Figure 7.
Patient samples resistant to ALK TKI show downregulation of PTPN1 and PTPN2 and upregulation of SHP2. (A) Representative hematoxylin-eosin and immunohistochemistry stainings of ALK, CD30, PTPN1, and PTPN2 in 1 ALK+ case expressing low PTPN1 and low PTPN2 (top) and 1 ALK+ ALCL case expressing high PTPN1 and high PTPN2 (bottom). Tumor cells are identified by ALK and CD30 stainings. High expression was determined by an H score >200. Scale bar, 100 μm. (B) Percentage of cases with high PTPN1 or PTPN2 protein expression of PTPN1 and PTPN2 evaluated by immunohistochemistry in human T-cell lymphoma subtypes: ALK+ ALCL (n = 30), ALK− ALCL (n = 18), AITL (n = 10), and peripheral T-cell lymphoma (n = 10). High expression was determined by an H score >200. (C) RNA-seq data from chemotherapy-relapsed/refractory (n = 2) and ALK TKI–resistant (n = 2) patients to evaluate mRNA expression of PTPN1, PTPN2, and PTPN11 (SHP2). ALK mutation status was analyzed by sequencing following a biopsy of relapsed lymphoma samples. The 2 patients that relapsed after chemotherapy showed WT ALK. Of the 2 patients relapsed during ALK TKI, 1 patient was WT, and 1 patient carried the L1196M mutation in ALK. See supplemental Figure 12 for treatment details. CPM, counts per million.

Patient samples resistant to ALK TKI show downregulation of PTPN1 and PTPN2 and upregulation of SHP2. (A) Representative hematoxylin-eosin and immunohistochemistry stainings of ALK, CD30, PTPN1, and PTPN2 in 1 ALK+ case expressing low PTPN1 and low PTPN2 (top) and 1 ALK+ ALCL case expressing high PTPN1 and high PTPN2 (bottom). Tumor cells are identified by ALK and CD30 stainings. High expression was determined by an H score >200. Scale bar, 100 μm. (B) Percentage of cases with high PTPN1 or PTPN2 protein expression of PTPN1 and PTPN2 evaluated by immunohistochemistry in human T-cell lymphoma subtypes: ALK+ ALCL (n = 30), ALK ALCL (n = 18), AITL (n = 10), and peripheral T-cell lymphoma (n = 10). High expression was determined by an H score >200. (C) RNA-seq data from chemotherapy-relapsed/refractory (n = 2) and ALK TKI–resistant (n = 2) patients to evaluate mRNA expression of PTPN1, PTPN2, and PTPN11 (SHP2). ALK mutation status was analyzed by sequencing following a biopsy of relapsed lymphoma samples. The 2 patients that relapsed after chemotherapy showed WT ALK. Of the 2 patients relapsed during ALK TKI, 1 patient was WT, and 1 patient carried the L1196M mutation in ALK. See supplemental Figure 12 for treatment details. CPM, counts per million.

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