11 research outputs found
Screening and Identification of a Prognostic Model of Ovarian Cancer by Combination of Transcriptomic and Proteomic Data
The integration of transcriptome and proteome analysis can lead to the discovery of a myriad of biological insights into ovarian cancer. Proteome, clinical, and transcriptome data about ovarian cancer were downloaded from TCGA’s database. A LASSO–Cox regression was used to uncover prognostic-related proteins and develop a new protein prognostic signature for patients with ovarian cancer to predict their prognosis. Patients were brought together in subgroups using a consensus clustering analysis of prognostic-related proteins. To further investigate the role of proteins and protein-coding genes in ovarian cancer, additional analyses were performed using multiple online databases (HPA, Sangerbox, TIMER, cBioPortal, TISCH, and CancerSEA). The final resulting prognosis factors consisted of seven protective factors (P38MAPK, RAB11, FOXO3A, AR, BETACATENIN, Sox2, and IGFRb) and two risk factors (AKT_pS473 and ERCC5), which can be used to construct a prognosis-related protein model. A significant difference in overall survival (OS), disease-free interval (DFI), disease-specific survival (DSS), and progression-free interval (PFI) curves were found in the training, testing, and whole sets when analyzing the protein-based risk score (p < 0.05). We also illustrated a wide range of functions, immune checkpoints, and tumor-infiltrating immune cells in prognosis-related protein signatures. Additionally, the protein-coding genes were significantly correlated with each other. EMTAB8107 and GSE154600 single-cell data revealed that the genes were highly expressed. Furthermore, the genes were related to tumor functional states (angiogenesis, invasion, and quiescence). We reported and validated a survivability prediction model for ovarian cancer based on prognostic-related protein signatures. A strong correlation was found between the signatures, tumor-infiltrating immune cells, and immune checkpoints. The protein-coding genes were highly expressed in single-cell RNA and bulk RNA sequencing, correlating with both each other and tumor functional states
A Multifunctional Nanocatalytic Metal-Organic Framework as a Ferroptosis Amplifier for Mild Hyperthermia Photothermal Therapy
Hyperthermia therapy is considered an effective anticancer strategy. However, high temperature can trigger an excessive inflammatory response, leading to tumor self-protection, immunosuppression, metastasis, and recurrence. To address this issue, we reported a multifunctional photothermal nanoplatform to achieve mild hyperthermia photothermal therapy (mild PTT) based on cisplatin (DDP) and a ferrocene metal-organic framework (MOF-Fc) nanocomposite, which can specifically enhance ferroptosis-triggered oxidative stress levels and synchronously amplify mild hyperthermia PTT-mediated anticancer responses. Both in vitro and in vivo antineoplastic results verify the superiority of mild PTT with DDP/MOF-Fc@HA. The combination of DDP and MOF-Fc exhibits Fenton catalytic activity and glutathione depletion capacity, magnifying mild hyperthermia effects via the radical oxygen species (ROS)-adenosine triphosphate (ATP)-HSP silencing pathway, with important implications for clinical hyperthermia therapy
Supplementary Material from Synthesis of 11-Oxygenated Androgens in Peripheral Tissue Revealed by Enzyme Gene Expression and LC-MS/MS Quantification
<p>Supplementary Material from Synthesis of 11-Oxygenated Androgens in Peripheral Tissue Revealed by Enzyme Gene Expression and LC-MS/MS Quantification</p>
Fabrication of Electrically Bistable Organic Semiconducting/Ferroelectric Blend Films by Temperature Controlled Spin Coating
A document level neural model integrated domain knowledge for chemical-induced disease relations
Aberrant epigenetic and genetic marks are seen in myelodysplastic leukocytes and reveal Dock4 as a candidate pathogenic gene on chromosome 7q.
Myelodysplastic syndromes (MDS) are characterized by abnormal and dysplastic maturation of all blood lineages. Even though epigenetic alterations have been seen in MDS marrow progenitors, very little is known about the molecular alterations in dysplastic peripheral blood cells. We analyzed the methylome of MDS leukocytes by the HELP assay and determined that it was globally distinct from age-matched controls and was characterized by numerous novel, aberrant hypermethylated marks that were located mainly outside of CpG islands and preferentially affected GTPase regulators and other cancer-related pathways. Additionally, array comparative genomic hybridization revealed that novel as well as previously characterized deletions and amplifications could also be visualized in peripheral blood leukocytes, thus potentially reducing the need for bone marrow samples for future studies. Using integrative analysis, potentially pathogenic genes silenced by genetic deletions and aberrant hypermethylation in different patients were identified. DOCK4, a GTPase regulator located in the commonly deleted 7q31 region, was identified by this unbiased approach. Significant hypermethylation and reduced expression of DOCK4 in MDS bone marrow stem cells was observed in two large independent datasets, providing further validation of our findings. Finally, DOCK4 knockdown in primary marrow CD34(+) stem cells led to decreased erythroid colony formation and increased apoptosis, thus recapitulating the bone marrow failure seen in MDS. These findings reveal widespread novel epigenetic alterations in myelodysplastic leukocytes and implicate DOCK4 as a pathogenic gene located on the 7q chromosomal region