We further sub-classified LH into patients with carcinomas expressing high levels of hormone receptors (LH-high; Allred score, oestrogen receptor [ER] and/or progesterone receptor [PgR] 4-8) (n=89 [53.6%]) or low levels (LH-low; Allred score, ER and/or PgR 2 or 3) (n=21 [12.7%]) for clinicohistomorphological characterization.
Staining of p53 and PARP1 in breast cancer TMAs and comparison with the TCGA database indicated a higher double-positive signal in basal-like breast cancer than in Luminal A or Luminal B subtypes.
In detail, higher expression levels of AKT1 and AKT2 negatively influenced overall patients' survival, and in particular, AKT2 expression levels defined a group of luminal B BC patients with shorter cancer-specific survival.
A supervised analysis of microarray data from the Alliance/ACOSOG Z1031 neoadjuvant aromatase inhibitor (AI) trial identified upregulated genes in Luminal B breast cancers that correlated with AI-resistant tumor proliferation (Pearson's correlation r ≥ 0.4 with Ki67) (33 cases Ki67 >10% on AI) versus Luminal-B breast cancers that were more AI-sensitive (33 cases Ki67 <10% on AI).
In conclusion, we show that PCA-PAM50 enhances the consistency of breast cancer intrinsic and clinical subtyping by reclassifying an aggressive subset of LA tumors into LB.
In subset univariate analyses, the infiltration by MPO-positive cells was associated with significantly better overall survival in the Luminal B/HER2-negative subtype (p = 0.005), the HER2 enriched subtype (p = 0.011), and the Triple Negative subtype (p < 0.001).
Furthermore, some pivotal fusion genes like ESR1-C6orf97 with COBRA1-C9orf167 and VAPB-IKZF3 with ACACA-STAC2 were found in Luminal A and Luminal B breast cancer, respectively.
Breast cancer tissues of HER2 overexpression and Basal-like were more significant than Luminal A and Luminal B. MIIP was obviously downregulated and IGFBP2 was upregulated in MDA-MB-231, SKBR3 and MCF-7 versus MCF-10A especially in MDA-MB-231.
The subsequent analysis of the Kaplan-Meier plotter cohort also demonstrated that CCL28 was a favorable prognostic factor for luminal-like cases [luminal A (P<0.001) and luminal B (P=0.031)], but a poor prognostic indicator for the patients with triple-negative phenotype (P<0.001).
Furthermore, some pivotal fusion genes like ESR1-C6orf97 with COBRA1-C9orf167 and VAPB-IKZF3 with ACACA-STAC2 were found in Luminal A and Luminal B breast cancer, respectively.
Breast cancer tissues of HER2 overexpression and Basal-like were more significant than Luminal A and Luminal B. MIIP was obviously downregulated and IGFBP2 was upregulated in MDA-MB-231, SKBR3 and MCF-7 versus MCF-10A especially in MDA-MB-231.
Moreover, each CIC subtype tended to preferentially affect different categories of breast cancer, with TiT (<i>P</i> < 0.0001) and oCICs (<i>P</i> = 0.008) targeting luminal B (Her2<sup>+</sup>), TiM (<i>P</i> = 0.011) targeting HR<sup>-</sup> (Her2<sup>+</sup>/HR<sup>-</sup> and TNBC), and MiT targeting luminal A (<i>P</i> = 0.017) and luminal B (Her<sup>-</sup>) (<i>P</i> = 0.006).
MCM2, MCM4, MCM6, and Ki-67 are highly expressed in breast cancer of high histological grades that comprise clinically aggressive tumors such as luminal B, HER2-positive, and triple-negative subtypes.
Our analysis showed that both MIF and IL-17A were associated with increased risk of breast cancer (OR 3.85 CI 95% 1.98-7.50 and OR 4.51 95% 1.83-11.15, respectively), higher in aggressive subtypes Luminal B, HER2 and TN.
In detail, higher expression levels of AKT1 and AKT2 negatively influenced overall patients' survival, and in particular, AKT2 expression levels defined a group of luminal B BC patients with shorter cancer-specific survival.
Furthermore, some pivotal fusion genes like ESR1-C6orf97 with COBRA1-C9orf167 and VAPB-IKZF3 with ACACA-STAC2 were found in Luminal A and Luminal B breast cancer, respectively.
Furthermore, some pivotal fusion genes like ESR1-C6orf97 with COBRA1-C9orf167 and VAPB-IKZF3 with ACACA-STAC2 were found in Luminal A and Luminal B breast cancer, respectively.