Krzysztof Skiba 09.12 2015 Wrocaw What is SCS? History of SCS - - PowerPoint PPT Presentation

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Krzysztof Skiba 09.12 2015 Wrocaw What is SCS? History of SCS - - PowerPoint PPT Presentation

Krzysztof Skiba 09.12 2015 Wrocaw What is SCS? History of SCS Clonal diversity and evolution in primary tumors Circulating tumor cells and metastatic dissemination Delineating complex chromosome rearrangements in single


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Krzysztof Skiba 09.12 2015 Wrocław

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 What is SCS?  History of SCS  Clonal diversity and evolution in primary tumors  Circulating tumor cells and metastatic dissemination  Delineating complex chromosome rearrangements in single cells  Evolution of therapy resistance  Mutator phenotypes  SCS in animal models  Translational applications of SCS in the clinic  Technical challenges and emerging technologies  Conclusions and future directions

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 Single cell sequencing  NGS on single cells  Huge impact on cancer research

Differences to NGS?

 Single cell extraction  WGA (whole genome amplification) before

NGS (genomic input in ng)

 Looped amplicons

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 Intratumor heterogeneity (phylogenetic lineages

for cells in tumor mass)

 Clonal evolution:

  • by SCS
  • mostly CNVs in early tumor cells development
  • SNPs accumulation over time

 Single cells share common founder mutations,

suggesting evolution from a common origin

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 Cells that circulate in blood  RARE (1 cel in 1 000 000)  Carry ~60% SNPs from primary and

metastatic tumors (prostate, lung, breast)

 Blood markers for tumors? (non invasive)  CTCs express their own extracellular matrix

proteins in the blood

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 Tumor evolution = chromosome structural

rearrangments = gene dosage effects

 Evolution dynamics  SCS represents cells at differnet evolution

time

 CNA – copy number aberrations, early in

tumor evolution

 Chromothripsis – within single chromosome

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 Initial response to therapy, but eventually

resistance to treatment

 Epithelial-to-mesenchymal transition (EMT)  Resistance clones preexisting (adaptive)  Induced new mutations (acquired)  SCS: Androgen gene amplification in CTCs

(prostate cancer = adaptive resistance)

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 Human cancers = higher mutation rate ?  Estimated mutation rate: 210 x normal cells  SCS: 2.5 nucleotide error per cell division

marginally higher then normal

 SCS: breast cancer – 13.3 x normal  SCS limited to few patients – need more

research

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 Genetically engineered mice (GEM)  Xenografts  SCS: transplantation of breast cancer from

human to mouse1 -> mouse2 ->… mouseN. Selection of tumor cells and high mutation rate.

 RNA-SCS: pancreatic cancer, CTCs and

fluorescent markers.

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 Phylogenetic trees -> therapeutic targets  CTCs and cancer cells in bodily fluids -> early

noninvasive detection

 SCS advantage -> very small clinical samples

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 Drop-seq (uses nanoliter droplets and

barcoded beads to capture single cells and performWTA, enabling RNA-SCS on 10,000– 100,000 cells in a single run )

 https://vimeo.com/128484564

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 SCS improoved understanding of

decelopment , heterogeneity, metastasis, invasion of tumor cells.

 SCS for gene expression analysis.  SCS as a tool for connecting genotypes with

phenotypes.

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The first five years of single-cell cancer genomics and beyond Nicholas E. Navin, doi:10.1101/gr.191098.115Genome Res. 2015. 25:1499-1507

https://en.wikipedia.org/wiki/MALBAC