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With the considerable understanding of intrinsic molecular subtypes, it is far from satisfactory to determine the clinical outcome exclusively by HR status.
Although this observation does not have a direct impact on the clinical utility of the 'intrinsic' molecular subtypes, it has led to the assumption that different subtypes of breast cancer would originate from different cell types [ 13, 39- 42].
Furthermore, in a study on methylation in breast cancer and breast cancer molecular subtypes it was shown that RASSF1A is hypermethylated in HER2 positive breast tumors (ERBB2 and luminal B) [ 35].
When the impact of ER-β expression on DFS was examined in the context of different BC molecular subtypes, it proved to be of further prognostic value in LA and LB patients, depending on their nodal status.
Looking at Ki67 values in different molecular subtypes, it seemed that patients with triple-negative or hormone receptor-positive, HER2-negative breast cancer had a more favorable prognosis when a pCR was achieved, although these patient groups had a higher Ki67 proliferation rate.
Similar(55)
Although standard gene centering is commonly applied prior to molecular subtyping, it produces inaccurate molecular subtype classifications when the study and training cohorts differ in their clinicopathological composition.
One case failed to be classified in one of the molecular subtypes, because it exhibited staining for PR, CK8, and high Ki67, but not for ER, HER2, and CK5/6.
If the same tendency is true for defects in other high penetrance breast cancer genes, tumors from genetically related patients would exhibit related molecular subtypes, as it is the case for BRCA1 and BRCA2 families.
Standard gene centering is routinely done prior to molecular subtyping, but it can produce inaccurate classifications when the distribution of clinicopathological characteristics in the study cohort differs from that of the training cohort used to derive the classifier.
Given the various molecular subtypes of medulloblastoma, it will be important to ensure that patients with relapsed disease receive subgroup-appropriate therapies (e.g., SMO inhibitors or future DDX3X inhibitors).
Although the HIS was an independent prognostic predictor across the different molecular subtypes of breast cancer, it remains unclear whether similar metastatic programs are involved in mediating metastasis in these other subtypes.
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