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This proof-of-concept evaluation demonstrates that next-generation sequencing-based liquid biopsy can detect genomic alterations in the blood of cats with cancer and the absence of such alterations in the blood of presumably cancer-free cats. Two cats with cytologically confirmed lymphoma and nine presumably cancer-free cats were included in this analysis. Whole blood was collected from each subject and samples were subjected to DNA extraction, library preparation, and next-generation sequencing. Both cancer-diagnosed subjects had somatic copy number variants (a "cancer signal") identified in cell-free DNA, suggesting the current presence of cancer in these subjects. All nine presumably cancer-free subjects had unremarkable genomic profiles, suggesting the absence of cancer in these subjects. Liquid biopsy using nextgeneration sequencing of cell-free DNA allows for blood-based detection of cancer-associated genomic alterations in cats. Such technology has the potential to offer considerable utility in veterinary medicine, particularly for the non-invasive prioritization of small cell intestinal lymphoma versus inflammatory bowel disease in cats with gastrointestinal signs. This study lays the foundation for future studies to fully validate this type of testing for use in clinical practice. [ABSTRACT FROM AUTHOR]

Fish aquaculture has become the fastest growing sector in global food production. Thus, ensuring the sustainability of aquaculture practices is of the utmost importance. Studies in higher vertebrates (i.e. mammals) have demonstrated the role of the host microbiome in physiological processes from nutrient acquisition to pathogen protection. Therefore, analysis of fish microbiomes is an important factor to consider with regard to overall animal health and welfare. Rainbow trout (Oncorhynchus mykiss) are an economically valued fish cultured worldwide. Several studies have identified microbial constituents inhabiting the intestinal tract of rainbow trout. To better elucidate some of the core constituents of the rainbow trout intestinal microbiome, this systematic literature review analysed the relative abundance results from 25 articles published on the rainbow trout intestinal microbiome from 2017 to 2021. Bacteria classified within the phyla Firmicutes and Proteobacteria were observed in every study. At the family level, Lactobacillaceae was consistently observed. Additionally, bacteria in the Actinobacteria, Bacteroides, and Tenericutes phyla were identified in at least 50% of the studies. Interestingly, Mycoplasma spp. were occasionally the most dominant organisms present in the microbiome. Overall, the results here identify bacteria that are commonly found members of the rainbow trout intestinal microbiome. [ABSTRACT FROM AUTHOR]

Simple Summary: In humans there is a biological phenomenon known as CHIP (clonal hematopoiesis of indeterminate potential) in which somatic (acquired) mutations cause blood cells of a certain type to grow disproportionately by making many copies (or "clones") of themselves. Although most people who are found to have CHIP do not have cancer, they are known to be at higher risk of developing cancer. CHIP has been studied extensively in humans, where it occurs more frequently with increasing age and is thought to be present in 10–20% of people over the of age 70; however, CHIP has not been well-studied in other species. This study provides the first population-level evidence for the potential existence of CHIP-like findings in dogs. Further research is needed to determine the clinical significance of these findings in canine patients. Age-related somatic genomic alterations in hematopoietic cell lines have been well characterized in humans; however, this phenomenon has not been well studied in other species. Next-generation sequencing-based liquid biopsy testing for cancer detection was recently developed for dogs and has been used to study the genomic profiles of blood samples from thousands of canine patients since 2021. In this study, 4870 client-owned dogs with and without a diagnosis or suspicion of cancer underwent liquid biopsy testing by this method. Copy number variants detected exclusively in genomic DNA derived from white blood cells (WBC gDNA-specific CNVs) were observed in 126 dogs (2.6%; 95% CI: 2.2–3.1); these copy number variants were absent from matched plasma cell-free DNA, and from tumor tissue in dogs with concurrent cancer. These findings were more common in older dogs and were persistent in WBC gDNA in over 70% of patients, with little to no change in the amplitude of the signal across longitudinal samples. Many of these alterations were observed at recurrent locations in the genome across subjects; the most common finding was a partial loss on CFA25, typically accompanied by a partial gain on the same chromosome. These early findings suggest that age-related somatic alterations may be present at an appreciable frequency in the general canine population. Further research is needed to determine the clinical significance of these findings. [ABSTRACT FROM AUTHOR]

