Figure 2
Apoptosis induced by Cdc42 or Rac1 deletion impairs NPM-ALK lymphoma development in vivo. (A) Representative histology of lymphoma arising in NPM-ALK, NPM-ALK;CD4Cre;Cdc42fl/fl (NPM-ALK/Cdc42KO), or NPM-ALK;CD4Cre;Rac1fl/fl (NPM-ALK/Rac1KO) mice (top). Immunostainings for Ki-67 (middle) and activated caspase-3 (bottom) in tumors of the indicated genotypes are shown. Scale bar, 50 μm. (B) Histograms represent the average diameter quantified by counting at least 100 cells for each genotype. Error bars indicated SEM. ***P < .001. (C) Quantification of the percentages of proliferating cells based on Ki-67 counts on sections stained by immunohistochemistry. Data were obtained from 10 different areas in 3 independent mice for each genotype. (D) Quantification of the percentages of apoptotic cells based on activated caspase-3 counts on sections stained by immunohistochemistry. Data were obtained from 10 different areas in 3 independent mice for each genotype. Error bars indicated SEM. ***P < .001.

Apoptosis induced by Cdc42 or Rac1 deletion impairs NPM-ALK lymphoma development in vivo. (A) Representative histology of lymphoma arising in NPM-ALK, NPM-ALK;CD4Cre;Cdc42fl/fl (NPM-ALK/Cdc42KO), or NPM-ALK;CD4Cre;Rac1fl/fl (NPM-ALK/Rac1KO) mice (top). Immunostainings for Ki-67 (middle) and activated caspase-3 (bottom) in tumors of the indicated genotypes are shown. Scale bar, 50 μm. (B) Histograms represent the average diameter quantified by counting at least 100 cells for each genotype. Error bars indicated SEM. ***P < .001. (C) Quantification of the percentages of proliferating cells based on Ki-67 counts on sections stained by immunohistochemistry. Data were obtained from 10 different areas in 3 independent mice for each genotype. (D) Quantification of the percentages of apoptotic cells based on activated caspase-3 counts on sections stained by immunohistochemistry. Data were obtained from 10 different areas in 3 independent mice for each genotype. Error bars indicated SEM. ***P < .001.

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