Ge-modified Si(100) substrates for the growth of 3C-SiC (100)

An alternative route to improve the epitaxial growth of 3C-SiC (100) on Si(100) was developed. It consists in covering the silicon wafers with germanium prior to the carbonization step of the silicon substrate. Transmission electron microscopy and μ -Raman investigations revealed an improvement in the residual strain and crystalline quality of the grown 3C-SiC layers comparable to or better than in the case of 3C-SiC grown on silicon on insulator substrates. These beneficial effects were reached by using a Ge coverage in the range of 0.5-1 monolayer

Raman studies of Ge-promoted stress modulation in 3C-SiC grown on Si(111)

We present a study of the stress state in cubic silicon carbide (3C-SiC) thin films (120 and 300 nm) grown by solid-source molecular-beam epitaxy (SSMBE) on Si(111) substrates modified by the deposition of germanium prior to the carbonization of Si. μ -Raman measurements were used to determine the residual stress existing in the 3C-SiC layers. The stress is found to decrease linearly with increasing Ge quantity but with different strength depending on the 3C-SiC thickness deposited after the introduction of Ge. Based on secondary ions mass spectroscopy (SIMS) and transmission electron microscopy (TEM) analyses it is suggested that the Ge introduced prior to the carbonization step remains in the near-interface region and reduces the Si outdiffusion, which further reduces the stress state of the 3C-SiC layers

PIK3CA exon9 mutations associate with reduced survival, and are highly concordant between matching primary tumors and metastases in endometrial cancer

Mutations of the phosphoinositide-3-kinase (PI3K) catalytic subunit alpha gene (PIK3CA) are frequent in endometrial cancer. We sequenced exon9 and exon20 of PIK3CA in 280 primary endometrial cancers to assess the relationship with clinicopathologic variables, patient survival and associations with PIK3CA mRNA and phospho-AKT1 by gene expression and protein data, respectively. While PIK3CA mutations generally had no impact on survival, and were not associated with clinicopathological variables, patients with exon9 charge-changing mutations, providing a positive charge at the substituted amino acid residue, were associated with poor survival (p = 0.018). Furthermore, we characterized PIK3CA mutations in the metastatic setting, including 32 patients with matched primary tumors and metastases, and found a high level of concordance (85.7%; 6 out of 7 patients), suggesting limited heterogeneity. PIK3CA mRNA levels were increased in metastases compared to the primary tumors (p = 0.031), independent of PIK3CA mutation status, which rather associated with reduced PIK3CA mRNA expression. PIK3CA mutated tumors expressed higher p-AKT/AKT protein levels, both within primary (p < 0.001) and metastatic lesion (p = 0.010). Our results support the notion that the PI3K signaling pathway might be activated, both dependent- and independently of PIK3CA mutations, an aspect that should be considered when designing PIK3 pathway targeting strategies in endometrial cancer