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  1. Data from Adaptive Therapy Exploits Fitness Deficits in Chemotherapy-Resistant Ovarian Cancer to Achieve Long-Term Tumor Control
  2. Figure 1 from Adaptive Therapy Exploits Fitness Deficits in Chemotherapy-Resistant Ovarian Cancer to Achieve Long-Term Tumor Control
  3. Figure 2 from Adaptive Therapy Exploits Fitness Deficits in Chemotherapy-Resistant Ovarian Cancer to Achieve Long-Term Tumor Control
  4. Figure 3 from Adaptive Therapy Exploits Fitness Deficits in Chemotherapy-Resistant Ovarian Cancer to Achieve Long-Term Tumor Control
  5. Figure 4 from Adaptive Therapy Exploits Fitness Deficits in Chemotherapy-Resistant Ovarian Cancer to Achieve Long-Term Tumor Control
  6. Figure 5 from Adaptive Therapy Exploits Fitness Deficits in Chemotherapy-Resistant Ovarian Cancer to Achieve Long-Term Tumor Control
  7. Figure 6 from Adaptive Therapy Exploits Fitness Deficits in Chemotherapy-Resistant Ovarian Cancer to Achieve Long-Term Tumor Control
  8. Figure 7 from Adaptive Therapy Exploits Fitness Deficits in Chemotherapy-Resistant Ovarian Cancer to Achieve Long-Term Tumor Control
  9. Figure 8 from Adaptive Therapy Exploits Fitness Deficits in Chemotherapy-Resistant Ovarian Cancer to Achieve Long-Term Tumor Control
  10. Supplementary Figure 1 from Adaptive Therapy Exploits Fitness Deficits in Chemotherapy-Resistant Ovarian Cancer to Achieve Long-Term Tumor Control
  11. Supplementary Figure 2 from Adaptive Therapy Exploits Fitness Deficits in Chemotherapy-Resistant Ovarian Cancer to Achieve Long-Term Tumor Control
  12. Supplementary Figure 3 from Adaptive Therapy Exploits Fitness Deficits in Chemotherapy-Resistant Ovarian Cancer to Achieve Long-Term Tumor Control
  13. Supplementary Figure 4 from Adaptive Therapy Exploits Fitness Deficits in Chemotherapy-Resistant Ovarian Cancer to Achieve Long-Term Tumor Control
  14. Supplementary Figure 5 from Adaptive Therapy Exploits Fitness Deficits in Chemotherapy-Resistant Ovarian Cancer to Achieve Long-Term Tumor Control
  15. Supplementary Figure 6 from Adaptive Therapy Exploits Fitness Deficits in Chemotherapy-Resistant Ovarian Cancer to Achieve Long-Term Tumor Control
  16. Supplementary Figure 7 from Adaptive Therapy Exploits Fitness Deficits in Chemotherapy-Resistant Ovarian Cancer to Achieve Long-Term Tumor Control
  17. Supplementary Figure 8 from Adaptive Therapy Exploits Fitness Deficits in Chemotherapy-Resistant Ovarian Cancer to Achieve Long-Term Tumor Control
  18. Supplementary Figure 9 from Adaptive Therapy Exploits Fitness Deficits in Chemotherapy-Resistant Ovarian Cancer to Achieve Long-Term Tumor Control
  19. Supplementary Table 1 from Adaptive Therapy Exploits Fitness Deficits in Chemotherapy-Resistant Ovarian Cancer to Achieve Long-Term Tumor Control
  20. Supplementary Table 2 from Adaptive Therapy Exploits Fitness Deficits in Chemotherapy-Resistant Ovarian Cancer to Achieve Long-Term Tumor Control
  21. Mathematical modelling of cancer cell evolution and plasticity
  22. Quantitative measurement of phenotype dynamics during cancer drug resistance evolution using genetic barcoding
  23. Adaptive Therapy Exploits Fitness Deficits in Chemotherapy-Resistant Ovarian Cancer to Achieve Long-Term Tumor Control
  24. Quantitative measurement of phenotype dynamics during cancer drug resistance evolution using genetic barcoding
