S A Quezada

Summary

Publications

  1. Swanton C, McGranahan N, Starrett G, Harris R. APOBEC Enzymes: Mutagenic Fuel for Cancer Evolution and Heterogeneity. Cancer Discov. 2015;5:704-12 pubmed publisher
    ..APOBEC family members might represent a new class of drug target aimed at limiting tumor evolution, adaptation, and drug resistance. ..
  2. Turajlic S, Sottoriva A, Graham T, Swanton C. Resolving genetic heterogeneity in cancer. Nat Rev Genet. 2019;: pubmed publisher
    ..Nevertheless, an evolutionary framework is a powerful aid to understand cancer progression and therapy failure. Indeed, such a framework could be applied to predict individual tumour behaviour and support treatment strategies. ..
  3. Rosenthal R, Cadieux E, Salgado R, Bakir M, Moore D, Hiley C, et al. Neoantigen-directed immune escape in lung cancer evolution. Nature. 2019;: pubmed publisher
  4. Turajlic S, McGranahan N, Swanton C. Inferring mutational timing and reconstructing tumour evolutionary histories. Biochim Biophys Acta. 2015;1855:264-75 pubmed publisher
    ..We discuss how this knowledge can be used to illuminate the genes and pathways that drive cancer initiation and relapse; and to support drug development and clinical trial design. ..
  5. Turajlic S, Xu H, Litchfield K, Rowan A, Chambers T, Lopez J, et al. Tracking Cancer Evolution Reveals Constrained Routes to Metastases: TRACERx Renal. Cell. 2018;173:581-594.e12 pubmed publisher
    ..Finally, we observed early divergence of primitive ancestral clones and protracted latency of up to two decades as a feature of pancreatic metastases. ..
  6. Turajlic S, Xu H, Litchfield K, Rowan A, Horswell S, Chambers T, et al. Deterministic Evolutionary Trajectories Influence Primary Tumor Growth: TRACERx Renal. Cell. 2018;173:595-610.e11 pubmed publisher
    ..Our insights reconcile the variable clinical behavior of ccRCC and suggest evolutionary potential as a biomarker for both intervention and surveillance. ..
  7. McGranahan N, Favero F, de Bruin E, Birkbak N, Szallasi Z, Swanton C. Clonal status of actionable driver events and the timing of mutational processes in cancer evolution. Sci Transl Med. 2015;7:283ra54 pubmed publisher
    ..The frequent presence of subclonal driver mutations suggests the need to stratify targeted therapy response according to the proportion of tumor cells in which the driver is identified. ..
  8. Abbosh C, Birkbak N, Swanton C. Early stage NSCLC - challenges to implementing ctDNA-based screening and MRD detection. Nat Rev Clin Oncol. 2018;15:577-586 pubmed publisher
    ..We explain the technical and analytical challenges to low-frequency mutation detection using NGS-based ctDNA profiling and evaluate the feasibility of ctDNA profiling in both screening and MRD assessment contexts. ..
  9. Mitchell T, Turajlic S, Rowan A, Nicol D, Farmery J, O Brien T, et al. Timing the Landmark Events in the Evolution of Clear Cell Renal Cell Cancer: TRACERx Renal. Cell. 2018;173:611-623.e17 pubmed publisher
    ..Early development of ccRCC follows well-defined evolutionary trajectories, offering opportunity for early intervention. ..

