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Abstract Objectives Gastrointestinal stromal tumors (GISTs) carrying different KIT exon 11 (KIT-11) mutations exhibit varying prognoses and responses to Imatinib. Herein, we aimed to determine whether computed tomography (CT) radiomics can accurately stratify KIT-11 mutation genotypes to benefit Imatinib therapy and GISTs monitoring. Methods Overall, 1143 GISTs from 3 independent centers were separated into a training cohort (TC) or validation cohort (VC). In addition, the KIT-11 mutation genotype was classified into 4 categories: no KIT-11 mutation (K11-NM), point mutations or duplications (K11-PM/D), KIT-11 557/558 deletions (K11-557/558D), and KIT-11 deletion without codons 557/558 involvement (K11-D). Subsequently, radiomic signatures (RS) were generated based on the arterial phase of contrast CT, which were then developed as KIT-11 mutation predictors using 1408 quantitative image features and LASSO regression analysis, with further evaluation of its predictive capability. Results The TC AUCs for K11-NM, K11-PM/D, K11-557/558D, and K11-D ranged from 0.848 (95% CI 0.812–0.884), 0.759 (95% CI 0.722–0.797), 0.956 (95% CI 0.938–0.974), and 0.876 (95% CI 0.844–0.908), whereas the VC AUCs ranged from 0.723 (95% CI 0.660–0.786), 0.688 (95% CI 0.643–0.732), 0.870 (95% CI 0.824–0.918), and 0.830 (95% CI 0.780–0.878). Macro-weighted AUCs for the KIT-11 mutant genotype ranged from 0.838 (95% CI 0.820–0.855) in the TC to 0.758 (95% CI 0.758–0.784) in VC. TC had an overall accuracy of 0.694 (95%CI 0.660–0.729) for RS-based predictions of the KIT-11 mutant genotype, whereas VC had an accuracy of 0.637 (95%CI 0.595–0.679). Conclusions CT radiomics signature exhibited good predictive performance in estimating the KIT-11 mutation genotype, especially in prediction of K11-557/558D genotype. RS-based classification of K11-NM, K11-557/558D, and K11-D patients may be an indication for choice of Imatinib therapy.

Transition-metal-catalyzed allenes-involved C–H functionalizations demonstrate unique selectivity and undergo exceptional pathways due to the existence of elusive orthogonal cumulative CCC bonds. As a result, it allows for a diverse array of C–H activation reactions, such as allylation, alkenylation, allenylation, dienylation, propargylation, and annulation. In this review, we comprehensively summarize the noteworthy aspects of transition-metal-catalyzed C–H functionalizations involving variously substituted allenes.

Abstract Background Emerging evidence manifests that cyclin‐dependent kinase 6 (CDK6) plays an essential part in the initiation and progression of several types of human cancer, and its descending expression is correlated with an adverse prognosis. However, the precise role of CDK6 in Pancreatic cancer (PC) remains obscure. Aims To identify the potential ceRNA regulatory axis of CDK6 in PC and explore its relationship with immune cells and immune checkpoints. Materials & Methods Using The Cancer Genome Atlas TCGA and GTEx data analyze the expression and survival of CDK6 in patients in pan‐cancer, and cellular experiments were performed to verify the effect of CDK6 on cell function. Using GEPIA and STARBASE databases to analyze prognosis, expression and survival, and identify non coding RNA (ncRNA) that mediates CDK6 overexpression. The TIMER 2.0 database was used for immune correlation analysis. Results We revealed CDK6 might be an oncogene in PC, and the HOXA11‐AS /NR2F1‐AS1‐ miR‐454‐3p axis was identified as the possible upstream ncRNA‐associated pathway of CDK6 in PC. In addition, CDK6 show significant association with three immune checkpoints (PD‐L1, PD‐L2, and HAVCR2), the infiltration level of immune cells, and immunity biomarkers. Discussion We discussed some applications of CDK6 in breast cancer, melanoma, and hemorrhagic malignancies. The role of miR‐15a‐5p, HOXA11‐AS and NR2F1‐AS1 in tumor development was also discussed based on existing studies. The potential mechanism of CDK6 affecting immune cells in pancreatic cancer was discussed. Conclusions Overall, these results established that nc‐RNA‐mediated high expression of CDK6 is associated with patient outcomes and immune invasion in pancreatic cancer.

Trichomes are specialized structures developed from epidermal cells and can protect plants against biotic and abiotic stresses. Trichomes cover carrots during the generative phase. However, the morphology of the carrot trichomes and candidate genes controlling the formation of trichomes are still unclear. This study found that carrot trichomes were non-glandular and unbranched hairs distributed on the stem, leaf, petiole, pedicel, and seed of carrot. Resequencing analysis of a trichome mutant with sparse and short trichomes (sst) and a wild type (wt) with long and dense trichomes on carrot stems was conducted. A total of 15 396 genes containing nonsynonymous mutations in sst were obtained, including 42 trichome-related genes. We also analyzed the transcriptome of the trichomes on secondary branches when these secondary branches were 10 cm long between wt and sst and obtained 6 576 differentially expressed genes (DEGs), including 24 trichome-related genes. qRT-PCR validation exhibited three significantly up-regulated DEGs, 20 significantly down-regulated, and one with no difference. We considered both the resequencing and transcriptome sequencing analyses and found that 12 trichome-related genes that were grouped into five transcription factor families containing nonsynonymous mutations and significantly down-regulated in sst. Therefore, these genes are potentially promising candidate genes whose nonsynonymous mutations and down-regulation may result in scarce and short trichomes mutation on carrot stems in sst.

Numerous studies have accumulatively discovered mitochondrial genome (mtDNA) diversity in the natural populations of the same species, and some of the mtDNA variations may be selected by the host's environment. However, it remains unclear about the molecular mechanisms by which this long-term coexistence of mtDNA variations in the same species affects the metabolism and evolution of the host. By comparing two mitochondrial genomes of cultured population of Hermetia illucens, our study reveals that the mtDNAs of both strains (Ref-strain and Sub-strain) have great structural divergences, and mitochondria of the Sub-strain may be functionally defective, which is consistent with the observed lower body weights and higher oxidative stress levels in the midgut of Sub-strain. Moreover, the differentially expressed genes and differential metabolites between the midguts of both strains were related to the mitochondrial functions including oxidative stress, antioxidant and electron transport chain. Interesting, the midgut microbial compositions differed significantly in both strains. Additionally, 25 of 310 the potentially positively selected genes were related to mitochondrial function. Combination of these multidimensional investigations of both strains helped to reveal how the host insects adapt to mtDNA variations through cyto-nuclear interactions. This study can provide new evidence for understanding the nuclear response to the mitochondria dysfunction in insects, and its role in differentiation of the natural populations and even in the process of speciation. [ABSTRACT FROM AUTHOR]