EGAGenomicsIllumina Genome Analyzer IIx, Illumina HiSeq 2000Otherhttps://ega-archive.org/studies/EGAS00001000883EGAEGA study EGAS00001000883Dataset for the "Study on the proliferation history of colorectal adenomas"EGArestrictedPapillary Adenomas, Proliferating, study, acinar cell adenoma (morphologic abnormality), Follicular Adenoma, Microcystic Adenomas, Trabecular Adenomas, Adenomas, Adenoma, Aspect, Basal Cell, acinar cell adenoma, proliferating, Monomorphic Adenoma, adenoma, benign, Histories, Historical Aspects, historical aspects, Microcystic Adenoma, Historical Aspect, Microcystic, Monomorphic Adenomas, Papillary, Trabecular., Monomorphic, Papillary Adenoma, Proliferation, historical notes, Trabecular, Basal Cell Adenoma, Follicular Adenomas, Trabecular Adenoma, Aspects, Basal Cell Adenomas, Follicular, HistoricalProliferating, dmBest1, Procedures, Trabecular Adenomas, Adenomas, Aspect, Neoplasms, low frequency, postnatal development, BEST1, Benign Neoplasm, adenoma, organization and administration, Non-Governmental Organizations, cd206, X Chromosomes, growth and development, Tumor, anon-WO0118547.380, C-type lectin domain family 13 member D-like, composed of, Malignant, Repair, Microcystic, Chromosomes, DmelCG6264, Monomorphic Adenomas, Mutations, method, Techniques, Monomorphic, Method, method used in an experiment, Genetic heterogeneity, Studies, ARB, Non-Governmental, (2Z)-but-2-enedioate, methodology., Technique, BEST1_HUMAN, Follicular, male, treatment, study, acinar cell adenoma (morphologic abnormality), Organization, Follicular Adenoma, Microcystic Adenomas, MutS/MutL/MutH pathway, clec13d, Malignancy, Adenoma, VMD2, proliferating, DNA Mismatch, composition, procedures, benign, X, BMD, Histories, Microcystic Adenoma, MRC1L1, genetic, Neoplasias, Study, Non-Governmental Organization, Methodological Studies, malignant neoplasm, disease management, Basal Cell Adenoma, Therapies, Malignancies, Basal Cell Adenomas, Organizations, organization, CD206, constitutitional genetic, Mismatch, infrequent, Cancer, Tumors, RP50, Papillary Adenomas, vitelliform macular dystrophy 2 (Best disease, Therapy, Malignant Neoplasm, CG6264, organisation, organizational structure, Basal Cell, Males, familial, compositionality, Historical Aspects, Procedure, Tree, historical aspects, Historical Aspect, not genetically inherited, Cell, development, Benign, MT, Algorithm, Trabecular, Neoplasm, MMR, macrophage mannose receptor 1-like protein 1, techniques, Nongovernmental Organizations, TU15B, CLEC13DL, bestrophin), dBest1, administrative management, long patch mismatch repair system, Dbest, primary cancer, mismatch repair, growth pattern, best, maleate, Nongovernmental, acinar cell adenoma, non-developmental growth, content, administrative structure, Monomorphic Adenoma, dbest1, Mismatch Repair, postnatal growth, Heterogeneity, mmr, common, Benign Neoplasms, MutL-like pathway, Cancers, Methodological, Methodological Study, Treatments, malignant tumor, Malignant Neoplasms, male human body, plan specification, Papillary, Non Governmental Organizations, CLEC13D, Chromosome, Therapeutic, Papillary Adenoma, Proliferation, historical notes, structure, Follicular Adenomas, Trabecular Adenoma, organizational management, Treatment, inherited genetic, DNA, Aspects, other neoplasm, growth, Nongovernmental Organization, hereditary, BEST, Neoplasia, HistoricalfalseStudy on the proliferation history of colorectal adenomasMismatch repair (MMR) deficient colorectal adenomas are composed of transformed cells that descend from a common founder and progressively accumulate genomic alterations but their proliferation history is still largely unknown. Here we rebuilt the proliferation history of four MMR deficient colorectal adenomas from male individuals by deep sequencing the X chromosome and mapping the somatic mutations that were progressively acquired during tumor growth. We developed a novel method to call high and low frequency mutations, to cluster them according to their frequencies and rebuild the proliferation trees directly from these mutation clusters using a recursive algorithm. The trees of all four lesions were formed of a dominant subclone that coexisted with other genetically heterogeneous subpopulations of cells. Despite this similar hierarchical organization, however, the growth dynamics varied among and within tumors, likely depending on a combination of tumor-specific genetic and environmental factors. Our study provides insights into the biological properties of individual MMR deficient colorectal adenomas that may influence their growth and also the response to therapy. Extended to other solid tumors, our approach could inform on the mechanisms of cancer progression, thus providing insight into the best choice of cancer treatment methods.2017-07-26 15:39:25EGAS000010008839606EGAD00001000882EGAC00001000209