Although the role of evolutionary process in cancer progression is widely accepted, increasing attention is being given to the evolutionary mechanisms that can lead to differences in clinical outcome. Recent studies suggest that the temporal order in which somatic mutations accumulate during cancer progression is important. Single-cell sequencing (SCS) provides a unique opportunity to examine the effect that the mutation order has on cancer progression and treatment effect. However, the error rates associated with single-cell sequencing are known to be high, which greatly complicates the task. We propose a novel method for inferring the order in which somatic mutations arise within an individual tumor using noisy data from single-cell sequencing. Our method incorporates models at two levels in that the evolutionary process of somatic mutation within the tumor is modeled along with the technical errors that arise from the single-cell sequencing data collection process. Through analyses of simulations across a wide range of realistic scenarios, we show that our method substantially outperforms existing approaches for identifying mutation order. Most importantly, our method provides a unique means to capture and quantify the uncertainty in the inferred mutation order along a given phylogeny. We illustrate our method by analyzing data from colorectal and prostate cancer patients, in which our method strengthens previously reported mutation orders. Our work is an important step towards producing meaningful prediction of mutation order with high accuracy and measuring the uncertainty of predicted mutation order in cancer patients, with the potential to lead to new insights about the evolutionary trajectories of cancer.
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http://dx.doi.org/10.1371/journal.pcbi.1010560 | DOI Listing |
Pol J Vet Sci
December 2024
University of Warmia and Mazury, Department of Animal Genetics, 10-719 Olsztyn, Oczapowskiego 5. Email: Tel.: +48/89/5234714.
The aim of the study was to find out whether carriers of new genetic defect Muscle Weakness (MW) occur in the population of Polish Holstein-Friesian bulls. Fifty bulls were included in the analysis. Bulls were selected as having in the pedigree known carrier of MW.
View Article and Find Full Text PDFZhonghua Yi Xue Za Zhi
December 2024
Neurofibromatosis type 1 (NF1) is an autosomal dominant genetic disorder caused by mutations in the NF1 gene, affecting approximately 1 in 3 000 newborns worldwide. Plexiform neurofibroma (PNF) is one of the common clinical manifestations of NF1. PNF can lead to a range of clinical symptoms, with a high rate of disability and teratogenesis; furthermore, there is a risk for malignant transformation that poses significant threats to the life and health of patients.
View Article and Find Full Text PDFSci Rep
December 2024
Department of Forensic Medicine, Guizhou Medical University, Guiyang, 550025, China.
Multi-insertion/deletion polymorphisms (Multi-InDels), as the novel genetic markers, show great potential in forensic research. Whereas, forensic researchers mainly focus on the multi-InDels on the autosomes, which can provide relatively limited information in some complex paternity cases. In this study, a novel X chromosomal multi-InDel multiplex amplification system was designed, containing 22 multi-InDels and one STR locus on the X chromosome.
View Article and Find Full Text PDFSci Rep
December 2024
Laboratory of Respiratory Diseases and Thoracic Surgery (BREATHE), Department of Chronic Diseases and Metabolism, KU Leuven, Leuven, Belgium.
The lungs of people with cystic fibrosis (PwCF) are characterized by recurrent bacterial infections and inflammation. Infections in cystic fibrosis (CF) are left unresolved despite excessive neutrophil infiltration. The role of CFTR in neutrophils is not fully understood.
View Article and Find Full Text PDFProtein Sci
January 2025
Department of Neuroscience, Biomedicine and Movement Sciences, Section of Biochemistry, University of Verona, Verona, Italy.
Human succinic semialdehyde dehydrogenase is a mitochondrial enzyme fundamental in the neurotransmitter γ-aminobutyric acid catabolism. It catalyzes the NAD-dependent oxidative degradation of its derivative, succinic semialdehyde, to succinic acid. Mutations in its gene lead to an inherited neurometabolic rare disease, succinic semialdehyde dehydrogenase deficiency, characterized by mental and developmental delay.
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