Relevant bibliographies by topics / Clonal heterogeneity

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Clonal heterogeneity'

Author: Grafiati
Published: 1 February 2023

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Journal articles on the topic "Clonal heterogeneity"

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Schuringa, Jan Jacob, and Constanze Bonifer. "Dissecting Clonal Heterogeneity in AML." Cancer Cell 38, no. 6 (December 2020): 782–84. http://dx.doi.org/10.1016/j.ccell.2020.11.011.

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Campos, Paulo R. A., Pedro S. C. A. Neto, Viviane M. de Oliveira, and Isabel Gordo. "ENVIRONMENTAL HETEROGENEITY ENHANCES CLONAL INTERFERENCE." Evolution 62, no. 6 (June 2008): 1390–99. http://dx.doi.org/10.1111/j.1558-5646.2008.00380.x.

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Rousselot, Philippe. "Clonal heterogeneity in acute lymphoblastic leukemias." Hématologie 17, no. 2 (March 2011): 120–22. http://dx.doi.org/10.1684/hma.2011.0601.

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Shlush, Liran I., and Dov Hershkovitz. "Clonal Evolution Models of Tumor Heterogeneity." American Society of Clinical Oncology Educational Book, no. 35 (May 2015): e662-e665. http://dx.doi.org/10.14694/edbook_am.2015.35.e662.

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Somatic/clonal evolution is the process of sequential acquisition of vertically transmittable genetic/epigenetic elements in multicellular organisms. Cancer is the result of somatic evolution. Understanding the processes that shape the evolution of individual tumors might help us to treat cancer more efficiently. The initiating genetic/epigenetic events occur in functional cells and provide the cell of origin a selective advantage under a changing environment. The initiating genetic events tend to be enriched in specific tissues (and are sometimes specific for those tissues), as different tissues undergo different changes in the environment that will activate selective forces on different cells of origin. For the initial clonal expansion to occur premalignant clones need to have a relative fitness advantage over their competitors. It is estimated that the premalignant phase can take several years. Once the premalignant clonal expansion is established, the premalignant cells will contribute to the changing environment and will start competing among themselves. In late stages of cancer evolution the environmental changes might be similar across different tissues, including a lack of physical space, a shortage of energy, and activation of the immune system, and more and more of the hallmarks of cancer will evolve. In this review we will explore the possible clinical relevance of the heterogeneity that evolves during this long somatic evolution. Above all, it should be stressed that the earlier the clonal expansion is recognized, the less diverse and less fit for survival the cells in the population are.
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Quinn, Jason George, and Irene Sadek. "Clonal heterogeneity in plasma cell myeloma." Lancet 387, no. 10022 (March 2016): e22. http://dx.doi.org/10.1016/s0140-6736(15)00384-0.

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Takhaveev, Vakil, and Matthias Heinemann. "Metabolic heterogeneity in clonal microbial populations." Current Opinion in Microbiology 45 (October 2018): 30–38. http://dx.doi.org/10.1016/j.mib.2018.02.004.

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García-Marqués, Jorge, and Laura López-Mascaraque. "Clonal Identity Determines Astrocyte Cortical Heterogeneity." Cerebral Cortex 23, no. 6 (May 22, 2012): 1463–72. http://dx.doi.org/10.1093/cercor/bhs134.

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Alonso-Alvarez, Sara, Alba Redondo-Guijo, Óscar Blanco, Miguel Alcoceba, Ana Balanzategui, Juan C. Caballero, Julio Dávila, et al. "Lymphoma Heterogeneity: Three Different Histological Pictures and One Unique Clone." Case Reports in Hematology 2016 (2016): 1–4. http://dx.doi.org/10.1155/2016/3947510.

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We report a patient who developed up to three different lymphomas with the same clonal IGH rearrangement. She was first diagnosed of splenic zone marginal lymphoma and relapsed for the first time with Hodgkin lymphoma histology and later with diffuse large B-cell lymphoma histology. Subsequent biopsies and analysis of clonally rearranged IGH genes helped to elucidate the clonal relationship between the three histologies and to confirm a common origin from the three tissue histologies. An integrated diagnosis should always be performed in order to achieve the most accurate diagnosis and be able to choose the best therapeutic options for our patients.
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Nepstad, Ina, Kimberley Joanne Hatfield, Tor Henrik Anderson Tvedt, Håkon Reikvam, and Øystein Bruserud. "Clonal Heterogeneity Reflected by PI3K-AKT-mTOR Signaling in Human Acute Myeloid Leukemia Cells and Its Association with Adverse Prognosis." Cancers 10, no. 9 (September 14, 2018): 332. http://dx.doi.org/10.3390/cancers10090332.

