Fig. 2.
Fig. 2. Contribution of human liver to myelomatous SCID-hu hosts' response to thalidomide. / (A) Final hIg levels (mean + SEM) in thalidomide- and CMC-treated myelomatous SCID-hu B (n = 10) and SCID-hy B+L (n = 8) mice. The asterisk denotes that the change in tumor burden in thalidomide-treated SCID-hu B+L hosts is significantly different from that in CMC-treated controls (P < .0009), whereas the difference in the final hIg levels between these 2 groups is significant at P < .05 (Mann-Whitney U test). The hIg levels in thalidomide- and CMC-treated control SCID-hu B mice were not significantly different. (B-C) Examples of 2 experiments demonstrating the effect of the presence of human liver tissue on myeloma growth and response to thalidomide in SCID-hu hosts inoculated with myeloma cells from patients 9 (B) and 10 (C). Values are means ± SEM of replicate readings.

Contribution of human liver to myelomatous SCID-hu hosts' response to thalidomide.

(A) Final hIg levels (mean + SEM) in thalidomide- and CMC-treated myelomatous SCID-hu B (n = 10) and SCID-hy B+L (n = 8) mice. The asterisk denotes that the change in tumor burden in thalidomide-treated SCID-hu B+L hosts is significantly different from that in CMC-treated controls (P < .0009), whereas the difference in the final hIg levels between these 2 groups is significant at P < .05 (Mann-Whitney U test). The hIg levels in thalidomide- and CMC-treated control SCID-hu B mice were not significantly different. (B-C) Examples of 2 experiments demonstrating the effect of the presence of human liver tissue on myeloma growth and response to thalidomide in SCID-hu hosts inoculated with myeloma cells from patients 9 (B) and 10 (C). Values are means ± SEM of replicate readings.

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