Figure 1
Figure 1. Molecular diagnostic signatures of PTCL subgroups. (A) Unique gene expression signatures were identified for major PTCL entities using compound covariate prediction model (see Materials and methods for details), and the predictor score from top ranking genes for each subtype was used to classify a PTCL patient. ALCL and ENKTL groups are further differentiated into ALK(+)ALCL and ALK(–)ALCL, and NK and γδ T-cell subgroups, respectively. Each column represents a PTCL patient and each row represents a unique gene of the classifier. The relative gene expression scale is indicated below. (B) Pathological vs molecular diagnosis comparison. Substantial number of cases from PTCL-NOS were molecularly classified into WHO recognized PTCL subgroups: (i) AITL (n = 21, 14%); (ii) ALK(–)ALCL (n = 17, 11%); (iii) ATLL (n = 4, 3%); (iv) γδ-PTCL (n = 13, 9%). However, 26 AITL cases (22%) were not molecularly classifiable and changed to PTCL-NOS.

Molecular diagnostic signatures of PTCL subgroups. (A) Unique gene expression signatures were identified for major PTCL entities using compound covariate prediction model (see Materials and methods for details), and the predictor score from top ranking genes for each subtype was used to classify a PTCL patient. ALCL and ENKTL groups are further differentiated into ALK(+)ALCL and ALK(–)ALCL, and NK and γδ T-cell subgroups, respectively. Each column represents a PTCL patient and each row represents a unique gene of the classifier. The relative gene expression scale is indicated below. (B) Pathological vs molecular diagnosis comparison. Substantial number of cases from PTCL-NOS were molecularly classified into WHO recognized PTCL subgroups: (i) AITL (n = 21, 14%); (ii) ALK(–)ALCL (n = 17, 11%); (iii) ATLL (n = 4, 3%); (iv) γδ-PTCL (n = 13, 9%). However, 26 AITL cases (22%) were not molecularly classifiable and changed to PTCL-NOS.

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