More Information

Publications27

  1. Hiley C, Le Quesne J, Santis G, Sharpe R, De Castro D, Middleton G, et al. Challenges in molecular testing in non-small-cell lung cancer patients with advanced disease. Lancet. 2016;388:1002-11 pubmed publisher
    ..The use of next generation sequencing to recruit for molecularly stratified clinical trials is discussed in the context of the UK Stratified Medicine Programme and The UK National Lung Matrix Trial. ..
  2. Hiley C, Swanton C. Pruning Cancer's Evolutionary Tree with Lesion-Directed Therapy. Cancer Discov. 2016;6:122-4 pubmed publisher
    ..Next-generation sequencing of spatially and temporally separated biopsies and circulating tumor DNA directs therapy in response to tumor evolution and acquired resistance in colorectal cancer. ..
  3. Turajlic S, Swanton C. Metastasis as an evolutionary process. Science. 2016;352:169-75 pubmed publisher
    ..We also discuss the practical challenges associated with these studies and how they might be overcome. ..
  4. Szikriszt B, Póti A, Pipek O, Krzystanek M, Kanu N, Molnar J, et al. A comprehensive survey of the mutagenic impact of common cancer cytotoxics. Genome Biol. 2016;17:99 pubmed publisher
    ..Our results suggest genetic reversion due to cisplatin-induced mutations as a distinct mechanism for developing resistance. ..
  5. Kanu N, Cerone M, Goh G, Zalmas L, Bartkova J, Dietzen M, et al. DNA replication stress mediates APOBEC3 family mutagenesis in breast cancer. Genome Biol. 2016;17:185 pubmed publisher
  6. McGranahan N, Swanton C. Cancer Evolution Constrained by the Immune Microenvironment. Cell. 2017;170:825-827 pubmed publisher
    ..These complex interactions are highlighted in this issue of Cell by the results from Jiménez-Sánchez et al. of a deep analysis of one patient with advanced serous carcinoma of the ovary. ..
  7. McGranahan N, Rosenthal R, Hiley C, Rowan A, Watkins T, Wilson G, et al. Allele-Specific HLA Loss and Immune Escape in Lung Cancer Evolution. Cell. 2017;171:1259-1271.e11 pubmed publisher
    ..Characterizing HLA LOH with LOHHLA refines neoantigen prediction and may have implications for our understanding of resistance mechanisms and immunotherapeutic approaches targeting neoantigens. VIDEO ABSTRACT. ..
  8. McGranahan N, Swanton C. Clonal Heterogeneity and Tumor Evolution: Past, Present, and the Future. Cell. 2017;168:613-628 pubmed publisher
    ..We suggest that bold approaches to drug development, harnessing the adaptive properties of the immune-microenvironment while limiting those of the tumor, combined with advances in clinical trial-design, will improve patient outcome. ..
  9. BURRELL R, Swanton C. Re-Evaluating Clonal Dominance in Cancer Evolution. Trends Cancer. 2016;2:263-276 pubmed publisher
    ..Major shifts in current clinical practice and trial designs, aimed at understanding cancer evolution on a patient-by-patient basis, may be necessary to achieve more successful treatment of heterogeneous metastatic disease. ..
  10. Litchfield K, Turajlic S, Swanton C. The GENIE Is Out of the Bottle: Landmark Cancer Genomics Dataset Released. Cancer Discov. 2017;7:796-798 pubmed publisher
    ..i>Cancer Discov; 7(8); 796-8. ©2017 AACR.See related article by The AACR Project GENIE Consortium, p. 818. ..
  11. Turajlic S, Litchfield K, Xu H, Rosenthal R, McGranahan N, Reading J, et al. Insertion-and-deletion-derived tumour-specific neoantigens and the immunogenic phenotype: a pan-cancer analysis. Lancet Oncol. 2017;18:1009-1021 pubmed publisher
  12. Venkatesan S, Birkbak N, Swanton C. Constraints in cancer evolution. Biochem Soc Trans. 2017;45:1-13 pubmed publisher
    ..These constraints on cancer evolution may help us identify cancer evolutionary rule books, which could eventually inform both diagnostic and therapeutic approaches to improve survival outcomes. ..
  13. Berenjeno I, Piñeiro R, Castillo S, Pearce W, McGranahan N, Dewhurst S, et al. Oncogenic PIK3CA induces centrosome amplification and tolerance to genome doubling. Nat Commun. 2017;8:1773 pubmed publisher
    ..While this can limit the impact of PI3K-targeted therapies, these findings also open the opportunity for therapeutic approaches aimed at limiting tumour heterogeneity and evolution. ..
  14. Rosenthal R, McGranahan N, Herrero J, Taylor B, Swanton C. DeconstructSigs: delineating mutational processes in single tumors distinguishes DNA repair deficiencies and patterns of carcinoma evolution. Genome Biol. 2016;17:31 pubmed publisher
    ..deconstructSigs confers the ability to define mutational processes driven by environmental exposures, DNA repair abnormalities, and mutagenic processes in individual tumors with implications for precision cancer medicine. ..
  15. Lopez Garcia C, Sansregret L, Domingo E, McGranahan N, Hobor S, Birkbak N, et al. BCL9L Dysfunction Impairs Caspase-2 Expression Permitting Aneuploidy Tolerance in Colorectal Cancer. Cancer Cell. 2017;31:79-93 pubmed publisher
    ..Efforts to exploit aneuploidy tolerance mechanisms and the BCL9L/caspase-2/BID axis may limit cancer diversity and evolution. ..
  16. Jamal Hanjani M, Wilson G, Horswell S, Mitter R, Sakarya O, Constantin T, et al. Detection of ubiquitous and heterogeneous mutations in cell-free DNA from patients with early-stage non-small-cell lung cancer. Ann Oncol. 2016;27:862-7 pubmed publisher
    ..Further validation of mPCR-NGS in cfDNA is required to define its potential use in clinical practice. ..
  17. Birkbak N, Hiley C, Swanton C. Evolutionary Precision Medicine: A Role for Repeat Epidermal Growth Factor Receptor Analysis in ALK-Rearranged Lung Adenocarcinoma?. J Clin Oncol. 2015;33:3681-3 pubmed publisher
  18. Turajlic S, Larkin J, Swanton C. Academically led clinical trials: challenges and opportunities. Ann Oncol. 2015;26:2010-1 pubmed publisher