We therefore assessed whether these previously defined molecular subtypes were reproduced in the low and high-risk groups as defined by our 19-gene profile in the 2nd validation set (Figure 3).
Our finding that these molecular subtypes were overrepresented (enriched) in the high and low risk groups identified by our 19-gene profile, further attests to the notion that the profile is tracking true and reproducible outcome phenotypes in EOC.
Five molecular subtypes were identified, characterized by WNT signaling (A; 9 cases), SHH signaling (B; 15 cases), expression of neuronal differentiation genes (C and D; 16 and 11 cases, respectively) or photoreceptor genes (D and E; both 11 cases).
Molecular subtypes were defined by PAM50 [ 17].
Molecular subtypes were defined by immunohistochemistry (IHC).
Molecular subtypes were also evaluated as described below.
Five molecular subtypes were defined according to clinico-pathologic criteria.
Differences among the other three molecular subtypes were small.
Molecular subtypes were determined using PAM50 centroids [ 23].
All the intrinsic molecular subtypes were identified within TNBC, with BLBCs predominating (55 81.2%).
How the different molecular subtypes were defined by IHC is shown in Table 5.
