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