Relationship between PET/CT images and KRAS gene mutations in colorectal cancer in Vietnamese patients

OBJECTIVE: We conducted this study to determine the relationship among standardized uptake value (SUV), metabolic tumor volume (MTV), and total lesion glycolysis (TLG) indexes of Flourine-18 fluorodeoxyglucose positron emission tomography/computed tomography18 (FDG-PET/CT) imaging and Kirsten rat sarcoma (KRAS) gene mutations in colorectal cancer (CRC). PATIENTS AND METHODS: This cross-sectional study was conducted in Bach Mai Hospital from 2020 to 2022. It included newly diagnosed CRC patients who underwent PET/CT examination prior to primary tumor resection. The maximum SUV (SUVmax – SUVmean), MTV, and TLG were considered. All pathologically confirmed CRC patients were accepted with further KRAS mutation status analysis. RESULTS: We enrolled 63 newly diagnosed CRC patients who underwent PET/CT examination prior to primary tumor resection. Among them, 31 (49.2%) patients had KRAS gene mutation. Patients with KRAS mutation status showed significantly different and higher SUVmax (p-value = 0.025), SUVmax t/b (p-value = 0.013), SUVmax t-b (p-value = 0.014), MTV (p-value = 0.023), and TLG (p-value = 0.011) than patients with WT KRAS. Other characteristics, including age, gender, tumor location, SUVb, SUVmean, SUVmax of lymph nodes, and SUVmax of liver metastasis, were insignificantly different between the two groups of patients with KRAS mutation status. Receiver operating curve analysis showed that the area under the curve was 0.672 for SUVmax (p-value = 0.019), SUVt/b (p-value = 0.045), and SUVt-b (p-value = 0.020). CONCLUSIONS: We observed a relationship, considering the quantitative parameters (SUVmax, SUVmax, SUVmax t-b, MTV, and TLG), between 18FDG-PET/CT images and the KRAS gene mutation in CRC by analyzing 63 patients prior to treatment

The chromatin landscape of healthy and injured cell types in the human kidney

There is a need to define regions of gene activation or repression that control human kidney cells in states of health, injury, and repair to understand the molecular pathogenesis of kidney disease and design therapeutic strategies. Comprehensive integration of gene expression with epigenetic features that define regulatory elements remains a significant challenge. We measure dual single nucleus RNA expression and chromatin accessibility, DNA methylation, and H3K27ac, H3K4me1, H3K4me3, and H3K27me3 histone modifications to decipher the chromatin landscape and gene regulation of the kidney in reference and adaptive injury states. We establish a spatially-anchored epigenomic atlas to define the kidney’s active, silent, and regulatory accessible chromatin regions across the genome. Using this atlas, we note distinct control of adaptive injury in different epithelial cell types. A proximal tubule cell transcription factor network of ELF3, KLF6, and KLF10 regulates the transition between health and injury, while in thick ascending limb cells this transition is regulated by NR2F1. Further, combined perturbation of ELF3, KLF6, and KLF10 distinguishes two adaptive proximal tubular cell subtypes, one of which manifested a repair trajectory after knockout. This atlas will serve as a foundation to facilitate targeted cell-specific therapeutics by reprogramming gene regulatory networks. © 2024, The Author(s).Open access journalThis item from the UA Faculty Publications collection is made available by the University of Arizona with support from the University of Arizona Libraries. If you have questions, please contact us at [email protected]