Table 3 Properties of Raju cells and their mitotic derivatives:

   1. Short cell cycle duration of nascent Raju cells (before they undergo first mitosis) – an indication of lack of G1 phase? [5, 6].

   2. Reactivation of telomerase conferring extended mitotic life span [139-141].

   3. Is it possible to expand Raju cell population without differentiation under proper culture conditions such as EGF or FGF2 [43, 144-148].

   4. Increase in cell size accompanied by increase in cell cycle duration-introduction of G1 phase in the cell cycle [Rajaraman, unpublished; 143].

   5. Resistance to genotoxins – Expression of multidrug resistance genes? [192, 193].

   6. Are they transiently expressing tissue stem cell specific surface markers? (e.g., CD34+ for hematopoietic cells [8]; CD133+ for brain cells [12, 13], CD44+, CD33-, LowLin- for breast cells [9-11]; CD20+ for skin cells [40]; CD44+,α 2β 1hi/CD133+ for prostate cancer cells [41].

   7. Are they transiently expressing stem cell specific growth genes? (E.g. Nanog, Oct-4, Wnt, Bmi1 etc.) [188-191]

   8. Potential to differentiate, although aberrantly.

Somatic cell properties of mitotic derivatives of Raju cells:

   1. Resumption of symmetric mitotic division.

   2. Increase in cell size – Introduction of G1 phase in the cell cycle? [143].

   3. Progressive, but, aberrant differentiation.

   4. Loss of tissue specific stem cell surface markers due to differentiation during extended mitotic proliferation?

   5. Loss of expression of stem cell specific self-renewal genes?

   6. Loss of expression of multidrug resistance genes?

   7. They are subject to aging and associated senescence brought about by telomere attrition.

   8. Therefore, they have limited division potential.

   9. Telomere attrition, chromosome breakage-fusion-bridge cycle or genetic stress will result in senescent phase with MN/PG formation, mitotic crisis, and mitotic catastrophe.

   10. Absence of senescent check points constitutes a built-in mechanism for accumulation of additional mutations via breakage-fusion-bridge cycle, setting in motion the next cycle of S/T-neosis [66, 67].