Relevant bibliographies by topics / Tumour sequencing

Academic literature on the topic 'Tumour sequencing'

Author: Grafiati
Published: 10 December 2022
Last updated: 28 January 2023

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Journal articles on the topic "Tumour sequencing"

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Oey, Harald, Marissa Daniels, Vandana Relan, Tian Mun Chee, Morgan R. Davidson, Ian A. Yang, Jonathan J. Ellis, Kwun M. Fong, Lutz Krause, and Rayleen V. Bowman. "Whole-genome sequencing of human malignant mesothelioma tumours and cell lines." Carcinogenesis 40, no. 6 (April 25, 2019): 724–34. http://dx.doi.org/10.1093/carcin/bgz066.

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Abstract Pleural mesothelioma is a cancer of serosal surfaces caused by environmental exposure to asbestos. Clinical outcome remains poor and while trials of new treatments are ongoing it remains an understudied cancer. Mesothelioma cell lines can readily be grown from primary tumour and from tumour cells shed into pleural effusion with the latter representing a particularly valuable source of DNA in clinical settings, procurable without the need for additional invasive procedures. However, it is not well understood how accurately patient-derived cultured tumour cells represent the molecular characteristics of their primary tumour. We used whole-genome sequencing of primary tumour and matched cultured cells to comprehensively characterize mutations and structural alterations. Most cases had complex rearranged genomes with evidence of chromoanagenesis and rearrangements reminiscent of chromoplexy. Many of the identified driver mutations were structural, indicating that mesothelioma is often caused by structural alterations and catastrophic genomic events, rather than point mutations. Because the majority of genomic changes detected in tumours were also displayed by the genomes of cultured tumour cells, we conclude that low-passage cultured tumour cells are generally suitable for molecular characterization of mesothelioma and may be particularly useful where tissue samples with high tumour cell content are not available. However, the subclonal compositions of the cell lines did not fully recapitulate the subclonal diversity of the primary tumours. Furthermore, longitudinal acquisition of major alterations in subclonal cell populations was observed after long-term passaging. These two factors define limitations of tumour-derived cell lines as genomic substrate for clinical purposes.
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Lolkema, M. P. "Platforms for Tumour Sequencing: Pertinence and Practicability." Annals of Oncology 25 (September 2014): iv9. http://dx.doi.org/10.1093/annonc/mdu294.2.

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Navin, Nicholas, Jude Kendall, Jennifer Troge, Peter Andrews, Linda Rodgers, Jeanne McIndoo, Kerry Cook, et al. "Tumour evolution inferred by single-cell sequencing." Nature 472, no. 7341 (March 13, 2011): 90–94. http://dx.doi.org/10.1038/nature09807.

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Muers, Mary. "Sequencing to detect tumour DNA in circulation." Nature Reviews Genetics 14, no. 1 (December 18, 2012): 4. http://dx.doi.org/10.1038/nrg3397.

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Tang, Ka-Wei, and Erik Larsson. "Tumour virology in the era of high-throughput genomics." Philosophical Transactions of the Royal Society B: Biological Sciences 372, no. 1732 (September 11, 2017): 20160265. http://dx.doi.org/10.1098/rstb.2016.0265.

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With the advent of massively parallel sequencing, oncogenic viruses in tumours can now be detected in an unbiased and comprehensive manner. Additionally, new viruses or strains can be discovered based on sequence similarity with known viruses. Using this approach, the causative agent for Merkel cell carcinoma was identified. Subsequent studies using data from large collections of tumours have confirmed models built during decades of hypothesis-driven and low-throughput research, and a more detailed and comprehensive description of virus–tumour associations have emerged. Notably, large cohorts and high sequencing depth, in combination with newly developed bioinformatical techniques, have made it possible to rule out several suggested virus–tumour associations with a high degree of confidence. In this review we discuss possibilities, limitations and insights gained from using massively parallel sequencing to characterize tumours with viral content, with emphasis on detection of viral sequences and genomic integration events. This article is part of the themed issue ‘Human oncogenic viruses’.
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de Ruiter, J. R., L. F. A. Wessels, and J. Jonkers. "Mouse models in the era of large human tumour sequencing studies." Open Biology 8, no. 8 (August 2018): 180080. http://dx.doi.org/10.1098/rsob.180080.

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Cancer is a complex disease in which cells progressively accumulate mutations disrupting their cellular processes. A fraction of these mutations drive tumourigenesis by affecting oncogenes or tumour suppressor genes, but many mutations are passengers with no clear contribution to tumour development. The advancement of DNA and RNA sequencing technologies has enabled in-depth analysis of thousands of human tumours from various tissues to perform systematic characterization of their (epi)genomes and transcriptomes in order to identify (epi)genetic changes associated with cancer. Combined with considerable progress in algorithmic development, this expansion in scale has resulted in the identification of many cancer-associated mutations, genes and pathways that are considered to be potential drivers of tumour development. However, it remains challenging to systematically identify drivers affected by complex genomic rearrangements and drivers residing in non-coding regions of the genome or in complex amplicons or deletions of copy-number driven tumours. Furthermore, functional characterization is challenging in the human context due to the lack of genetically tractable experimental model systems in which the effects of mutations can be studied in the context of their tumour microenvironment. In this respect, mouse models of human cancer provide unique opportunities for pinpointing novel driver genes and their detailed characterization. In this review, we provide an overview of approaches for complementing human studies with data from mouse models. We also discuss state-of-the-art technological developments for cancer gene discovery and validation in mice.
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Patel, Areeba, Helin Dogan, Alexander Jung, Zaira Seferbekova, Alexander Payne, Michael Ritter, Daniel Schrimpf, et al. "PATH-46. COMPUTATIONAL HISTOPATHOLOGY INFORMED RAPID TARGETED NANOPORE SEQUENCING ENABLES AFFORDABLE NEXT DAY REPORTING OF COMPREHENSIVE MOLECULAR MARKERS FOR CNS TUMOUR DIAGNOSTICS." Neuro-Oncology 24, Supplement_7 (November 1, 2022): vii161. http://dx.doi.org/10.1093/neuonc/noac209.619.