  25. Deep Learning for Biomarker Discovery in Cancer Genomes
  26. Phenotypic noise and plasticity in cancer evolution
  27. Gene mutant dosage determines prognosis and metastatic tropism in 60,000 clinical cancer samples
  28. Contribution of pks+ E. coli mutations to colorectal carcinogenesis
  29. Adaptive therapy achieves long-term control of chemotherapy resistance in high grade ovarian cancer
  30. Bridging clinic and wildlife care with AI-powered pan-species computational pathology
  31. First passage time analysis of spatial mutation patterns reveals sub-clonal evolutionary dynamics in colorectal cancer
  32. Whole genome sequencing of 2,023 colorectal cancers reveals mutational landscapes, new driver genes and immune interactions
  33. Cell Competition in Carcinogenesis
  34. The mutational signatures of formalin fixation on the human genome
  35. Lineage tracing in human tissues
  36. AI-powered pan-species computational pathology: bridging clinic and wildlife care
  37. CNETML: Maximum likelihood inference of phylogeny from copy number profiles of spatio-temporal samples
  38. AI-powered pan-species computational pathology: bridging clinic and wildlife care
  39. First passage time analysis of spatial mutation patterns reveals evolutionary dynamics of pre-existing resistance in colorectal cancer
  40. Evolutionary dynamics in Barrett oesophagus: implications for surveillance, risk stratification and therapy
  41. LiquidCNA: Tracking subclonal evolution from longitudinal liquid biopsies using somatic copy number alterations
  42. Predicting Colorectal Cancer Occurrence in IBD
  43. The mutational signatures of formalin fixation on the human genome
  44. LiquidCNA: tracking subclonal evolution from longitudinal liquid biopsies using somatic copy number alterations
  45. Genomic landscape and clonal architecture of mouse oral squamous cell carcinomas dictate tumour ecology
  46. Platinum resistance induces diverse evolutionary trajectories in high grade serous ovarian cancer
  47. Navigating the path to distant metastasis
  48. Author Correction: The effects of mutational processes and selection on driver mutations across cancer types
  49. Measuring the distribution of fitness effects in somatic evolution by combining clonal dynamics with dN/dS ratios
  50. Measuring single cell divisions in human tissues from multi-region sequencing data
  51. A novel use of random priming-based single-strand library preparation for whole genome sequencing of formalin-fixed paraffin-embedded tissue samples
  52. Author Correction: Resolving genetic heterogeneity in cancer
  53. Spatially constrained tumour growth affects the patterns of clonal selection and neutral drift in cancer genomic data
  54. Measuring the distribution of fitness effects in somatic evolution by combining clonal dynamics with dN/dS ratios
  55. Niche engineering drives early passage through an immune bottleneck in progression to colorectal cancer
  56. Resolving genetic heterogeneity in cancer
  57. Model-based tumor subclonal reconstruction
  58. Crypt fusion as a homeostatic mechanism in the human colon
  59. Measuring single cell divisions in human cancers from multi-region sequencing data
  60. Spatially constrained tumour growth affects the patterns of clonal selection and neutral drift in cancer genomic data
