Table 1.

Clinical, pathologic, and genetic features of breast implant–associated ALCLs

ParameterNo. positive/no. studiedPercent positive
Capsular infiltration (T3*4/33 12 
Mass/infiltration beyond capsule (T4) 10/33 30 
Lymph node involvement 4/30 13 
ALK (IHC0/36 
DUSP22 rearrangement (FISH) 0/36 
TP63 rearrangement (FISH) 0/36 
pSTAT3Y705 (IHC) 27/27 100 
JAK1 mutation (NGS) 1/15 7§ 
JAK3 mutation (NGS) 0/15 
STAT3 mutation (NGS) 3/15 20 
STAT5A mutation (NGS) 0/15 
STAT5B mutation (NGS) 0/15 
ParameterNo. positive/no. studiedPercent positive
Capsular infiltration (T3*4/33 12 
Mass/infiltration beyond capsule (T4) 10/33 30 
Lymph node involvement 4/30 13 
ALK (IHC0/36 
DUSP22 rearrangement (FISH) 0/36 
TP63 rearrangement (FISH) 0/36 
pSTAT3Y705 (IHC) 27/27 100 
JAK1 mutation (NGS) 1/15 7§ 
JAK3 mutation (NGS) 0/15 
STAT3 mutation (NGS) 3/15 20 
STAT5A mutation (NGS) 0/15 
STAT5B mutation (NGS) 0/15 

FISH, fluorescence in situ hybridization; IHC, immunohistochemistry; NGS, next-generation sequencing.

*

Based on the TNM staging system of Clemens et al. T staging data were not available in 3 patients. Clinical data on 17 cases were previously reported in Miranda et al.

Extramammary staging data were not available in 6 patients; no spread to other organs/distant sites (M1) was identified in 30 evaluable patients.

Additional immunohistochemistry results are shown in supplemental Table 1.

§

Mutational frequencies are for mutations known or predicted to be activating.

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