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Abstract BACKGROUND Integrative brain tumour diagnostics indisputably requires comprehensive reporting of molecular markers. The 2021 WHO classification of central nervous system (CNS) tumours substantially increased the set of markers for routine evaluation, with greater significance to DNA methylation analysis in diagnostics. Limited by investment and batching, smaller labs and clinics might suffer major delays in delivering clinical decisions. To make precision diagnostics accessible, we introduce an integrated computational histopathology and adaptive nanopore sequencing workflow for next day CNS tumour diagnostics. METHODS We used CNS-CHiP- a multitask deep transfer learning model to predict key molecular alterations and methylation classification from H&E stained CNS tumour slides. For further characterisation and subtyping, we used the predictions to formulate a custom panel for each patient. Targeted sequencing and analyses were performed using Rapid-CNS2- a custom neurooncology nanopore sequencing pipeline for parallel copy-number, mutational and methylation analysis that is flexible in target selection with no additional library preparation and can be initiated upon receipt of frozen sections. Sequencing was performed on a portable MinION or GridION. RESULTS We demonstrate our workflow on diagnostic samples received by the Department of Neuropathology, University Hospital Heidelberg. CNS-CHiP predicted multiple pathognomonic alterations (eg. IDH mutation, 7 gain/10 loss) with reasonable accuracy. This provided basic information regarding the tumor type instantly. Personalised panels enabled small target sizes, resulting in low sequencing time (up to 24h) and competitive costs. The GPU-accelerated bioinformatics pipeline reduced analysis time from > 24h to < 3h. CONCLUSIONS Our workflow harnessing histology-based molecular predictions to instruct targeted nanopore sequencing can be set up with low initial investment and has the potential to facilitate reporting of molecular results on the next day of sample collection. CNS-CHiP combined with Rapid-CNS2 thus aims to make CNS tumour diagnostics affordable and accessible to smaller hospitals and labs especially in low- and middle-income countries.
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Knudsen, Erik S., Uthra Balaji, Brian Mannakee, Paris Vail, Cody Eslinger, Christopher Moxom, John Mansour, and Agnieszka K. Witkiewicz. "Pancreatic cancer cell lines as patient-derived avatars: genetic characterisation and functional utility." Gut 67, no. 3 (January 10, 2017): 508–20. http://dx.doi.org/10.1136/gutjnl-2016-313133.

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ObjectivePancreatic ductal adenocarcinoma (PDAC) is a therapy recalcitrant disease with the worst survival rate of common solid tumours. Preclinical models that accurately reflect the genetic and biological diversity of PDAC will be important for delineating features of tumour biology and therapeutic vulnerabilities.Design27 primary PDAC tumours were employed for genetic analysis and development of tumour models. Tumour tissue was used for derivation of xenografts and cell lines. Exome sequencing was performed on the originating tumour and developed models. RNA sequencing, histological and functional analyses were employed to determine the relationship of the patient-derived models to clinical presentation of PDAC.ResultsThe cohort employed captured the genetic diversity of PDAC. From most cases, both cell lines and xenograft models were developed. Exome sequencing confirmed preservation of the primary tumour mutations in developed cell lines, which remained stable with extended passaging. The level of genetic conservation in the cell lines was comparable to that observed with patient-derived xenograft (PDX) models. Unlike historically established PDAC cancer cell lines, patient-derived models recapitulated the histological architecture of the primary tumour and exhibited metastatic spread similar to that observed clinically. Detailed genetic analyses of tumours and derived models revealed features of ex vivo evolution and the clonal architecture of PDAC. Functional analysis was used to elucidate therapeutic vulnerabilities of relevance to treatment of PDAC.ConclusionsThese data illustrate that with the appropriate methods it is possible to develop cell lines that maintain genetic features of PDAC. Such models serve as important substrates for analysing the significance of genetic variants and create a unique biorepository of annotated cell lines and xenografts that were established simultaneously from same primary tumour. These models can be used to infer genetic and empirically determined therapeutic sensitivities that would be germane to the patient.
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Stankunaite, Reda, Sally L. George, Lewis Gallagher, Sabri Jamal, Ridwan Shaikh, Lina Yuan, Debbie Hughes, et al. "Circulating tumour DNA sequencing to determine therapeutic response and identify tumour heterogeneity in patients with paediatric solid tumours." European Journal of Cancer 162 (February 2022): 209–20. http://dx.doi.org/10.1016/j.ejca.2021.09.042.

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Tanner, Georgette, David R. Westhead, Alastair Droop, and Lucy F. Stead. "Simulation of heterogeneous tumour genomes with HeteroGenesis and in silico whole exome sequencing." Bioinformatics 35, no. 16 (January 4, 2019): 2850–52. http://dx.doi.org/10.1093/bioinformatics/bty1063.

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Abstract Summary Tumour evolution results in progressive cancer phenotypes such as metastatic spread and treatment resistance. To better treat cancers, we must characterize tumour evolution and the genetic events that confer progressive phenotypes. This is facilitated by high coverage genome or exome sequencing. However, the best approach by which, or indeed whether, these data can be used to accurately model and interpret underlying evolutionary dynamics is yet to be confirmed. Establishing this requires sequencing data from appropriately heterogeneous tumours in which the exact trajectory and combination of events occurring throughout its evolution are known. We therefore developed HeteroGenesis: a tool to generate realistically evolved tumour genomes, which can be sequenced using weighted-Wessim (w-Wessim), an in silico exome sequencing tool that we have adapted from previous methods. HeteroGenesis simulates more complex and realistic heterogeneous tumour genomes than existing methods, can model different evolutionary dynamics, and enables the creation of multi-region and longitudinal data. Availability and implementation HeteroGenesis and w-Wessim are freely available under the GNU General Public Licence from https://github.com/GeorgetteTanner, implemented in Python and supported on linux and MS Windows. Supplementary information Supplementary data are available at Bioinformatics online.
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Dissertations / Theses on the topic "Tumour sequencing"

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Burns, Alice Sin Ying Wai. "The role of the p53 tumour suppressor pathway in central primitive neuroectodermal tumours." Thesis, University of Newcastle Upon Tyne, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.300357.

