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Our understanding on the genetic alterations in gliomas has led to the recognition of several molecular subtypes with distinct clinical, prognostic, and imaging characteristics [9,10].
Recent findings indicate that PDAC, formerly presumed a homogeneous entity, has distinct morphological and molecular subtypes with different biological behavior and prognosis.
We hypothesized that variation in the transcriptional programming of AC tumors might distinguish molecular subtypes with differential outcomes after CRS/HIPEC.
Gene expression profiling of human breast cancers has identified a number of distinct molecular subtypes with different biological properties and prognoses [19].
The relatively poor outcome in adult ALL has been explained by an increased frequency of high-risk molecular subtypes with more aggressive clinical behavior and greater drug resistance, poorer tolerance and compliance with treatment, and less effective treatment regimens compared with childhood ALL [6], [8], [9].
It was indicating that RRM2 protein levels were higher in the molecular subtypes with poor outcomes.
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In the present study, only shifts to a molecular subtype with worse prognosis were observed.
Of the 295 data sets, 26 had unspecified molecular subtype with unknown ER, PR or HER2 expression status.
Group B was the most predominant molecular subtype with 68% (n = 126) of the strains in this cluster.
When comparing BluePrint molecular subtyping with clinical stratification, the prognosis (10-year DMFS) was significantly different in 10-year DMFS between the different molecular subtypes (p < 0.001).
Luminal A was the most frequent molecular subtype with 140 patients (46%), followed by luminal B with 102 women (34%), 38 TN (12%), and 24 HER2 positive (nonluminal) (8%).
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