Cancer markers shown to be a cause as well as a consequence of cancer activityIngenieur d'etude au CNRS France, Scientific Attache, Molecular International Research, Inc., New York, NY
Aims: -Show a correlation between the excessive unwinding of the secondary structure of non-supercoiled DNA, proper to cancer DNA, and the amount of cancer markers. -Show that the same markers become in turn a contributing factor to further unwinding of cancer-DNA, producing more initiation sites for cancer cell proliferation. -Conversely, show that through the use of an intercalating alkaloid that trigger a tightening of the DNA double helix (hypochromicity), such a re-winding causes a progressive disappearance of cancer markers in both plants and mammals. Methods: DNA preparations isolated from breast cancer DNA * incubated in the presence of increasing concentrations of cancer markers; unwinding of cancer DNA was measured through hyperchronicity.. * or used as template to synthesize new DNAs in presence of increasing doses of cancer markers. In presence of increasing doses of an intercalating alkaloid, measurements were made of * breast cancer's hypochromicity and synthesis * cancer cells' proliferation and marker production Results: increasing doses of marker like AFP increases both the unwinding of breast cancer DNA and its rate of synthesis. Inversely, increasing doses of intercalating alkaloid reduces the unwinding of same DNA, its template activity, the proliferation of cancer cells and provokes the disappearance of markers in the serums of patients using a natural extract containing this alkaloid Conclusions: By directly modulating the cancer-DNA double strand, tumor markers or, conversely, intercalating agents act as switch molecules in the cancer cell multiplication and consequently, in the production of tumor markers.
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Paper presented at the International Symposium on Predictive Oncology and Intervention Strategies; Paris, France; February 9 - 12, 2002; in the section on Predictive Markers.