Ignatiadis, M., Sledge, G. W. & Jeffrey, S. S. Liquid biopsy enters the clinic—implementation points and future challenges. Nat. Rev. Clin. Oncol. 18, 297–312 (2021).
Weber, Z. T. et al. Modeling clonal construction over slender time frames through circulating tumor DNA in metastatic breast most cancers. Genome Med. 13, 89 (2021).
Abbosh, C. et al. Phylogenetic ctDNA evaluation depicts early-stage lung most cancers evolution. Nature 545, 446–451 (2017).
Parikh, A. R. et al. Liquid versus tissue biopsy for detecting acquired resistance and tumor heterogeneity in gastrointestinal cancers. Nat. Med. 25, 1415–1421 (2019).
Cresswell, G. D. et al. Mapping the breast most cancers metastatic cascade onto ctDNA utilizing genetic and epigenetic clonal monitoring. Nat. Commun. 11, 1446 (2020).
Annala, M. et al. Evolution of castration-resistant prostate most cancers in ctDNA throughout sequential androgen receptor pathway inhibition. Clin. Most cancers Res. 27, 4610–4623 (2021).
Wyatt, A. W. et al. Concordance of circulating tumor DNA and matched metastatic tissue biopsy in prostate most cancers. J. Natl Most cancers Inst. 109, djx118 (2017).
Razavi, P. et al. Alterations in PTEN and ESR1 promote medical resistance to alpelisib plus aromatase inhibitors. Nat. Most cancers 1, 382–393 (2020).
Siravegna, G. et al. Radiologic and genomic evolution of particular person metastases throughout HER2 blockade in colorectal most cancers. Most cancers Cell 34, 148–162 (2018).
O’Leary, B. et al. The genetic panorama and clonal evolution of breast most cancers resistance to palbociclib plus fulvestrant within the PALOMA-3 trial. Most cancers Discov. 8, 1390–1403 (2018).
Noorani, A. et al. Genomic proof helps a clonal diaspora mannequin for metastases of esophageal adenocarcinoma. Nat. Genet. 52, 74–83 (2020).
Woodcock, D. J. et al. Prostate most cancers evolution from multilineage major to single lineage metastases with implications for liquid biopsy. Nat. Commun. 11, 5070 (2020).
Snyder, M. W., Kircher, M., Hill, A. J., Daza, R. M. & Shendure, J. Cell-free DNA includes an in vivo nucleosome footprint that informs its tissues-of-origin. Cell 164, 57–68 (2016).
Ulz, P. et al. Inference of transcription issue binding from cell-free DNA allows tumor subtype prediction and early detection. Nat. Commun. 10, 4666 (2019).
Zhu, G. et al. Tissue-specific cell-free DNA degradation quantifies circulating tumor DNA burden. Nat. Commun. 12, 1–11 (2021).
Ulz, P. et al. Inferring expressed genes by whole-genome sequencing of plasma DNA. Nat. Genet. 48, 1273–1278 (2016).
Peneder, P. et al. Multimodal evaluation of cell-free DNA whole-genome sequencing for pediatric cancers with low mutational burden. Nat. Commun. 12, 3230 (2021).
Solar, Ok. et al. Orientation-aware plasma cell-free DNA fragmentation evaluation in open chromatin areas informs tissue of origin. Genome Res. 29, 418–427 (2019).
Khalaf, D. J. et al. Optimum sequencing of enzalutamide and abiraterone acetate plus prednisone in metastatic castration-resistant prostate most cancers: a multicentre, randomised, open-label, section 2, crossover trial. Lancet Oncol. 20, 1730–1739 (2019).
Quigley, D. A. et al. Genomic hallmarks and structural variation in metastatic prostate most cancers. Cell 174, 758–769 (2018).
