Deficiency in the breast cancer type 1 (BRCA1) gene expression predisposes to triple-negative breast cancer (TNBC) and ovarian cancer (OC). We previously identified by Comparative Genomic Hybridization (CGH) array a gain in the 17q25.3 genomic region in 90% of the BRCA1 mutated TNBC tissues, where 17 genes were up-regulated. A second region (Chr19_45681759_54221324) was identified as the second most frequent gain in the BRCA1-mutated population and has not yet been described in the context of BRCA1 mutation. We thus aimed to validate the expression of the Casein kinase 1 delta (CSNK1D) gene of Chr17 in TNBC and OC cell lines and to investigate the expression of genes of Chr19 in TNBC cell lines and tissues as well as in OC cell lines. Expression level of the genes of the 17q25.3, 19q13.32,13.33 and 13.41 chromosomal regions was analyzed using RT-PCR in BRCA1 deficient TNBC and OC cell lines, as well as in 10 BRCA1-mutated TNBC tissues versus 10 wild type carriers. Our results revealed a significant upregulation of CSNK1D gene expression in BRCA1 deficient TNBC and OC cell lines when compared to control ones, and a significant aberration in the expression of the other six genes of Chr19 was observed. Interestingly, upregulation of kallikrein-related peptidase 6 (KLK6) was detected among the BRCA1 deficient TNBC (cell lines and tissues) and OC cell lines. In conclusion, our results suggested that CSNK1D and KLK6 expression levels could be very promising in the search for biomarkers for BRCA1 deficient TNBC and OC.
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http://dx.doi.org/10.1080/15257770.2024.2357267 | DOI Listing |
Eur J Epidemiol
January 2025
Department of Neurobiology, Care Sciences and Society, Division of Family Medicine and Primary Care, Karolinska Institutet, Stockholm, Sweden.
The Stockholm Early Detection of Cancer Study (STEADY-CAN) cohort was established to investigate strategies for early cancer detection in a population-based context within Stockholm County, the capital region of Sweden. Utilising real-world data to explore cancer-related healthcare patterns and outcomes, the cohort links extensive clinical and laboratory data from both inpatient and outpatient care in the region. The dataset includes demographic information, detailed diagnostic codes, laboratory results, prescribed medications, and healthcare utilisation data.
View Article and Find Full Text PDFNPJ Precis Oncol
January 2025
Zentalis Pharmaceuticals, Inc., San Diego, CA, USA.
Upregulation of Cyclin E1 and subsequent activation of CDK2 accelerates cell cycle progression from G1 to S phase and is a common oncogenic driver in gynecological malignancies. WEE1 kinase counteracts the effects of Cyclin E1/CDK2 activation by regulating multiple cell cycle checkpoints. Here we characterized the relationship between Cyclin E1/CDK2 activation and sensitivity to the selective WEE1 inhibitor azenosertib.
View Article and Find Full Text PDFSci Rep
January 2025
School of Medicine, Nankai University, Tianjin, 300071, China.
Cholangiocarcinoma (CCA), a highly aggressive form of cancer, is known for its high mortality rate. A Disintegrin and Metalloprotease Domain-like Protein Decysin-1 (ADAMDEC1) can promote the development and metastasis in various tumors by degrading the extracellular matrix. However, its regulatory mechanism in CCA remains unclear.
View Article and Find Full Text PDFAnn Hematol
January 2025
Department of Hematology, Navy Medical Center of PLA, Naval Medical University, No. 338 West Huaihai Road, Changning District, Shanghai, 200052, China.
Multiple myeloma(MM) remains incurable with high relapse and chemoresistance rates. Differentially expressed genes(DEGs) between newly diagnosed myeloma and secondary plasma cell leukemia(sPCL) were subjected to a weighted gene co-expression network analysis(WGCNA). Drug resistant myeloma cell lines were established.
View Article and Find Full Text PDFSci Rep
January 2025
School of Physics, Engineering and Technology, University of York, Heslington, York, YO10 5DD, UK.
Prostate cancer is a disease which poses an interesting clinical question: Should it be treated? Only a small subset of prostate cancers are aggressive and require removal and treatment to prevent metastatic spread. However, conventional diagnostics remain challenged to risk-stratify such patients; hence, new methods of approach to biomolecularly sub-classify the disease are needed. Here we use an unsupervised self-organising map approach to analyse live-cell Raman spectroscopy data obtained from prostate cell-lines; our aim is to exemplify this method to sub-stratify, at the single-cell-level, the cancer disease state using high-dimensional datasets with minimal preprocessing.
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