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Clonal heterogeneity detected by karyotyping is a biomarker associated with adverse prognosis in acute myeloid leukemia (AML). Constitutive activation of the phosphatidylinositol-3-kinase-Akt-mechanistic target of rapamycin (PI3K-Akt-mTOR) pathway is present in AML cells, and this pathway integrates signaling from several upstream receptors/mediators. We suggest that this pathway reflects biologically important clonal heterogeneity. We investigated constitutive PI3K-Akt-mTOR pathway activation in primary human AML cells derived from 114 patients, together with 18 pathway mediators. The cohort included patients with normal karyotype or single karyotype abnormalities and with an expected heterogeneity of molecular genetic abnormalities. Clonal heterogeneity reflected as pathway mediator heterogeneity was detected for 49 patients. Global gene expression profiles of AML cell populations with and without clonal heterogeneity differed with regard to expression of ectopic olfactory receptors (a subset of G-protein coupled receptors) and proteins involved in G-protein coupled receptor signaling. Finally, the presence of clonal heterogeneity was associated with adverse prognosis for patients receiving intensive antileukemic treatment. The clonal heterogeneity as reflected in the activation status of selected mediators in the PI3K-Akt-mTOR pathway was associated with a different gene expression profile and had an independent prognostic impact. Biological heterogeneity reflected in the intracellular signaling status should be further investigated as a prognostic biomarker in human AML.
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de Mel, Sanjay, Su Hong Lim, Moon Ley Tung, and Wee-Joo Chng. "Implications of Heterogeneity in Multiple Myeloma." BioMed Research International 2014 (2014): 1–12. http://dx.doi.org/10.1155/2014/232546.

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Multiple myeloma is the second most common hematologic malignancy in the world. Despite improvement in outcome, the disease is still incurable for most patients. However, not all myeloma are the same. With the same treatment, some patients can have very long survival whereas others can have very short survival. This suggests that there is underlying heterogeneity in myeloma. Studies over the years have revealed multiple layers of heterogeneity. First, clinical parameters such as age and tumor burden could significantly affect outcome. At the genetic level, there are also significant heterogeneity ranging for chromosome numbers, genetic translocations, and genetic mutations. At the clonal level, there appears to be significant clonal heterogeneity with multiple clones coexisting in the same patient. At the cell differentiation level, there appears to be a hierarchy of clonally related cells that have different clonogenic potential and sensitivity to therapies. These levels of complexities present challenges in terms of treatment and prognostication as well as monitoring of treatment. However, if we can clearly delineate and dissect this heterogeneity, we may also be presented with unique opportunities for precision and personalized treatment of myeloma. Some proof of concepts of such approaches has been demonstrated.
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Dissertations / Theses on the topic "Clonal heterogeneity"

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Beer, Philip. "The human myeloproliferative disorders : molecular pathogenesis and clonal heterogeneity." Thesis, University of Cambridge, 2009. https://www.repository.cam.ac.uk/handle/1810/226756.

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The classical myeloproliferative disorders (MPD), comprising essential thrombocythaemia (ET), polycythaemia vera (PV) and idiopathic myelofibrosis (IMF), are clonal premalignant haematopoietic neoplasms associated with activating mutations in signalling pathway molecules and a variable tendency to develop acute myeloid leukaemia (AML). This thesis examined genotype-phenotype associations of JAK2 and MPL mutations, the presence of clonal diversity in the MPD and the genetic events associated with progressive disease. Mutations in MPL were identified in 4% of ET and 7% of IMF but not in PV. Three different acquired MPL mutations were identified, one of which had been reported as an inherited allele. Although MPL mutations did not delineate a distinct clinical or histopathological subtype of ET, molecular testing provides an important new tool in the diagnostic armamentarium. Clones homozygous for the JAK2 V617F mutation were identified in female but not male patients with ET, suggesting that gender differences may be important in the determination of disease phenotype. In patients with two acquired genetic alterations, a signalling pathway mutation and a cytogenetic abnormality were usually present within the same clone. By contrast, coexistence of two signalling pathway mutations indicated the presence of biclonal disease that in two patients had arisen independently and not from a shared founder clone. RAS mutations were identified as potential cooperating events in patients with JAK2 or MPL mutant IMF. In patients developing AML following a JAK2 V617F-positive MPD, those with V617F-positive leukaemia had progressed via an accelerated phase of disease and harboured acquired alterations of RUNX1 or EVI1. V617F-negative leukaemias tended to follow directly from ET or PV, and loss of the JAK2 mutation by reversion to wild-type due to mitotic recombination, gene deletion or gene conversion was excluded. The thesis concludes with a discussion of how clonal heterogeneity can be integrated into current models of MPD disease pathogenesis.
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Nguyen, Long Viet. "Clonal heterogeneity of normal and transformed mammary stem cells." Thesis, University of British Columbia, 2014. http://hdl.handle.net/2429/47023.