Abida, W. et al. Genomic correlates of medical final result in superior prostate most cancers. Proc. Natl Acad. Sci. USA. 116, 11428–11436 (2019).
van Dessel, L. F. et al. The genomic panorama of metastatic castration-resistant prostate cancers reveals a number of distinct genotypes with potential medical affect. Nat. Commun. 10, 5251 (2019).
Alexandrov, L. B. et al. The repertoire of mutational signatures in human most cancers. Nature 578, 94–101 (2020).
Wu, Y.-M. et al. Inactivation of CDK12 delineates a definite immunogenic class of superior prostate most cancers. Cell 173, 1770–1782 (2018).
Black, J. R. M. & McGranahan, N. Genetic and non-genetic clonal variety in most cancers evolution. Nat. Rev. Most cancers 21, 379–392 (2021).
Dentro, S. C. et al. Characterizing genetic intra-tumor heterogeneity throughout 2,658 human most cancers genomes. Cell 184, 2239–2254 (2021).
Tarabichi, M. et al. A sensible information to most cancers subclonal reconstruction from DNA sequencing. Nat. Strategies 18, 144–155 (2021).
Bielski, C. M. et al. Genome doubling shapes the evolution and prognosis of superior cancers. Nat. Genet. 50, 1189–1195 (2018).
Quinton, R. J. et al. Complete-genome doubling confers distinctive genetic vulnerabilities on tumour cells. Nature 590, 492–497 (2021).
Cohen-Sharir, Y. et al. Aneuploidy renders most cancers cells weak to mitotic checkpoint inhibition. Nature 590, 486–491 (2021).
Zaccaria, S. & Raphael, B. J. Correct quantification of copy-number aberrations and whole-genome duplications in multi-sample tumor sequencing information. Nat. Commun. 11, 4301 (2020).
Chen, C. D. et al. Molecular determinants of resistance to antiandrogen remedy. Nat. Med. 10, 33–39 (2004).
Henzler, C. et al. Truncation and constitutive activation of the androgen receptor by various genomic rearrangements in prostate most cancers. Nat. Commun. 7, 13668 (2016).
Takeda, D. Y. et al. A somatically acquired enhancer of the androgen receptor is a noncoding driver in superior prostate most cancers. Cell 174, 422–432 (2018).
Li, Y. et al. Various AR gene rearrangements mediate resistance to androgen receptor inhibitors in metastatic prostate most cancers. Clin. Most cancers Res. 26, 1965–1976 (2020).
Annala, M. et al. Circulating tumor dna genomics correlate with resistance to abiraterone and enzalutamide in prostate most cancers. Most cancers Discov. 8, 444–457 (2018).
Baca, S. C. et al. Punctuated evolution of prostate most cancers genomes. Cell 153, 666–677 (2013).
Viswanathan, S. R. et al. Structural alterations driving castration-resistant prostate most cancers revealed by linked-read genome sequencing. Cell 174, 433–447 (2018).
Esfahani, M. S. et al. Inferring gene expression from cell-free DNA fragmentation profiles. Nat. Biotechnol. 40, 585–597 (2022).
Davies, A. H., Beltran, H. & Zoubeidi, A. Mobile plasticity and the neuroendocrine phenotype in prostate most cancers. Nat. Rev. Urol. 15, 271–286 (2018).
Pomerantz, M. M. et al. The androgen receptor cistrome is extensively reprogrammed in human prostate tumorigenesis. Nat. Genet. 47, 1346–1351 (2015).
Morova, T. et al. Androgen receptor-binding websites are extremely mutated in prostate most cancers. Nat. Commun. 11, 832 (2020).
Rebello, R. J. et al. Prostate most cancers. Nat Rev. Dis. Primers 7, 9 (2021).
Chi, Ok. N. et al. A prognostic index mannequin for predicting general survival in sufferers with metastatic castration-resistant prostate most cancers handled with abiraterone acetate after docetaxel. Ann. Oncol. 27, 454–460 (2016).