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Duarte, Antonio. "Regulation of gene expression by the Wilms' tumour suppressor, WT1." Thesis, University of Oxford, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.389178.

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Murtaza, Muhammed. "Identification and monitoring of somatic mutations in solid cancers by sequencing circulating tumour DNA." Thesis, University of Cambridge, 2015. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.708647.

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Ross, Edith. "Inferring tumour evolution from single-cell and multi-sample data." Thesis, University of Cambridge, 2018. https://www.repository.cam.ac.uk/handle/1810/274604.

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Tumour development has long been recognised as an evolutionary process during which cells accumulate mutations and evolve into a mix of genetically distinct cell subpopulations. The resulting genetic intra-tumour heterogeneity poses a major challenge to cancer therapy, as it increases the chance of drug resistance. To study tumour evolution in more detail, reliable approaches to infer the life histories of tumours are needed. This dissertation focuses on computational methods for inferring trees of tumour evolution from single-cell and multi-sample sequencing data. Recent advances in single-cell sequencing technologies have promised to reveal tumour heterogeneity at a much higher resolution, but single-cell sequencing data is inherently noisy, making it unsuitable for analysis with classic phylogenetic methods. The first part of the dissertation describes OncoNEM, a novel probabilistic method to infer clonal lineage trees from noisy single nucleotide variants of single cells. Simulation studies are used to validate the method and to compare its performance to that of other methods. Finally, OncoNEM is applied in two case studies. In the second part of the dissertation, a comprehensive collection of existing multi-sample approaches is used to infer the phylogenies of metastatic breast cancers from ten patients. In particular, shallow whole-genome, whole exome and targeted deep sequencing data are analysed. The inference methods comprise copy number and point mutation based approaches, as well as a method that utilises a combination of the two. To improve the copy number based inference, a novel allele-specific multi-sample segmentation algorithm is presented. The results are compared across methods and data types to assess the reliability of the different methods. In summary, this thesis presents substantial methodological advances to understand tumour evolution from genomic profiles of single cells or related bulk samples.
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Fewings, Eleanor Rose. "The use of whole exome sequencing data to identify candidate genes involved in cancer and benign tumour predisposition." Thesis, University of Cambridge, 2019. https://www.repository.cam.ac.uk/handle/1810/285963.

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The development of whole exome sequencing has transformed the study of disease predisposition. The sequencing of both large disease sets and smaller rare disease families enables the identification of new predisposition variants and potentially provide clinical insight into disease management. There is no standard protocol for analysing exome sequencing data. Outside of extremely large sequencing studies including thousands of individuals, statistical approaches are often underpowered to detect rare disease associated variants. Aggregation of variants into functionally related regions, including genes, gene clusters, and pathways, allows for the detection of biological processes that, when interrupted, may impact disease risk. In silico functional studies can also be utilised to further understand how variants disrupt biological processes and identify genotype-phenotype relationships. This study describes the exploration of sequencing datasets from cancers and benign tumour diseases including: i) hereditary diffuse gastric cancer, ii) sweat duct proliferation tumours, iii) adrenocortical carcinoma, and iv) breast cancer. Each set underwent germline whole exome sequencing followed by additional tumour or targeted sequencing to identify associated predisposition genes. Variants within a cluster of risk genes that are involved in double strand break repair were identified as associated with hereditary diffuse gastric cancer risk via gene ontology enrichment analysis. This cluster included PALB2 within which, using externally collated data, loss of function variants were identified as significantly associated with hereditary diffuse gastric cancer risk. Germline protein-affecting variants in the myosin gene MYH9 were identified in all individuals with a rare sweat duct proliferative syndrome, suggesting a role for MYH9 in skin development, regulation and tumorigenesis. These MYH9 variants were analysed in silico to identify a genotype-phenotype relationship between the clinical presentation and variants in the ATP binding pocket of the protein. Tumour matched normal sequence data from adrenocortical carcinoma cases was used to elucidate the role of Lynch syndrome genes in disease pathogenesis. Within the breast cancer set, candidate genes were selected to undergo targeted sequencing in a larger set of cases to further explore their role in breast cancer risk. Risk associated genes identified within this study may ultimately aid in diagnosis and management of disease. This thesis has also generated multiple novel tools and sequencing analysis techniques that may be of use for further studies by aiding in the prioritisation of candidate variants. The described techniques will provide support to researchers working on rare, statistically underpowered datasets and to provide standard analysis pipelines for a range of dataset sizes and types, including familial data and unrelated individuals.
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Asante, Du-Bois. "Development and evaluation of methodologies for analysis of CTC and ctDNA in patients with ovarian carcinoma." Thesis, Edith Cowan University, Research Online, Perth, Western Australia, 2022. https://ro.ecu.edu.au/theses/2570.

