Background: Breast cancer (BRCA), the hormone related malignant tumor, is well-known for poor prognosis. ZNF208 mainly acts as a transcription factor in various tumors, and the single nucleotide polymorphisms (SNPs) of ZNF208 are related to telomere length. Nevertheless, its role in breast tumorigenesis is largely unknown.
Methods: We systematically investigated the gene expression, prognostic value, and promoter methylation of in BRCA with Gene Expression Profiling Interactive Analysis (GEPIA) and DNA Methylation Interactive Visualization Database (DNMIVD). Meanwhile, we clarified the association of ZNF208 with tumor-infiltrating immune cells (TICs) from Tumor Immune Estimation Resource (TIMER). Furthermore, we determined the biological process and functional enrichment from Cancer single-cell state atlas (CancerSEA). Finally, we verified our results with prognostic analysis and immunohistochemistry (IHC) assay.
Results: We discovered that ZNF208 was downregulated in breast cancer, and low expression of ZNF208 predicted worse prognosis of BRCA patients. The promoter methylation level of was obviously increased, and ZNF208 was associated with TlCs in BRCA. In addition, ZNF208 could inhibit the metastasis and invasion biological processes, and regulate the MAPK and RAS signaling pathways in BRCA.
Conclusion: Our findings illustrate that ZNF208 can function as a tumor suppressor and predict prognosis of breast cancer.
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http://dx.doi.org/10.1177/11795549241301341 | DOI Listing |
Health Serv Insights
December 2024
Department of Surgery, Faculty of Medicine, Universiti Malaya, Kuala Lumpur, Malaysia.
One of the main challenges in breast cancer management is health system literacy to provide optimal and timely diagnosis and treatments within complex and multidisciplinary health system environments. Digitalised patient navigation programs have been developed and found to be helpful in high- and low-resource settings, but gaps remain in finding cost-effective navigation in the public sector in Malaysia, where resources are scarce and unstable. Hence, we set out to develop a virtual patient navigation application for breast cancer patients to enhance knowledge about cancer diagnosis and treatments and provide a tracking mechanism to ensure quality care.
View Article and Find Full Text PDFFront Oncol
December 2024
Analysis of Circulating Tumor Cells, Laboratory of Analytical Chemistry, Department of Chemistry, University of Athens, Athens, Greece.
Introduction: Detection of mutations in primary tumors and liquid biopsy samples is of increasing importance for treatment decisions and therapy resistance in many types of cancer. The aim of the present study was to directly compare the efficacy of a relatively inexpensive ultrasensitive real-time PCR with the well-established and highly sensitive technology of ddPCR for the detection of the three most common hotspot mutations of , in exons 9 and 20, that are all of clinical importance in various types of cancer.
Patients And Methods: We analyzed 42 gDNAs from primary tumors (FFPEs), 29 plasma-cfDNA samples, and 29 paired CTC-derived gDNAs, all from patients with ER+ metastatic breast cancer, and plasma from 10 healthy donors.
Ann Surg Open
December 2024
Duke Cancer Institute, Duke University, Durham, NC.
Nanoscale Adv
December 2024
Department of "Scienze e Tecnologie Biologiche, Chimiche e Farmaceutiche" (STEBICEF), University of Palermo Via Archirafi 32 90123 Palermo Italy nicolo.mauroatunipa.it.
Carbon dot (CD)-based theranostics offers a promising approach for breast cancer (BC) treatment, integrating ultra-localized chemo-photothermal effects to address chemoresistance and enhance therapeutic control. Herein, the development of a targeted theranostic nanosystem for the chemo-phototherapy of breast cancer is described. Fluorescent and biocompatible CDs were passivated with 1,2-bis(3-aminopropylamino)ethane (bAPAE) and decorated with the targeting agent folic acid (FA) through conjugation with a PEG spacer.
View Article and Find Full Text PDFActivation of PLCβ enzymes by G and G proteins is a common mechanism to trigger cytosolic Ca increase. We and others reported that G inhibitor FR900358 (FR) can inhibit both and G - and, surprisingly, G -mediated intracellular Ca mobilization. Thus, the G -G -PLCβ-Ca signaling axis depends entirely on the presence of active G , which reasonably explained FR-inhibited G -induced Ca release.
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