γδ T-cells in human malignancies: insights from single-cell studies and analytical considerations.

γδ T-cells are a rare population of T-cells with both adaptive and innate-like properties. Despite their low prevalence, they have been found to be implicated various human diseases. γδ T-cell infiltration has been associated with improved clinical outcomes in solid cancers, prompting renewed interest in understanding their biology.

Comparison of an amplicon-based large panel next generation sequencing (NGS) assay with conventional testing methods for MET and HER2 amplification in lung and breast cancers.

The frequency of MET and HER2 amplification being detected by next generation sequencing (NGS) is increasing due to NGS being increasingly adopted for molecular profiling of cancers. However, the accuracy of NGS in detecting these gene amplifications remains uncertain due to conflicting reports in the scientific literature. We studied the accuracy of an amplicon-based large panel NGS assay in detecting MET and HER2 amplification in lung and breast cancers, respectively, by comparing it against conventional testing methods.

Cord blood-derived V2 and V2 T cells acquire differential cell state compositions upon in vitro expansion.

Human cord blood-derived γδ T cells (CB) display a highly diverse TCR repertoire and have a unique subtype composition different from fetal or adult peripheral blood counterparts. We expanded CB in vitro using an irradiated Epstein-Barr virus-transformed feeder cell-based modified rapid expansion protocol (REP). Single-cell RNA sequencing tracked progressive differentiation of naïve CB into cells expressing neoantigen-reactive tumor-infiltrating lymphocyte as well as tissue-resident memory precursor-like and antigen-presenting cell-like gene signatures.

Deep learning for de-convolution of Smad2 versus Smad3 binding sites.

Background: The transforming growth factor beta-1 (TGF β-1) cytokine exerts both pro-tumor and anti-tumor effects in carcinogenesis. An increasing body of literature suggests that TGF β-1 signaling outcome is partially dependent on the regulatory targets of downstream receptor-regulated Smad (R-Smad) proteins Smad2 and Smad3. However, the lack of Smad-specific antibodies for ChIP-seq hinders convenient identification of Smad-specific binding sites.

R248Q mutation--Beyond p53-DNA binding.

R248 in the DNA binding domain (DBD) of p53 interacts directly with the minor groove of DNA. Earlier nuclear magnetic resonance (NMR) studies indicated that the R248Q mutation resulted in conformation changes in parts of DBD far from the mutation site. However, how information propagates from the mutation site to the rest of the DBD is still not well understood.