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About 70% of patients with ovarian cancer (OC) are diagnosed at an advanced stage (III-IV), with associated poor prognosis, even after chemotherapeutic interventions (mostly platinum taxane-based), leading to poor survival rates. The current biomarkers available in the clinic are not enough for efficient prognostication and surveillance of OC. Hence, more accurate and reliable biomarkers of patient disease status are urgently required. Currently, histopathological evaluation of tumour biopsies is the gold standard in clinical practice with the purpose of evaluating specific biomarkers to predict therapeutic response. However, this is invasive, and associated complications may occur. Liquid biopsy is a minimally invasive test and has the advantage of allowing real-time monitoring of treatment response and comprehensive serial/repetitive phenotypic and genotypic profiling of the primary, metastatic and recurrent tumours. Circulating tumour cells (CTC) and circulating tumour DNA (ctDNA) represent a new generation of biomarkers that can be used for predicting therapy responsiveness and longitudinal monitoring of OC patients undergoing therapy. This thesis describes a series of investigations in OC which include, a methodological study to improve phenotypic characterization of detected CTCs, genomic validation of putative CTCs, and the evaluation of the clinical validity of ctDNA as biomarker of response to neoadjuvant chemotherapy (NACT). This thesis consists of six chapters: a general introduction to OC (Chapter 1); a thorough review of the literature regarding CTCs and ctDNA in OC (Chapter 2); three results chapters (Chapters 3 - 5); and a final chapter that comprises of a general discussion of the main findings, the limitations of the study and future directions (Chapter 6). The first chapter (Chapter 1) of the thesis includes a review of the literature, which consist of the characterisation and clinical landscape of OC, while briefly introducing the topic of liquid biopsy. This is then followed by a comprehensive review (Chapter 2) that highlights the progress in the field of liquid biopsy for OC from 2011 to 2019, focusing specifically on CTCs and ctDNA as potential biomarkers for the management of the disease. Based on the limitations identified in this review (in Chapter 2), a multi-marker antibody staining protocol was developed to target epithelial (cytokeratin (CK) and EpCAM), mesenchymal (vimentin), and OC specific (PAX8) markers for detection of CTCs (Chapter 3). CD45/16 and CD31 were used for the exclusion of white blood and vascular endothelial cells, respectively. PD-L1 was used for CTC characterisation. Optimisation of the CTC markers were done using OC cell lines, SKOV-3 and OVCA432. CTCs were enriched using the ParsortixTM (Angle plc.) system, and further detected using the multifluorescent markers from 16 OC patients. Patients were found to have heterogeneous CTCs, with 113/157 (72%) cells positive for CK/EpCAM (epithelial marker), 58/157 (37%) positive for vimentin (mesenchymal marker), and 17/157 (11%) positive for both (hybrid). Positivity for PD-L1 was significantly associated with the hybrid phenotype when compared with the epithelial (p = 0.0009) and mesenchymal (p = 0.007) expressing CTCs. In Chapter 4, we performed copy number alteration (CNA) profiling on putative CTCs that were previously identified in Chapter 3. CNA were detected in both CK/EpCAM and vimentin positive CTCs. However, a proportion of cells expressing CK/EpCAM, PD-L1 and CD31 were found not to carry CNAs. Further characterisation of CTCs in combination with clinical outcomes is needed to provide insight into the role that epithelial to mesenchymal plasticity and vasculogenic mimicry plays in OC and its relationship with PD-L1 expression. In addition, ctDNA was analysed in 58 patients with high grade serous ovarian cancer (HGSOC) enrolled in a neoadjuvant chemotherapy (NACT) plus immune checkpoint inhibitor clinical trial (iPRIME, ACTRN12618000109202) (Chapter 5). Cell free DNA (cfDNA) was sequenced using the Oncomine™ Breast cfDNA Research Assay V2, and selected mutations were validated using droplet digital PCR (ddPCR). For ctDNA, the frequencies of genes affected by non-synonymous somatic mutations included TP53 (67%), KRAS (11%), PIK3CA (2%) and SF3B1 (2%). A total of 41 gene variants were identified in either pre- or post-NACT samples; 36 (87.8%) of them had variants in TP53 alone, and 3 (7.4%) in KRAS and 1 (2.4%) each for PIK3CA and SF3B1. Undetectable levels of ctDNA post, but not prior to NACT was associated with chemotherapy response score 3 (CRS3) (p = 0.04) when compared with CRS1/2. Comparison of mutant copies per mL of plasma quantified by NGS and ddPCR demonstrated a strong correlation (Pearson’s r = 0.929; p < 0.0001) between the two platforms. Longitudinal monitoring of ctDNA specific mutant gene variants using ddPCR, showed a predictive lead time, and anticipates disease progression earlier (7-12 weeks) compared to monitoring patients by analysis of serum levels of CA-125. These results suggest that ctDNA could be used as a biomarker to determine patients’ clinical outcomes and serve as a potential endpoint for clinical trials. Finally, Chapter 6 provides a general discussion of the studies covered in this thesis, highlighting potential contributions to the growing field of liquid biopsy and its application for the clinical management of OC patients. The limitations inherent to both CTCs and ctDNA analysis, and suggestions for improvements before its successful implementation in routine clinical practice, are comprehensively discussed.
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Naven, Marc. "Development of a pipeline and protocols for next generation sequencing of blood and formalin-fixed, paraffin-embedded tumour DNA samples." Thesis, Cardiff University, 2015. http://orca.cf.ac.uk/91435/.

