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• A108846B

  Whole genome sequencing for single cells for library A108846B 1636 cells; filetype=bam

  Dataset EGAD00001007092

• Whole Exome sequencing of colorectal cancer patients (SG-BULK)

  DNA-seq libraries were captured to exome regions using xGen Exome Research Panel v1.0 (IDT), and libraries were prepared using the KAPA Hyper prep kit. DNA libraries were sequenced to a target depth of ×200 for tumor sample, ×100 for normal samples on the Illumina HiSeq platform.

  Dataset EGAD00001008543

• A90679

  Whole genome sequencing for single cells for library A90679 1034 samples; filetype=bam

  Dataset EGAD00001008219

• A95635B

  Whole genome sequencing for single cells for library A95635B 593 samples; filetype=bam

  Dataset EGAD00001008223

• A95635D

  Whole genome sequencing for single cells for library A95635D 367 samples; filetype=bam

  Dataset EGAD00001008224

• A95654A

  Whole genome sequencing for single cells for library A95654A 901 samples; filetype=bam

  Dataset EGAD00001008225

• A95662A

  Whole genome sequencing for single cells for library A95662A 637 samples; filetype=bam

  Dataset EGAD00001008226

• A95664B

  Whole genome sequencing for single cells for library A95664B 630 samples; filetype=bam

  Dataset EGAD00001008227

• The long term effects of chemotherapy on normal blood - Nanoseq dataset

  In developed countries, ~10% of individuals are exposed to systemic chemotherapy for cancer and other diseases. Many chemotherapeutic agents act by increasing DNA damage in cancer cells, hence triggering cell death. However, there is limited understanding of the extent and consequences of collateral DNA damage to normal tissues. To investigate the impact of chemotherapy on mutation burdens and cell population structure of a normal tissue we sequenced blood cell genomes from 23 individuals, aged 3-80 years, treated with a range of chemotherapy regimens. Substantial additional mutation loads with characteristic mutational signatures were imposed by some chemotherapeutic agents, but there were differences in burden between different classes of agent, different agents of the same class and different blood cell types. Chemotherapy also induced premature changes in the cell population structure of normal blood, similar to those of normal ageing. The results constitute an initial survey of the long-term biological consequences of cytotoxic agents to which a substantial fraction of the population is exposed during the course of their disease management, raising mechanistic questions and highlighting opportunities for mitigation of adverse effects.

  Dataset EGAD00001015340

• Human microglial transitions at the Aβ–Tau inflection point associate with divergent pathways to dementia and resilience

  Alzheimer's disease depends not just on plaques and tangles, but on how brain cells respond to them. Using spatial and single-cell genomics across cognitively impaired octogenarians, healthy octogenarians, and cognitively intact centenarians with similar amyloid levels, we identified six spatial tissue states forming a disease continuum with a critical transition point where amyloid-driven inflammation gives way to tau-linked cellular programs. Microglia drive this shift, progressing from early inflammatory to late antigen-presenting states — and resilient individuals diverged here: healthy octogenarians never activated the late microglial program, while centenarians did so without the expected tau accumulation. This positions microglial state transitions at the amyloid-to-tau boundary as key targets for understanding and promoting resilience to Alzheimer's disease.

  Study EGAS50000001692