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Chromosomal instability of cancer can be quantitatively measured by phylogenetic analysis of 200 tumor cells while using evolutionary principles to account for cellular selection.

Unique mechanisms of genetic exchange in the important protozoan pathogen Trypanosome cruzi were characterized in detail using genome analyses of hybrid clones at different time points, showing initial tetraploids followed by genome erosion.

Non-coding mutations in microsatellite-instable (MSI) colorectal tumors are prevalent and activate cancer-specific enhancers, thereby disrupting gene expression control.

Based on the proteomics results, T1 CRC LNM prediction models were built using machine learning, the functional differences and biomarkers between LNM-negative and LNM-positive patients were revealed.

Exosomes secreted from pancreatic cancer cells can function as a classic initiator in the multi-step cellular transformation process.

Transcription elongation by the elongation factor P-TEFb promotes the epithelial–mesenchymal transition and metastasis of breast cancer cells, implicating inhibition of this factor as a potential treatment for the late stages of this cancer.

Mice studies show that the 'just-right' balance optimal for BRAF^V600E-induced cecal tumor formation can be achieved through FAK alteration.

Previously uncharacterized long repeat sequences are associated with significant genome variation that can increase fitness and promote antifungal drug resistance in diverse isolates of Candida albicans.

Genomic approaches can be integrated with epidemiological and ecological studies to provide high-resolution answers to open questions about schistosomiasis transmission dynamics, offering a level of precision that is actionable, such that schistosomiasis-control programming can be tailored to regional contexts.