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Using existing software and six novel scripts, we developed a pipeline for variant calling using exome re-sequencing data of germline blood deoxyribonucleic acid (DNA) samples. We observed >99% (6,723/6,739) concordance between calls from our pipeline and previous genotyping. We identified >93% of single nucleotide variants (SNVs) and >94% of insertion/deletions called by a commercial partner using the same sequencing reads. Using a subset of genes, we showed that around half of predicted pathogenic variants could be validated in vitro. Together, these data showed that our pipeline was reliable for variant calling. Next generation sequencing (NGS) of DNA from formalin-fixed, paraffin-embedded (FFPE) tumours is technically challenging. We sought to determine the sensitivity of NGS to detect known somatic hotspot mutations (n=25) in 19 FFPE advanced colorectal cancers and to optimise it for the identification of novel somatic variants. Analysis using Illumina’s MiSeq software identified 100% of somatic mutations with 93% specificity, whereas the Genome Analysis Tool Kit’s (GATK) HaplotypeCaller identified 80-92% of somatic mutations with 100% specificity. We investigated the background mutator profile and found that normal FFPE DNA had 3-fold more SNVs than matched blood DNA, with an excess of FFPE-associated C:G>T:A substitutions (27.1 vs. 5.3%). Uracil DNA glycosylase treatment reduced this excess. Only ~5% of variants were consistently called in replicate runs and were likely to be genuine somatic variants. We detected potential candidates for genetic biomarkers of cetuximab-resistance in colorectal cancers that were previously shown to be wild type for KRAS, NRAS, BRAF and PIK3CA. We found that 7/21 (33%) of the CRCs analysed harboured mutations at either codon 12 or 61, whileother CRCs carried truncating KRAS mutations. NRAS also carried a codon 12 mutation in 1 CRC, and PIK3CA possessed mutations at codons 542 and 545. PTEN was found to harbour 5 truncating mutations at codons 71, 140, 155, 178 and 189, potentially leading to loss of function.
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Bucher, Katharina M. I. "The tumour suppressor gene p53 in the horse : identification, cloning and sequencing : its possible role in the pathogenesis of equine sarcoid /." [S.l.] : [s.n.], 1995. http://www.ub.unibe.ch/content/bibliotheken_sammlungen/sondersammlungen/dissen_bestellformular/index_ger.html.

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Choudhry, Hani. "Genome-wide analysis of the hypoxic breast cancer transcriptome using next generation sequencing." Thesis, University of Oxford, 2014. http://ora.ox.ac.uk/objects/uuid:9a66b553-a66c-4164-a854-5881be65ca45.

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Hypoxia pathways are associated with the pathogenesis of both ischaemic and neoplastic diseases. In response to hypoxia the transcription factor hypoxia‐inducible factor (HIF) induces the expression of hundreds of genes with diverse functions. These enable cells to adapt to low oxygen availability. To date, pan-genomic analyses of these transcriptional responses have focussed on protein-coding genes and microRNAs. However, the role of other classes of non-coding RNAs, in particular lncRNAs, in the hypoxia response is largely uncharacterised. My thesis aimed at improving understanding of the transcriptional regulation of the non-coding transcriptome in hypoxia. I performed an integrated genomic analysis of both non-coding and coding transcripts by massively parallel sequencing. This was interfaced with pan-genomic analyses of DNAse hypersensitivity and HIF, H3k4me3 and RNApol2 binding in hypoxic cells. These analyses have revealed that hypoxia profoundly regulated all RNA classes. snRNAs and tRNAs are globally downregulated in hypoxia, whilst miRNAs, mRNAs and lncRNAs are both up- and downregulated with an overall trend towards slight upregulation. In addition, a significant number of previously non-annotated (and largely hypoxia upregulated) transcripts were identified, including novel intergenic transcripts and natural antisense transcripts. HIF bound close to genes for mRNAs, miRNAs and lncRNAs that were upregulated by hypoxia, but was excluded from binding at genes for RNA classes that showed global downregulation. This suggests that HIF acts as a transcriptional activator (but not repressor), of lncRNAs as well as mRNAs and miRNAs. Consistent with direct regulation by HIF, many of these hypoxia-inducible, HIF-binding lncRNAs were downregulated following HIF knockdown. Analysis of RNApol2 binding and DNAse HSS signals at HIF transcriptional target genes indicated that HIF-dependent transcriptional activation occurs through release of RNApol2 that is pre-bound to open promoters of lncRNAs as well as mRNAs. In these datasets, NEAT1 was the most hypoxia-upregulated, HIF-targeted lncRNA in MCF-7 cells and, despite binding of both HIF-1 and HIF-2 isoforms at its promoter, was selectively regulated by HIF-2 alone. Furthermore, NEAT1 was induced by hypoxia in a wide range of breast cancer cell lines and in hypoxic xenograft models. Functionally, NEAT1 is required for the assembly of nuclear paraspeckle structures. Increased nuclear paraspeckle formation was observed in hypoxia and was dependent on both NEAT1 and HIF-2. Knockdown of hypoxia-induced NEAT1 significantly reduced cell proliferation and survival and induced apoptosis. Finally, high expression of NEAT1 correlated with poor clinical outcome in a large cohort of breast cancer patients. These findings extend the role of the hypoxic transcriptional response in cancer into the spectrum of non-coding transcripts and provide new insights into molecular roles of hypoxia-regulated lncRNAs, which may provide the basis for novel therapeutic targets in the future.
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Strakova, Andrea. "Genome diversity and evolution in canine transmissible venereal tumour." Thesis, University of Cambridge, 2018. https://www.repository.cam.ac.uk/handle/1810/276037.

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The canine transmissible venereal tumour (CTVT) is a contagious cancer that is naturally transmitted between dogs by the allogeneic transfer of living cancer cells during coitus. CTVT first arose several thousand years ago and has been reported in dog populations worldwide. The goals of this Thesis were (1) to gain further understanding of CTVT distribution patterns and prevalence around the world, (2) to use genetics to trace the historical spread of CTVT and (3) to map the genetic as well as phenotypic diversity of CTVT tumours around the world. To understand the distribution patterns of CTVT, I obtained information from 645 veterinarians and animal health workers in 109 countries, and generated a snapshot of the locations in which this disease is found. Additionally, as preparation for further genetic analysis, I collected samples from over one thousand CTVT cases from more than 50 countries, optimised methods for high-throughput DNA extraction and quantification and optimised a qPCR-based assay for CTVT diagnosis and host contamination detection. With the goal of tracing the historical spread of CTVT and learning about the genetic diversity of this disease, I sequenced complete mitochondrial genomes of 449 CTVT tumours and their matched hosts. The analysis of the CTVT mitochondrial diversity revealed that CTVT has captured mitochondrial DNA (mtDNA) through horizontal transfer events at least five times during the history of the lineage, delineating five tumour clades. CTVT appears to have spread rapidly around the world within the last 2,000 years, perhaps transported by dogs travelling along historic maritime trade routes. This work indicated that negative selection has operated to prevent accumulation of deleterious mutations in captured mtDNA, and that recombination has caused occasional mtDNA re-assortment. A histology-based screen of CTVT clades did not show any significant phenotypic differences between groups. In order to determine how the five mtDNA clades relate to each other, I analysed data from 539 CTVT exomes. This revealed that a single canine mtDNA haplogroup has recurrently and recently undergone multiple horizontal transfer events. Analysis of this haplotype highlighted a number of candidate genetic variants which may be conferring a selective advantage to this haplotype in CTVT, possibly by influencing mtDNA transcription or replication. Overall, genetic and phenotypic analysis of CTVT tumours from across the globe has broadened our understanding of CTVT diversity, and provided important insights into the biology of a unique transmissible cancer.
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Books on the topic "Tumour sequencing"

