells. The laboratory procedures presented here, the Cancer Profile (CA Profile, including glucose phosphate isomerase [GPI]), look not at the tumor itself, but rather, some of its products. Consequently, the realization of cancer can be detected at a very early stage, before the growth is large enough to otherwise be observed. According to epigenetics, individuals inherit cancer genes at the moment of conception. These genes remain dormant as long as they are not caused by internal and/or external environmental factors to express themselves. Actually, it may take 8 to 12 years for a tumor to become visible. Utilizing the GPI test, a developing tumor could be detected during these years. Once a tumor is large enough to be visualized, it may be too late for successful remedy. Some current methodologies depend on the presence of at least 2 million tumor cells. Targeting and altering metastatic spread of cancer are a major elements of therapy. The presence of autocrine motility factor (AMF, GPI, aka phosphohexose isomerase) and its receptor on the cell surface is an independent determinant of diagnostics and poor disease prognosis. GPI is a neurokine, stimulating cytokinesis of dislodged tumor cells, that regulates and promotes anaerobic glucose metabolism, ie, Emden-Meyerhof glycolytic and glucogenetic pathways. Amongst other functions, it is involved in the accumulation of ascites fluids and inhibits apoptosis. Metastatic cancer spread is only possible by 2 avenues: (1) mechanical, ie, biopsy or surgical knife, or (2) the elevated presence of this enzyme. For more than 30 years, GPI enzyme kinetic determinations have been an integral part of the CA Profile. It is proposed that GPI is the cause of generating circulating tumor cells. It is not only the cause of cell dislodgement, but it also jockeys the tumor cell to a new site for further proliferation. Furthermore, AMF (PHI) binds to HER2 and ablates the HER2 inhibitory effect of trastuzumab (Herceptin) in breast cancer cells.

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