pCSCs developed into various type of tumors in immunodeficient mice.

<p>A, Tumor incidence from 3 experiments. Equal numbers of sex matched SCID mice were injected s.c. or i.p. with 5×10⁶ pCSCs. No significant difference in incidence was observed between s.c. and i.p. injected mice. As a control, C57BL/6 mice injected s.c. (n = 10) or i.p. (n = 10) with 2C4 cells did not develop tumors within 5 months of observation (data not shown) “*” indicates that a mouse developed ascites, “**” indicates that the 3B6C cells infiltrated in the liver and spleen (see E). B, Kinetics of tumor growth: the data shown are from experiments 1 & 2 in A. Each color in B corresponds to a specific cell line. C, Comparison of tumorigenesis between pCSCs (2C4) and differentiated cancer cells (3B11); (n = 10/group, each group includes 5 males and 5 females). D, A representative of gross tumors from a mouse injected i.p. with 3B5C clone. E, A histological representative of pCSC-derived tumors from the mice injected i.p. with 2C4 or 3B5C clones. F, A histological representative from the spleen of mice injected i.p. or s.c. with 3B6C clone. Note that megakaryocytes in the spleen of normal SCID mice were replaced by atypical neutrophils or eosinophils. G, Benign differentiation of pCSCs in the liver with metastatic cancers: (a) H & E staining of a liver section with metastatic cancers from a mouse injected i.p. with 2C4 cells (original magnification: ×200). (b) Immunohistochemical staining of the liver section from the same mouse with antibody to neomycin, showing neomycin⁺ cancer cells (original magnification: ×400). (c) Immunohistochemical staining of pCSC-derived hepatoid cells in the regenerative area of the liver sections from the same mouse (original magnification: ×200). (d) The enlarged micrographs of hepatoid cells demonstrated in (c).