Turajlic, S. et al. Deterministic evolutionary trajectories affect major tumor development: TRACERx Renal. Cell 173, 595–610 (2018).
Gundem, G. et al. The evolutionary historical past of deadly metastatic prostate most cancers. Nature 520, 353–357 (2015).
Kumar, A. et al. Substantial interindividual and restricted intraindividual genomic variety amongst tumors from males with metastatic prostate most cancers. Nat. Med. 22, 369–378 (2016).
Quigley, D. et al. Evaluation of circulating cell-free DNA identifies multiclonal heterogeneity of reversion mutations related to resistance to PARP inhibitors. Most cancers Discov. 7, 999–1005 (2017).
Unterrainer, M. et al. Current advances of PET imaging in medical radiation oncology. Radiat. Oncol. 15, 88 (2020).
Brandão, M., Caparica, R., Eiger, D. & de Azambuja, E. Biomarkers of response and resistance to PI3K inhibitors in estrogen receptor-positive breast most cancers sufferers and mixture therapies involving PI3K inhibitors. Ann. Oncol. 30, x27–x42 (2019).
Parikh, A. et al. Systematic liquid biopsy identifies novel and heterogeneous mechanisms of acquired resistance in gastrointestinal (GI) most cancers sufferers. Ann. Oncol. 28, iii137 (2017).
Balanis, N. G. et al. Pan-cancer Convergence to a small-cell neuroendocrine phenotype that shares susceptibilities with hematological malignancies. Most cancers Cell 36, 17–34 (2019).
Herberts, C. & Wyatt, A. W. Technical and organic constraints on ctDNA-based genotyping. Developments Most cancers Res. 7, 995–1009 (2021).
Turajlic, S., Sottoriva, A., Graham, T. & Swanton, C. Resolving genetic heterogeneity in most cancers. Nat. Rev. Genet. 20, 404–416 (2019).
Scher, H. I. et al. Trial design and targets for castration-resistant prostate most cancers: up to date suggestions from the prostate most cancers medical trials working group 3. J. Clin. Oncol. 34, 1402–1418 (2016).
Warner, E. et al. BRCA2, ATM, and CDK12 defects differentially form prostate tumor driver genomics and medical aggression. Clin. Most cancers Res. 27, 1650–1662 (2021).
Martin, M. Cutadapt removes adapter sequences from high-throughput sequencing reads. EMBnet J. 17, 10 (2011).
Langmead, B. & Salzberg, S. L. Quick gapped-read alignment with Bowtie 2. Nat. Strategies 9, 357–359 (2012).
Faust, G. G. & Corridor, I. M. SAMBLASTER: quick duplicate marking and structural variant learn extraction. Bioinformatics 30, 2503–2505 (2014).
Quinlan, A. R. & Corridor, I. M. BEDTools: a versatile suite of utilities for evaluating genomic options. Bioinformatics 26, 841–842 (2010).
Wang, Ok., Li, M. & Hakonarson, H. ANNOVAR: purposeful annotation of genetic variants from high-throughput sequencing information. Nucleic Acids Res. 38, e164 (2010).
Rosenthal, R., McGranahan, N., Herrero, J., Taylor, B. S. & Swanton, C. DeconstructSigs: delineating mutational processes in single tumors distinguishes DNA restore deficiencies and patterns of carcinoma evolution. Genome Biol. 17, 31 (2016).
Bergstrom, E. N. et al. SigProfilerMatrixGenerator: a software for visualizing and exploring patterns of small mutational occasions. BMC Genomics 20, 685 (2019).
Landrum, M. J. et al. ClinVar: bettering entry to variant interpretations and supporting proof. Nucleic Acids Res. 46, D1062–D1067 (2018).
Danecek, P. et al. Twelve years of SAMtools and BCFtools. Gigascience 10, giab008 (2021).
Eisenberg, E. & Levanon, E. Y. Human housekeeping genes, revisited. Developments Genet. 29, 569–574 (2013).