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Maher, Christopher J., and Elaine R. Mardis. Genomic Landscape of Cancer. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780190238667.003.0004.

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The study of cancer genomics has advanced rapidly during the last decade due to the development of next generation or massively parallel technology for DNA sequencing. The resulting knowledge is transforming the understanding of both inherited (germline) genetic susceptibility and the somatic changes in tumor tissue that drive abnormal growth and progression. The somatic alterations in tumor tissue vary depending on the type of cancer and its characteristic “genomic landscape.” New technologies have increased the speed and lowered the cost of DNA sequencing and have enabled high-volume characterization of RNA, DNA methylation, DNA-protein complexes, DNA conformation, and a host of other factors that, when altered, can contribute to the development and/or progression of the cancer. Technologic advances have greatly expanded research on somatic changes in tumor tissue, revealing both the singularity of individual cancer genomes and the commonality of genetic alterations that drive cancer in different tissues.
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Ramaswamy, Vijay, Jason T. Huse, and Yasmin Khakoo. Pediatric Brain Tumors. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0140.

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Cerebellar astrocytoma of childhood most commonly refers to cerebellar pilocytic astrocytoma, a World health Organization (WHO) Grade I tumor. However, on occasion cerebellar astrocytomas may demonstrate more aggressive histology including fibrillary astrocytomas, pilomyxoid astrocytomas, and rarely malignant lesions. In the near future, the diagnosis of cerebellar astrocytomas will be simplified by molecular analysis for BRAF fusions rather than a purely morphological approach. The emergence of next-generation sequencing can be expected to identify single nucleotide variations and further expand our understanding of both pilocytic astrocytomas as well as rare variants that occur in the cerebellum. Therapies targeting BRAF (B-raf protooncogene) are currently in clinical trial for adult malignancies and will eventually reach the pediatric population, allowing a targeted approach to recurrent and surgically inaccessible cases of pilocytic astrocytomas.
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Wu, Wei, and Hani Choudhry. Next Generation Sequencing in Cancer Research Vol. 1 : Volume 1: Decoding the Cancer Genome. Springer London, Limited, 2013.

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Tangen, Catherine M., Marian L. Neuhouser, and Janet L. Stanford. Prostate Cancer. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780190238667.003.0053.

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Prostate cancer is the most common solid tumor and the second leading cause of cancer-related mortality in American men. Worldwide, prostate cancer ranks second and fifth as a cause of cancer and cancer deaths, respectively. Despite the international burden of disease due to prostate cancer, its etiology is unclear in most cases. Established risk factors include age, race/ancestry, and family history of the disease. Prostate cancer has a strong heritable component, and genome-wide association studies have identified over 110 common risk-associated genetic variants. Family-based sequencing studies have also found rare mutations (e.g., HOXB13) that contribute to prostate cancer susceptibility. Numerous environmental and lifestyle factors (e.g., obesity, diet) have been examined in relation to prostate cancer incidence, but few modifiable exposures have been consistently associated with risk. Some of the variability in results may be related to etiological heterogeneity, with different causes underlying the development of distinct disease subgroups.
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Pezzella, Francesco, Mahvash Tavassoli, and David J. Kerr, eds. Oxford Textbook of Cancer Biology. Oxford University Press, 2019. http://dx.doi.org/10.1093/med/9780198779452.001.0001.

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The study of the biology of tumours has grown to become markedly interdisciplinary, involving chemists, statisticians, epidemiologists, mathematicians, bioinformaticians, and computer scientists alongside medical scientists. Oxford Textbook of Cancer Biology brings together the developments from different branches of research into one volume. Structured in seven sections, the book starts with a review of the development and biology of multicellular organisms, how they maintain a healthy homeostasis in an individual, and a description of the molecular basis of cancer development. The book then illustrates how, once cells become neoplastic, their signalling network is altered and pathological behaviour follows. Changes that cancer cells can induce in nearby normal tissue are explored, and the new relationship established between them and the stroma is explicated. Finally, the authors illustrate the contribution provided by high throughput techniques to map cancer at different levels, from genomic sequencing to cellular metabolic functions, and how information technology with its vast amounts of data are integrated with traditional cell biology to provide a global view of the disease. The book concludes by summarizing what we know to date about cancer, and in what direction our understanding of cancer is moving.
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Book chapters on the topic "Tumour sequencing"

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Subramanian, Ayshwarya, Stanley Shackney, and Russell Schwartz. "Tumor Phylogenetics in the NGS Era: Strategies, Challenges, and Future Prospects." In Next Generation Sequencing in Cancer Research, 335–57. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-7645-0_17.

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Su, Xiaoping, Gabriel G. Malouf, and Francisco J. Esteva. "Impact and Challenges in Assessing Tumor Purity by Next-Generation Sequencing." In Next Generation Sequencing in Cancer Research, 359–71. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-7645-0_18.