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The normal mammary gland contains “stem cells” with extensive in vivo growth and bi-lineage differentiation potential and a surface phenotype of basal cells (BCs). BCs also contain cells with more limited growth and differentiation activity in vitro. An analogous luminal-restricted progenitor (LPs) subset has surface characteristics of both basal and luminal cells. I hypothesized that the growth and differentiation activity displayed by individual mammary epithelial cells from both subsets would be highly diverse, and that the properties of tumours produced from these cells would be affected by their cell of origin. To address this hypothesis, I first developed a lentiviral-mediated barcoding strategy that involves transducing each cell with a unique 27-base pair non-coding DNA sequence so that the number of its clonal progeny can be inferred from high-throughput sequencing data obtained on the progeny of bulk-transduced populations. The use of “spiked-in” control cells carrying a known barcode provided an internal calibration for clone size calculations and allowed clones of ≥100 cells to be reliably detected. Application of this strategy to normal mouse and human mammary cells identified expected bi-lineage clones but an unanticipated predominance of lineage-restricted clones produced in primary transplants. These experiments also revealed that many clones apparent in secondary hosts were not detected in the primary hosts, indicating their origin from cells with very delayed growth activity. Application of the barcoding strategy to normal human BCs and LPs transduced with lentiviruses encoding KRASG¹²D ± PI3KCAH¹⁰⁴⁷R ± TP53R²⁷³C showed tumour formation in subsequently transplanted immunodeficient mice was rapid (within 8 weeks) and efficient from both cell types (8-12/18 donors, 1/200-1/4,000 transduced cells). However, tumours generated from LPs contained larger clones than tumours generated from BCs. Surprisingly, none of the LP-derived tumours were ERα⁺ (typical of luminal-like breast cancers) whereas 60% of the BC-derived tumours were. Earlier analysis of xenografts of similarly transduced cells revealed changes in both the number and phenotype of the cells present. Taken together, these findings underscore the diverse regenerative activity of normal mammary cells and provide definitive evidence that the cell of origin can affect the properties of human breast tumours generated using identical oncogenes.
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Zhao, Boyang. "Rational drug combinations design against intratumoral heterogeneity and clonal evolution." Thesis, Massachusetts Institute of Technology, 2016. http://hdl.handle.net/1721.1/103271.

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Thesis: Ph. D., Massachusetts Institute of Technology, Computational and Systems Biology Program, 2016.
Cataloged from PDF version of thesis.
Includes bibliographical references (pages 119-121).
Cancer is a clonal evolutionary process. This results in complex clonal architecture and intratumoral heterogeneity in each patient. This also presents challenges for effective therapeutic intervention - with constant selective pressure to induce or select pre-existing resistant subclones toward drug resistance. Mathematical/computational modeling from population genetics, evolutionary dynamics, and engineering are being utilized to a greater extent in recent times to study tumor progression, intratumoral heterogeneity, drug resistance, and rational drug scheduling/combinations design. In this thesis we present several joint quantitative and experimental approaches for the rational design of drug combinations to tackle the issue of intratumoral heterogeneity and clonal evolution. Using a tractable experimental system with pre-defined tumor compositions, we derived computational approaches to rationally design drug combinations with the goal of minimizing a given heterogeneous tumor. We found that the best drug combinations can oftentimes be non-intuitive as they do not contain component drugs most effective for the individual subpopulations. This was the result of a need for combinatorial considerations on the effects of each drug on all subpopulations, hence at times leading to non-intuitive drug regimens. We validated our computational model predictions in vitro and in vivo in a preclinical model of Burkitt's lymphoma, with predictable evolutionary trajectories upon treatment. Next, we extended this methodology to study the effects of more complex tumor heterogeneity on combinatorial drug design, with similar conclusions. Sampling and statistical analyses over a range of tumor compositions can further inform effective drug combinations under some uncertainty in initial tumor heterogeneity. Moving beyond a model where we have control of initial tumor composition, we sought to examine collateral resistance and sensitivity during clonal evolution. Using a murine model of Ph+ acute lymphoblastic leukemia, we performed drug selection and pharmacological screen experiments. We observed important evolutionary processes of selection and drift in giving rise to resistance to clinically used BCR-ABL1 inhibitors. Remarkably, the resistant population also became hyper-sensitized to nonclassical BCR-ABL1 inhibitors at intermediate stages of the clonal evolution, in this so-called 'temporally collateral sensitivity'. Mathematical modeling and experimentation brought additional insight into the evolutionary dynamics and mechanism of action, with demonstrated in vivo efficacy.
by Boyang Zhao.
Ph. D.
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Zucker, Mark Raymond. "Inferring Clonal Heterogeneity in Chronic Lymphocytic Leukemia From High-Throughput Data." The Ohio State University, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=osu1554049121307262.

