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FISH on a TMA of 239 ovarian tumours, including 73 of known molecular subtype found evidence for rearrangement between HACE1 and LIN28B in only a single core from a HG-SOC tumour of unknown molecular subtype (Table S6), suggesting this mechanism for LIN28B up-regulation is rare in ovarian carcinoma.
These relationships were reflected in the pattern of association with molecular subtype (Table 4).
Tumours detected by screening generally had more favourable outcomes than non-screen-detected cancers regardless of the molecular subtype (Table 3).
Within the multivariate model, the most significant hazard covariate for patient outcome was in fact the non-PN molecular subtype (Table 2: HR = 1.93, P-value = 1.4e-4).
The effect of screen detection on survival was then explored in a multivariate analysis after adjustment for tumour characteristics, the NPI, individual molecular biomarker expression and molecular subtype (Table 5).
This is reflected in the presentation rates of the metastatic disease, stratified by molecular subtype (Table 3).> Significantly, the relapse rates vary considerably by subtype, with HER2 + ve the highest (51.4%%), followed by luminal B (42.9 %), basal (35.1 %) and luminal A (27.8 %).
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We next applied the centroid model to the Rembrandt dataset to classify each of the samples to one of the four molecular subtypes (Table 2 and Figure 1A).
We then tested variables to identify predictors of survival outcomes by applying Cox proportional hazard models within strata of molecular subtypes (Table 5).
Although most FTD occurs in the absence of a known genetic mutation, each FTD clinical syndrome bears a different relationship to the FTLD genetic and molecular subtypes (Table 1).
In models that included age at and year of diagnosis, HIV status was also not associated with stages III or IV vs stages I and II; grades 2 and 3 vs grade 1; or molecular subtypes (Table 2).
Although patients in subgroup G1 experienced increased risk of late recurrence, this subgroup was not considered as a desired model for this study, because subgroup G1 showed an unbalanced distribution of breast cancer molecular subtypes (Table 2), and the upregulated gene cluster C2 was not directly correlated with late recurrence (Table 3).
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com