Changes in the three-dimensional (3D) structure of the genome are an emerging hallmark of cancer. Cancer-associated copy number variants and single nucleotide polymorphisms promote rewiring of chromatin loops, disruption of topologically associating domains (TADs), active/inactive chromatin state switching, leading to oncogene expression and silencing of tumor suppressors. However, little is known about 3D changes during cancer progression to a chemotherapy-resistant state. We integrated chromatin conformation capture (Hi-C), RNA-seq, and whole-genome sequencing obtained from triple-negative breast cancer patient-derived xenograft primary tumors (UCD52) and carboplatin-resistant samples and found increased short-range (< 2 Mb) interactions, chromatin looping, formation of TAD, chromatin state switching into a more active state, and amplification of ATP-binding cassette transporters. Transcriptome changes suggested the role of long-noncoding RNAs in carboplatin resistance. Rewiring of the 3D genome was associated with TP53, TP63, BATF, FOS-JUN family of transcription factors and led to activation of aggressiveness-, metastasis- and other cancer-related pathways. Integrative analysis highlighted increased ribosome biogenesis and oxidative phosphorylation, suggesting the role of mitochondrial energy metabolism. Our results suggest that 3D genome remodeling may be a key mechanism underlying carboplatin resistance. [ABSTRACT FROM AUTHOR]

Changes in the three-dimensional (3D) structure of the genome are an emerging hallmark of cancer. Cancer-associated copy number variants and single nucleotide polymorphisms promote rewiring of chromatin loops, disruption of topologically associating domains (TADs), active/inactive chromatin state switching, leading to oncogene expression and silencing of tumor suppressors. However, little is known about 3D changes during cancer progression to a chemotherapy-resistant state. We integrated chromatin conformation capture (Hi-C), RNA-seq, and whole-genome sequencing obtained from triple-negative breast cancer patient-derived xenograft primary tumors (UCD52) and carboplatin-resistant samples and found increased short-range (< 2 Mb) interactions, chromatin looping, formation of TAD, chromatin state switching into a more active state, and amplification of ATP-binding cassette transporters. Transcriptome changes suggested the role of long-noncoding RNAs in carboplatin resistance. Rewiring of the 3D genome was associated with TP53, TP63, BATF, FOS-JUN family of transcription factors and led to activation of aggressiveness-, metastasis- and other cancer-related pathways. Integrative analysis highlighted increased ribosome biogenesis and oxidative phosphorylation, suggesting the role of mitochondrial energy metabolism. Our results suggest that 3D genome remodeling may be a key mechanism underlying carboplatin resistance. [ABSTRACT FROM AUTHOR]

The document is a correction notice for an article titled "Rewiring of the 3D genome during acquisition of carboplatin resistance in a triple-negative breast cancer patient-derived xenograft" published in Scientific Reports. The correction addresses an error in the Acknowledgements section, updating the funding information and adding a new grant. The correction was made by a group of authors led by Mikhail G. Dozmorov and J. Chuck Harrell. [Extracted from the article]

Motivation Chromosome conformation capture technologies (Hi-C) revealed extensive DNA folding into discrete 3D domains, such as Topologically Associating Domains and chromatin loops. The correct binding of CTCF and cohesin at domain boundaries is integral in maintaining the proper structure and function of these 3D domains. 3D domains have been mapped at the resolutions of 1 kilobase and above. However, it has not been possible to define their boundaries at the resolution of boundary-forming proteins. Results To predict domain boundaries at base-pair resolution, we developed preciseTAD , an optimized transfer learning framework trained on high-resolution genome annotation data. In contrast to current TAD/loop callers, preciseTAD -predicted boundaries are strongly supported by experimental evidence. Importantly, this approach can accurately delineate boundaries in cells without Hi-C data. preciseTAD provides a powerful framework to improve our understanding of how genomic regulators are shaping the 3D structure of the genome at base-pair resolution. Availability and implementation preciseTAD is an R/Bioconductor package available at https://bioconductor.org/packages/preciseTAD/. Supplementary information Supplementary data are available at Bioinformatics online. [ABSTRACT FROM AUTHOR]

The whole genome sequencing data generated in this study have been submitted to the NCBI SRA database (https://www.ncbi.nlm.nih.gov/bioproject/) under accession number PRJNA832117, reviewer's accession link: https://dataview.ncbi.nlm.nih.gov/object/PRJNA832117. All original code has been deposited at Github (https://github.com/dozmorovlab/PDXHiC supplemental)." now reads: "All raw and processed sequencing data generated in this study have been submitted to the NCBI Gene Expression Omnibus (GEO; https://www.ncbi.nlm.nih.gov/geo/), under accession number GSE201435. The whole genome sequencing data generated in this study have been submitted to the NCBI SRA database (https://www.ncbi.nlm.nih.gov/bioproject/), under accession number PRJNA832117: https://dataview.ncbi.nlm.nih.gov/object/PRJNA832117. [Extracted from the article]