Tag: Single-Cell

Conquer

[PMID: 29481549] [Nature Methods]

Bias, robustness and scalability in single-cell differential expression analysis

“conquer, a repository of consistently processed, analysis-ready public scRNA-seq data sets that is aimed at simplifying method evaluation and reanalysis of published results.” “Currently, conquer contains 36 data sets: 31 generated with full-length protocols and 5 with 3′-end sequencing (UMI) protocols.”

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MEC by Single-Cell RNA-seq

[PMID: 29225342] [Nature Communications]

Differentiation dynamics of mammary epithelial cells revealed by single-cell RNA sequencing

“Here we report the use of single-cell RNA sequencing to determine the gene expression profile of MECs across four developmental stages; nulliparous, mid gestation, lactation and post involution. Our analysis of 23,184 cells identifies 15 clusters, few of which could be fully characterised by a single marker gene. We argue instead that the epithelial cells—especially in the luminal compartment—should rather be conceptualised as being part of a continuous spectrum of differentiation. Furthermore, our data support the existence of a common luminal progenitor cell giving rise to intermediate, restricted alveolar and hormone-sensing progenitors. This luminal progenitor compartment undergoes transcriptional changes in response to a full pregnancy, lactation and involution.”

CNA Evolution from Primary to CTCs

[PMID: 28487279] [Genome Research]

Single-cell sequencing deciphers a convergent evolution of copy number alterations from primary to circulating tumor cells

“Here, we studied genomic alterations in single primary tumor cells and circulating tumor cells (CTCs) from the same patient. Single-nucleotide variants (SNVs) in single cells from both samples occurred sporadically, whereas CNAs among primary tumor cells emerged accumulatively rather than abruptly, converging toward the CNA in CTCs. Focal CNAs affecting the MYC gene and the PTEN gene were observed only in a minor portion of primary tumor cells but were present in all CTCs, suggesting a strong selection toward metastasis. Single-cell structural variant (SV) analyses revealed a two-step mechanism, a complex rearrangement followed by gene amplification, for the simultaneous formation of anomalous CNAs in multiple chromosome regions.”