Figure 7
ERBB4 inhibition partially controls ALCL cell growth and disease progression of ERBB4-positive PDTs. (A) PDT explanted cells were treated with control diluent (DMSO) or neratinib at the indicated concentrations. Cell viability was measured over time by adenosine triphosphate–based luminescence assay. Results were normalized to DMSO controls at time 0 and represent the mean and standard error of 3 biological replicates. (B) In vivo tumor growth of PDT cells (5 × 104) subcutaneously injected into the flanks of 6 NSG mice. Mice with tumor masses of 0.5 cm diameter were treated with neratinib (40 mg/kg every 48 hours) or control diluent (Ctrl). Each data point represents the average tumor volume (mean ± standard error) for the indicated treatment condition (P = .0006). (C) Representative histologic sections stained with hematoxylin and eosin (H&E; top) of tumor masses derived from control or neratinib-treated animals. Tissue sections were stained for DNA breaks with the terminal deoxynucleotidyl transferase deoxyuridine triphosphate nick-end labeling method (bottom) and DAPI counterstained (middle). Original magnification ×20. (D) Box plot showing quantification of necrotic areas in 7 controls and in 9 neratinib-treated tumor masses (*P = .038). NT, no treatment.

ERBB4 inhibition partially controls ALCL cell growth and disease progression of ERBB4-positive PDTs. (A) PDT explanted cells were treated with control diluent (DMSO) or neratinib at the indicated concentrations. Cell viability was measured over time by adenosine triphosphate–based luminescence assay. Results were normalized to DMSO controls at time 0 and represent the mean and standard error of 3 biological replicates. (B) In vivo tumor growth of PDT cells (5 × 104) subcutaneously injected into the flanks of 6 NSG mice. Mice with tumor masses of 0.5 cm diameter were treated with neratinib (40 mg/kg every 48 hours) or control diluent (Ctrl). Each data point represents the average tumor volume (mean ± standard error) for the indicated treatment condition (P = .0006). (C) Representative histologic sections stained with hematoxylin and eosin (H&E; top) of tumor masses derived from control or neratinib-treated animals. Tissue sections were stained for DNA breaks with the terminal deoxynucleotidyl transferase deoxyuridine triphosphate nick-end labeling method (bottom) and DAPI counterstained (middle). Original magnification ×20. (D) Box plot showing quantification of necrotic areas in 7 controls and in 9 neratinib-treated tumor masses (*P = .038). NT, no treatment.

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