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X-Linked Dominant Growth Suppression of Transplanted Tumors in C57BL/6J-scid Mice

¹ Vascular Biology Program and Department of Surgery and ² Department of Ophthalmology, Children's Hospital Boston and Harvard Medical School, Boston, Massachusetts

Requests for reprints: Taturo Udagawa, Vascular Biology Program and Department of Surgery, Children's Hospital Boston and Harvard Medical School, Karp Family Research Laboratories, 1 Blackfan Circle, Boston, MA 02115. Phone: 617-919-2429; E-mail: taturo.udagawa{at}childrens.harvard.edu.

Tumor susceptibility, angiogenesis, and immune response differ between mouse strains. We, therefore, examined the growth rates of tumor xenografts in three genetically isolated strains of severe combined immunodeficient mice (C.B-17, C57BL/6J, and C3H). Tumors grew at significantly reduced rates in the C57BL/6J-scid strain. Engrafting bone marrow from the C57BL/6J-scid strain onto C.B-17-scid mice did not transfer the slow-growing tumor phenotype to the recipient mice; this counters the supposition that the slow-growing tumor phenotype is caused by a greater immune response to the xenograft in the C57BL/6J-scid strain. To establish the inheritance pattern of the slow-growing tumor phenotype, we reciprocally crossed C.B-17-scid mice and C57BL/6J-scid mice. Tumor growth was suppressed in all of the F₁ progeny except the male mice derived from the cross between C.B-17-scid female and C57BL/6J-scid male mice. The F₁ male mice that received the X chromosome from the C.B-17 strain displayed a fast-growing tumor phenotype. These results confirm that there are significant strain differences in capacity to support the growth of tumor xenografts. In addition, these results reveal the existence of a dominant allele involved in host suppression of tumor growth on the X chromosome of C57BL/6J mice.