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Prostate cancer (PCa) molecular subtypes have been defined by essentially mutually exclusive events, including ETS gene fusions (most commonly involving ERG) and SPINK1 overexpression.
Racial differences in molecular subtypes have been reported.
Breast cancers of different molecular subtypes have different survival rates.
Molecular subtypes have been shown to have prognostic and treatment predictive value.
Moreover, molecular subtypes have been associated with preferential sites of relapse.
Molecular subtypes have a clinical relevance inasmuch as they have different propensities to metastasize.
Similar(35)
For the 2nd validation dataset, favorable (C3 and C6) and unfavorable (C1, C2, C4, C5) prognostic molecular subtypes had already been defined by the authors [15].
Classifying breast cancers into molecular subtypes has significantly improved the understanding of preoperative chemotherapy outcomes and has helped guide the selection of treatment [ 9- 11].
Combining biological tumour markers into surrogate molecular subtypes has been shown to add prognostic information [ 6- 8, 10, 11] which may be of importance for recommendation of systemic therapy.
Considering a cohort of patients as a composite of a fixed set of molecular subtypes has distinct advantages when determining recurrent CNAs.
The greatest single difference between molecular subtypes has repeatedly been demonstrated to be between estrogen receptor-positive (ER+) luminal tumours and ER-negative basal tumours [ 6- 8, 13, 14].
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