Neosis is a newly discovered mechanism involved in origin and growth of tumors. Up to 10% of tumor cells are polyploid cells and their role in cancer formation is not well understood. They can undergo neosis, giving rise to Raju cells which can manifest stem cell properties. Chemotherapy or radiation can cause tumor cells to go into senescence, then through neosis to form Raju cells that are resistant to treatment. This may be the mechanism for the origin and continued growth of tumor cells and explain why recurrence and resistance to treatment is a major problem.
See Rengaswami Rajaraman. A new type of cancer cell growth. The Scientist, June 2006, p 14.
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Cell Biol Int. 2005 Dec;29(12):1084-97. Epub 2005 Nov 28
Department of Medicine, Division of Hematology, Dalhousie University, Sir Charles Tupper Medical Building, 5850 College Street, Halifax, B3H 1X5 NS, Canada. [email protected]
We recently described a novel form of cell division termed neosis, which appears to be the mode of escape of cells from senescence and is involved in the neoplastic transformation and progression of tumors (Cancer Biol & Therap 2004;3:207-18). Neosis is a parasexual somatic reduction division and is characterized by (1) DNA damage-induced senescence/mitotic crisis and polyploidization, (2) followed by production of aneuploid daughter cells via nuclear budding, (3) asymmetric cytokinesis and cellularization conferring extended, but, limited mitotic life span to the offspring, and (4) is repeated several times during tumor growth. The immediate neotic progeny are termed the Raju cells, which seem to transiently display stem cell properties. The Raju cells immediately undergo symmetric mitotic division and become mature tumor cells. Exposure of tumor cells to genotoxic agents yields neosis-derived Raju cell progenies that are resistant to genotoxins, thus contributing to the recurrence of drug-resistant tumor growth. Similar events have been described in the literature under different names through several decades, but have been neglected due to the lack of appreciation of the significance of this process in cancer biology. Here we review and interpret the literature in the light of our observations and the recent advances in self-renewal in cancer. Neosis paradigm of self-renewal of cancer growth is consistent with the telomere attrition, aging and origin of cancer cells after reactivation of telomerase, and constitutes an alternative to the cancer stem cell hypothesis. We summarize the arguments favoring Raju cells and not cancer stem cells, as the source of self-renewal in cancer and present a comprehensive hypothesis of carcinogenesis, encompassing various aspects of cancer biology including senescence, tumor suppressor genes, oncogenes, cell cycle checkpoints, genomic instability, polyploidy and aneuploidy, natural selection, apoptosis, endoapoptosis, development of resistance to radiotherapy and chemotherapy leading tumor progression into malignancy.
Neosis: a novel type of cell division in cancer.Sundaram M
, Guernsey DL
, Rajaraman MM
, Rajaraman R
.Cancer Biol Ther. 2004 Feb;3(2):207-18. Epub 2004 Feb 1.
Department of Medicine and Microbiology and Immunology, QEII Health Sciences Center
, Faculty of Medicine, Dalhousie University
, Halifax, Canada
Using computerized video time-lapse microscopy, we studied early cellular events during carcinogen-induced transformation of C3H10T1/2 cells. Multinucleate/polyploid giant cells (MN/PGs) formed due to DNA damage are thought to die via mitotic catastrophe. Before they die, some MN/PGs undergo a novel type of cell division, termed neosis, characterized by karyokinesis via nuclear budding followed by asymmetric, intracellular cytokinesis, producing several small mononuclear cells, termed the Raju cells, with extended mitotic life span (MLS). Mitotic derivatives of Raju cells give rise to transformed cell lines, inherit genomic instability, display a phenotype and transcriptome different from the neosis mother cell, and anchorage-independent growth. Neosis of MN/PGs also precedes spontaneous transformation of p53-/- mouse cells. Rodent neotic clones, and primary and metastatic human tumor cells undergo spontaneous or induced secondary/tertiary neosis. Neosis seems to extend the MLS of cells under conditions of genetic duress not favoring mitosis. It precedes tumorigenesis, occurs several times during tumor progression, yielding tumor-initiating Raju cells and introducing tumor cell heterogeneity subject to natural selection during tumor progression. Events during neosis, and its relevance to origin of established cell lines, multistep carcinogenesis, cancer stem cells, and therapeutic advantages of anti-neotic agents (neosicides) are discussed.