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Marass, Francesco, Francesc Castro-Giner, Barbara Maria Szczerba, Katharina Jahn, Jack Kuipers, Nicola Aceto, and Niko Beerenwinkel. "Computational Analysis of DNA and RNA Sequencing Data Obtained from Liquid Biopsies." In Tumor Liquid Biopsies, 347–68. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-26439-0_18.

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Watson, Geoffrey Alan, Kirsty Taylor, and Lillian L. Siu. "Innovation and Advances in Precision Medicine in Head and Neck Cancer." In Critical Issues in Head and Neck Oncology, 355–73. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-63234-2_24.

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AbstractThe clinical utility of precision medicine through molecular characterization of tumors has been demonstrated in some malignancies, especially in cases where oncogenic driver alterations are identified. Next generation sequencing data from thousands of patients with head and neck cancers have provided vast amounts of information about the genomic landscape of this disease. Thus far, only a limited number of genomic alterations have been druggable, such as NTRK gene rearrangements in salivary gland cancers (mainly mammary analogue secretory carcinoma), NOTCH mutations in adenoid cystic cancers, HRAS mutations in head and neck squamous cell cancers, and even a smaller number of these have reached regulatory approval status. In order to expand the scope of precision medicine in head and neck cancer, additional evaluation beyond genomics is necessary. For instance, there is increasing interest to perform transcriptomic profiling for target identification. Another advance is in the area of functional testing such as small interfering RNA and drug libraries on patient derived cell cultures. Liquid biopsies to detect specific tumor clones or subclones, or viral sequences such as HPV, are of great interest to enable non-invasive tracking of response or resistance to treatment. In addition, precision immuno-oncology is a tangible goal, with a growing body of knowledge on the interactions between the host immunity, the tumor and its microenvironment. Immuno-oncology combinations that are tailored to immunophenotypes of the host-tumor-microenvironment triad, personalized cancer vaccines, and adoptive cell therapies, among others, are in active development. Many therapeutic possibilities and opportunities lie ahead that ultimately will increase the reality of precision medicine in head and neck cancer.
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Sweeney, Robert T., and Matt van de Rijn. "Microarrays and High-Throughput Sequencing in Desmoid-Type Fibromatosis and Scar." In Desmoid Tumors, 181–93. Dordrecht: Springer Netherlands, 2011. http://dx.doi.org/10.1007/978-94-007-1685-8_12.

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Smith, C. C., L. M. Bixby, K. L. Miller, S. R. Selitsky, D. S. Bortone, K. A. Hoadley, B. G. Vincent, and J. S. Serody. "Using RNA Sequencing to Characterize the Tumor Microenvironment." In Biomarkers for Immunotherapy of Cancer, 245–72. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-9773-2_12.

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Vilimas, Tomas. "Measuring Tumor Mutational Burden Using Whole-Exome Sequencing." In Biomarkers for Immunotherapy of Cancer, 63–91. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-9773-2_3.

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Wang, Jinhua. "Tumor Sequencing: Enabling Personalized Targeted Treatments with Informatics." In Health Informatics, 161–74. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-18626-5_11.

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Qu, Kunbin, Joffre Baker, and Yan Ma. "Applications of NGS to Screen FFPE Tumours for Detecting Fusion Transcripts." In Next Generation Sequencing in Cancer Research, Volume 2, 155–77. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-15811-2_10.

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Chen, Mengjie, Lin Hou, and Hongyu Zhao. "Statistical Methods for the Analysis of Next Generation Sequencing Data from Paired Tumor-Normal Samples." In Statistical Analysis of Next Generation Sequencing Data, 379–404. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-07212-8_19.

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Conference papers on the topic "Tumour sequencing"

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Roze, JF, GM Monroe, JW Groeneweg, E. Stelloo, ST Paijens, HW Nijman, HS van Meurs, et al. "Whole genome sequencing of ovarian granulosa cell tumours show heterogeneity, genomic instability and tumour evolution." In ESGO Annual Meeting Abstracts. BMJ Publishing Group Ltd, 2019. http://dx.doi.org/10.1136/ijgc-2019-esgo.27.

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Shinde, Pravin V., Rajesh Deshmukh, and Preeti S. Patil. "Design of Deep Learning Approach for Expression of Genes by Tumour RNA-Sequencing Data." In 2022 IEEE 7th International conference for Convergence in Technology (I2CT). IEEE, 2022. http://dx.doi.org/10.1109/i2ct54291.2022.9825178.

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Koo, Si-Lin, Joe Poh Sheng Yeong, Andy Nguyen, Clarinda Wei Ling Chua, J. Zachary Sanborn, Steve Benz, Wah Siew Tan, et al. "Abstract 5725: Systematic identification of tumour-specific neoantigens(by whole-genome sequencing) and correlation between tumour neoantigen burden, PD-L1 expression and immune infiltrates in 158Asian colorectal cancers." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-5725.

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Peeters, Dieter JE, Ken Op De Beeck, Anja Brouwer, Geert Vandeweyer, Patrick Pauwels, Marc Peeters, Peter B. Vermeulen, et al. "Abstract P4-01-14: Whole exome sequencing of circulating and disseminated tumour cells in patients with metastatic breast cancer." In Thirty-Seventh Annual CTRC-AACR San Antonio Breast Cancer Symposium; December 9-13, 2014; San Antonio, TX. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.sabcs14-p4-01-14.

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Silva, Harini de, Niko Thio, Piers Blombery, Ella Thompson, Anand Deva, Miles Prince, Paul Neeson, and Criselle DSouza. "1442 Investigating the tumour immune microenvironment of breast implant associated anaplastic large cell lymphoma using single cell RNA sequencing." In SITC 37th Annual Meeting (SITC 2022) Abstracts. BMJ Publishing Group Ltd, 2022. http://dx.doi.org/10.1136/jitc-2022-sitc2022.1442.

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Mukhopadhyay, Asima, Nicola Curtin, and Richard Edmondson. "Evaluation of different methods to assess homologous recombination status and sensitivity to PARP inhibitors in ovarian cancer." In 16th Annual International Conference RGCON. Thieme Medical and Scientific Publishers Private Ltd., 2016. http://dx.doi.org/10.1055/s-0039-1685289.

