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Lotan, Y.

Publications and source records attributed to Lotan, Y..

2 recordsLinked to original sources

A Distinct Mode of Chromosome-End Genome Instability Revealed by Circulome Characterization and Analyses

Genome instability is a central hallmark of cancer and it is characterized largely from sequence: mutation, copy-number change and rearrangement scored against a linear reference. The genome has additional degrees of freedom, such as the physical form (topology) of the DNA itself. A specific mode of localized genome dynamics changes both dimensions (sequence and topology) at once: defined chromosomal regions are also represented as extrachromosomal circular DNA (eccDNA). The biogenesis of eccDNA is a feature of many cancers, supplying the tumor with genetic elements that can participate in phenotypic selection, and supplying the observer with a window into the genomic instability landscape. Genome-wide maps of where these circles arise have not been available at scale or at high resolution. Building such maps requires physical selection of circular species, because most sequenced reads from unselected DNA derive from unrearranged sequence, conflating the signal from dynamic rearrangements with that from bulk chromosomal DNA. Here we combine biophysical and biochemical isolation of circular DNA with next-generation sequencing, applying it to a panel of cancer cell lines and to patient tumors, with non-cancerous cells and adjacent normal tissues as controls. The resulting genome-wide maps of the circular-element repertoire, the Circulome, reveal a consistent and previously unreported enrichment of these elements at particular chromosome ends. The circles map to regions extending well past the telomeres, reaching varying distances up to tens of megabases inward. This activity is accompanied by corroborating rearrangements within the linear genome, consistent with regions of chromosomal instability. Together these features define a spatially localized mode of instability in cancer, which we term Erosion at Distal Genomic Ends (EDGE). We formulate a classification problem to discriminate bladder tumor from matched normal tissue, finding that the EDGE signal outperforms the mean of all interior chromosomal regions, for each chromosome. These findings define a distinct spatial signature of cancer chromosome instability detectable through Circulome analysis, and connect early models of region-specific instability to the human cancer genome.

genomics↗

Mitochondrial metabolism in primary and metastatic human kidney cancers

Most kidney cancers display evidence of metabolic dysfunction1-4 but how this relates to cancer progression in humans is unknown. We used a multidisciplinary approach to infuse 13C-labeled nutrients during surgical tumour resection in over 70 patients with kidney cancer. Labeling from [U-13C]glucose varies across cancer subtypes, indicating that the kidney environment alone cannot account for all metabolic reprogramming in these tumours. Compared to the adjacent kidney, clear cell renal cell carcinomas (ccRCC) display suppressed labelling of tricarboxylic acid (TCA) cycle intermediates in vivo and in organotypic slices cultured ex vivo, indicating that suppressed labeling is tissue intrinsic. Infusions of [1,2-13C]acetate and [U-13C]glutamine in patients, coupled with respiratory flux of mitochondria isolated from kidney and tumour tissue, reveal primary defects in mitochondrial function in human ccRCC. However, ccRCC metastases unexpectedly have enhanced labeling of TCA cycle intermediates compared to primary ccRCCs, indicating a divergent metabolic program during ccRCC metastasis in patients. In mice, stimulating respiration in ccRCC cells is sufficient to promote metastatic colonization. Altogether, these findings indicate that metabolic properties evolve during human kidney cancer progression, and suggest that mitochondrial respiration may be limiting for ccRCC metastasis but not for ccRCC growth at the site of origin.

cancer biology↗