  61. Evolutionary dynamics of neoantigens in growing tumours
  62. NeoPredPipe: High-Throughput Neoantigen Prediction and Recognition Potential Pipeline
  63. Reply to ‘Currently available bulk sequencing data do not necessarily support a model of neutral tumor evolution’
  64. Reply to ‘Revisiting signatures of neutral tumor evolution in the light of complexity of cancer genomic data’
  65. Detecting repeated cancer evolution from multi-region tumor sequencing data
  66. The evolutionary landscape of colorectal tumorigenesis
  67. Author Correction: Quantification of subclonal selection in cancer from bulk sequencing data
  68. Evolutionary history of human colitis-associated colorectal cancer
  69. Quantification of subclonal selection in cancer from bulk sequencing data
  70. The effects of mutational processes and selection on driver mutations across cancer types
  71. Reply: Neutral tumor evolution?
  72. Evolution of Barrett’s esophagus through space and time at single-crypt and whole-biopsy levels
  73. Robust RNA-based in situ mutation detection delineates colorectal cancer subclonal evolution
  74. Cumulative burden of inflammation predicts colorectal neoplasia risk in ulcerative colitis: a large single-centre study
  75. Insights Into the Pathophysiology of Esophageal Adenocarcinoma
  76. Reply: Uncertainties in tumor allele frequencies limit power to infer evolutionary pressures
  77. Detecting repeated cancer evolution in human tumours from multi-region sequencing data
  78. Quantification of within-sample genetic heterogeneity from SNP-array data
  79. Between-region genetic divergence reflects the mode and tempo of tumor evolution
  80. Catch my drift? Making sense of genomic intra-tumour heterogeneity
  81. Quantification of subclonal selection in cancer from bulk sequencing data
  82. Measuring cancer evolution from the genome
  83. New paradigms in clonal evolution: punctuated equilibrium in cancer
  84. Tumour Cell Heterogeneity
  85. Identification of neutral tumor evolution across cancer types
  86. Pan-cancer analysis of the extent and consequences of intratumor heterogeneity
  87. Derivation of genetic biomarkers for cancer risk stratification in Barrett’s oesophagus: a prospective cohort study
  88. Solutions to Peto's paradox revealed by mathematical modelling and cross-species cancer gene analysis
  89. Krt19+/Lgr5− Cells Are Radioresistant Cancer-Initiating Stem Cells in the Colon and Intestine
  90. Forty-Year Analysis of Colonoscopic Surveillance Program for Neoplasia in Ulcerative Colitis: An Updated Overview
  91. Characterization of LGR5 stem cells in colorectal adenomas and carcinomas
  92. A pan-cancer signature of neutral tumor evolution
  93. A Big Bang model of human colorectal tumor growth
  94. Gremlin 1 Identifies a Skeletal Stem Cell with Bone, Cartilage, and Reticular Stromal Potential
  95. Location, location, location! The reality of life for an intestinal stem cell in the crypt
  96. Quantification of Crypt and Stem Cell Evolution in the Normal and Neoplastic Human Colon
  97. Cell migration leads to spatially distinct but clonally related airway cancer precursors
  98. Re: Mitochondria and Tumor Progression in Ulcerative Colitis
  99. Stochastic homeostasis in human airway epithelium is achieved by neutral competition of basal cell progenitors
  100. Clonal Selection and Persistence in Dysplastic Barrettʼs Esophagus and Intramucosal Cancers After Failed Radiofrequency Ablation
  101. Crypt dysplasia in Barrett's oesophagus shows clonal identity between crypt and surface cells
  102. Lineage tracing reveals multipotent stem cells maintain human adenomas and the pattern of clonal expansion in tumor evolution
  103. What Can Be Learnt about Disease Progression in Breast Cancer Dormancy from Relapse Data?
  104. Pre-tumour clones, periodic selection and clonal interference in the origin and progression of gastrointestinal cancer: potential for biomarker development
  105. LRIG1 regulates cadherin-dependent contact inhibition directing epithelial homeostasis and pre-invasive squamous cell carcinoma development
  106. Modelling the evolution of genetic instability during tumour progression
  107. Resolving the stem-cell debate
  108. Field Cancerization in the Intestinal Epithelium of Patients With Crohn's Ileocolitis
  109. A basal gradient of Wnt and stem-cell number influences regional tumour distribution in human and mouse intestinal tracts
  110. Utilizing DNA Mutations to Trace Epithelial Cell Lineages in Human Tissues
  111. Barrett's metaplasia glands are clonal, contain multiple stem cells and share a common squamous progenitor
  112. Clonal architecture of human prostatic epithelium in benign and malignant conditions
  113. Field cancerization in the GI tract
  114. The human urothelium consists of multiple clonal units, each maintained by a stem cell
  115. Use of Methylation Patterns to Determine Expansion of Stem Cell Clones in Human Colon Tissue
  116. The Clonal Origins of Dysplasia From Intestinal Metaplasia in the Human Stomach
  117. Stem cells and their implications for colorectal cancer
  118. Stem Cells and Inflammation in the Intestine
  119. Field defects in DNA repair: is loss of MGMT an initial event in colorectal carcinogenesis?
  120. Breast Cancer Dormancy Can Be Maintained by Small Numbers of Micrometastases
  121. Spindles losing their bearings: Does disruption of orientation in stem cells predict the onset of cancer?
  122. Clonality Assessment and Clonal Ordering of Individual Neoplastic Crypts Shows Polyclonality of Colorectal Adenomas
  123. Genetic diversity during the development of Barrett's oesophagus-associated adenocarcinoma: how, when and why?
  124. Long-term proton pump induced hypergastrinaemia does induce lineage-specific restitution but not clonal expansion in benign Barrett's oesophagus in vivo
  125. Stem cells and solid cancers
  126. Clonality, Founder Mutations, and Field Cancerization in Human Ulcerative Colitis–Associated Neoplasia
  127. Investigating the fixation and spread of mutations in the gastrointestinal epithelium
  128. A comprehensive genetic profile of phyllodes tumours of the breast detects important mutations, intra-tumoral genetic heterogeneity and new genetic changes on recurrence
  129. Most low-level microsatellite instability in colorectal cancers can be explained without an elevated slippage rate
  130. Analysis of copy number changes suggests chromosomal instability in a minority of large colorectal adenomas