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Methods: Matched samples of ascites and tumor tissue were taken from patients undergoing surgery for epithelial ovarian cancer. Tumor samples were formalin fixed and paraffin embedded (FFPE); ascites samples were used to generate primary cultures (PC). HR status was determined in PCs as previously described.[1] IC50 for the PARP inhibitor Rucaparib was estimated using SRB assays. DNA was extracted from the FFPE tissue. The following techniques were evaluated in PCs or paired FFPE samples: DR-GFP reporter assay, PARP activity assay, BRCA1 expression on immunohistochemistry, BRCA1 methylation status and BRCA1/2 mutation analysis. A next generation sequencing based assay was used to detect mutations and other genomic alterations in a large panel of cancer-associated genes, including BRCA1/2. Results: Paired samples were collected from 64 patients and characterized for HR function. 47/64 (76%) were high grade serous. 44% (28/64)) were HR defective (HRD) by Rad51 assay and correlated with Rucaparib sensitivity (PPV-92%, NPV-100%). Molecular analysis revealed that all mutations and other genomic alterations detected in ascites derived PCs were also found in matched FFPE tumor tissues. All tumors with serous histology contained p53 mutations, whilst the remaining tumors without p53 mutations were non-serous in histology. DR-GFP assay was unreliable in PC due to poor transfection. In a subset of 50 cancers there was reduced BRCA1 expression in the HRD vs. HRC tumours (34.8% vs. 22.7%, ns) whilst in a further subset of 30 cases there was no difference in endogenous or stimulated PARP activity between HRD and HRC tumours. Deleterious BRCA2 mutations were identified in 7 tumors, 6 of which were HRD. Only 1 deleterious BRCA1 mutation was detected but methylation of BRCA1 was identified in 13 of 64 (20%) tumors, 7 of which were HRD. Mutation of BRCA2 was mutually exclusive to methylation of BRCA1. HRD vs. HRC tumours showed BRCA1 methylation (25% vs. 17%) and BRCA1/2 mutation (21% vs. 0.3%). 14/28 (50%) HR defective tumors do not have BRCA1/2 mutations or BRCA1 methylation, suggesting other mechanisms can also result in a HR defective phenotype. 28/64 (43%) of samples demonstrated the HR defective phenotype. In all cases HR status correlated with sensitivity to Rucaparib. Conclusion: As expected, deleterious BRCA2 mutations conferred a HRD phenotype in cells but methylation of BRCA1 was not universally associated with HRD. This may be as a result of only partial silencing of the gene by methylation and further work is required to identify thresholds of methylation which may predict HR status. The use of BRCA1/2 mutation testing alone is unlikely to identify the majority of HR defective ovarian tumors. Assessment of functional status of HRD is the preferred option and further technologies should be developed to simplify the Rad51 assay.
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Peeters, DJE, P. Kumar, N. Van der Aa, F. Rothé, K. Theunis, K. Op de Beeck, SJ Van Laere, et al. "Abstract P1-04-03: Genome-wide analysis of copy number variations and mutation profiles of single circulating tumour cells using massively parallel paired-end sequencing." In Abstracts: Thirty-Sixth Annual CTRC-AACR San Antonio Breast Cancer Symposium - Dec 10-14, 2013; San Antonio, TX. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/0008-5472.sabcs13-p1-04-03.

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De Laere, Bram, Dieter JE Peeters, Salgado Roberto, Vermeulen B. Peter, Van Dam A. Peter, Dirix Y. Luc, and Van Laere J. Steven. "Abstract P4-01-09: Exploring the intra-patientPIK3CAmutational heterogeneity of circulating tumour cells by massive parallel sequencing in patients with metastatic hormone receptor-positive breast cancer." In Thirty-Seventh Annual CTRC-AACR San Antonio Breast Cancer Symposium; December 9-13, 2014; San Antonio, TX. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.sabcs14-p4-01-09.

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Linch, E., L. Miller, T. Looney, A. Zheng, D. Topacio-Hall, G. Nistala, G. Lowman, F. Hyland, and M. Andersen. "PO-394 Performance of a targeted T cell receptor beta immune repertoire sequencing panel in several FFPE tissue types – a tool for interrogation of the tumour microenvironment." In Abstracts of the 25th Biennial Congress of the European Association for Cancer Research, Amsterdam, The Netherlands, 30 June – 3 July 2018. BMJ Publishing Group Ltd, 2018. http://dx.doi.org/10.1136/esmoopen-2018-eacr25.906.

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Baird, Richard D., Lucy Kilburn, Sarah Kernaghan, Andrew M. Wardley, Iain Macpherson, Rebecca Roylance, Peter Stephens, et al. "Abstract P1-19-14: Results from plasmaMATCH trial treatment cohort D: A phase II trial of capivasertib in patients with an AKT activation basket mutation identified via ctDNA testing or tumour sequencing (CRUK/15/010)." In Abstracts: 2019 San Antonio Breast Cancer Symposium; December 10-14, 2019; San Antonio, Texas. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.sabcs19-p1-19-14.

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Reports on the topic "Tumour sequencing"

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Wagle, Nikhil. Tumor Genomic Profiling in Breast Cancer Patients Using Targeted Massively Parallel Sequencing. Fort Belvoir, VA: Defense Technical Information Center, January 2014. http://dx.doi.org/10.21236/ada598724.

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Cooney, Kathleen A. High Throughput Sequencing of Germline and Tumor from Men With Early-Onset Metastatic Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, October 2014. http://dx.doi.org/10.21236/ada611828.

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Cooney, Kathleen A. High-Throughput Sequencing of Germline and Tumor From Men with Early-Onset Metastatic Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, October 2015. http://dx.doi.org/10.21236/ada624260.

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