A novel sensitizer reduces EGFR-TKI resistance by regulating the PI3K/Akt/mTOR pathway and autophagy.

Background: The incidence and mortality of lung cancer are high, and treatment with epidermal growth factor receptor-tyrosine kinase inhibitor (EGFR-TKI) is the preferred first-line treatment for patients suffering from non-small cell lung cancer (NSCLC) with EGFR mutations. However, EGFR-TKI resistance leads to treatment failure. Yifei-Sanjie pill (YFSJ) is a novel type of Chinese patent medicine for lung cancer.

Structures of vertebrate R2 retrotransposon complexes during target-primed reverse transcription and after second strand nicking.

R2 retrotransposons are model site-specific eukaryotic non-LTR retrotransposons that copy-and-paste into gene loci encoding ribosomal RNAs. Recently we demonstrated that avian A-clade R2 proteins achieve efficient and precise insertion of transgenes into their native safe-harbor loci in human cells. The features of A-clade R2 proteins that support gene insertion are not characterized.

The Ruminant Telomere-to-Telomere (RT2T) Consortium.

Telomere-to-telomere (T2T) assemblies reveal new insights into the structure and function of the previously 'invisible' parts of the genome and allow comparative analyses of complete genomes across entire clades. We present here an open collaborative effort, termed the 'Ruminant T2T Consortium' (RT2T), that aims to generate complete diploid assemblies for numerous species of the Artiodactyla suborder Ruminantia to examine chromosomal evolution in the context of natural selection and domestication of species used as livestock.

Fetal growth delay caused by loss of non-canonical imprinting is resolved late in pregnancy and culminates in offspring overgrowth.

Germline epigenetic programming, including genomic imprinting, substantially influences offspring development. Polycomb Repressive Complex 2 (PRC2) plays an important role in Histone 3 Lysine 27 trimethylation (H3K27me3)-dependent imprinting, loss of which leads to growth and developmental changes in mouse offspring. In this study, we show that offspring from mouse oocytes lacking the PRC2 protein Embryonic Ectoderm Development (EED) were initially developmentally delayed, characterised by low blastocyst cell counts and substantial growth delay in mid-gestation embryos.