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Okamoto, Takeshi. "Clonal heterogeneity in differentiation potential of immortalized human mesenchymal stem cells." Kyoto University, 2004. http://hdl.handle.net/2433/147533.

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Khattra, Jaswinder. "Charting clonal heterogeneity in breast cancers : from bulk tumor genomes to single-cell genotypes." Thesis, University of British Columbia, 2015. http://hdl.handle.net/2429/53485.

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Traditional classifications and treatment of human cancers have operated with limitations surrounding tumor homogeneity and mutational stasis. Clinical metrics of malignant tumors focused on descriptive and behavioral properties such as tissue of origin, cellular morphologic features and extent of spread. Missing has been an understanding of the dynamics of cellular subpopulations that underpin divergent functional properties in space and time. This dissertation is focused on the development and application of methods, including next generation DNA sequencing, computational modeling, and single-cell genotyping protocols to elucidate breast tumor heterogeneity and clonal evolution at single nucleotide and single-cell resolution. First, I present advances in our knowledge of the mutational spectrum that may occur and evolve in an individual epithelial cancer, namely a lobular breast cancer metastases and matched primary tumor separated by a nine year interval. This seminal study demonstrated clonal evolution in a patient’s breast cancer and the successful application of targeted deep sequencing for determining digital allelic prevalences and clonal genotypes in bulk tumors. Second, I describe the diversity of genomic sequence and clonal heterogeneity in tumors of the triple-negative breast cancer subtype. The study uncovered wide clonal diversity in these primary tumors at first diagnosis. Third, I demonstrate via genotyping single tumor cells, that computational inferences of tumor clonal architecture can be made reliably from bulk tissue-derived data sets. This was performed using both somatic point mutations and loss of heterozygosity loci as clonal marks. And fourth, I applied single-cell analysis to study the clonal evolution in breast tumor murine xenografts following engraftment and serial passaging. This research uncovered a range of outcomes in tumor clonal composition upon initial engraftment and serial passaging. The same clonal groups were found to arise independently in separate xenografts derived from the same primary tumor, suggesting selection of functionally significant genotypes. Comprehensive capabilities in the measurement and analysis of clonal structure in cancers offers improved classification and combinatorial treatments of subpopulations in heterogeneous tumors and better use of murine xenograft models. Functionally relevant subpopulations of tumor cells, irrespective of numerical abundance or spatiotemporal persistence, can thereby be targeted using clonally informative genomic profiles.
Medicine, Faculty of
Pathology and Laboratory Medicine, Department of
Graduate
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Lamprecht, Sebastian [Verfasser], and Andreas [Akademischer Betreuer] Jung. "Clonal dynamics and tumor cell heterogeneity in colorectal cancer / Sebastian Lamprecht ; Betreuer: Andreas Jung." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2018. http://d-nb.info/1161670726/34.

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Marass, Francesco. "Latent feature models and non-invasive clonal reconstruction." Thesis, University of Cambridge, 2017. https://www.repository.cam.ac.uk/handle/1810/267784.

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Intratumoural heterogeneity complicates the molecular interpretation of biopsies, as multiple distinct tumour genomes are sampled and analysed at once. Ignoring the presence of these populations can lead to erroneous conclusions, and so a correct analysis must account for the clonal structure of the sample. Several methods to reconstruct tumour clonality from sequencing data have been proposed, spanning methods that either do not consider phylogenetic constraints or posit a perfect phylogeny. Models of the first type are typically latent feature models that can describe the observed data flexibly, but whose results may not be reconcilable with a phylogeny. The second type, instead, generally comprises non-parametric mixture models, with strict assumptions on the tumour’s evolutionary process. The focus of this dissertation is on the development of a phylogenetic latent feature model that can bridge the advantages of these two approaches, allowing deviations from a perfect phylogeny. The work is recounted by three statistical models of increasing complexity. First, I present a non-parametric model based on the Indian Buffet Process prior, and highlight the need for phylogenetic constraints. Second, I develop a finite, phylogenetic extension of the previous model, and show that it can outperform competing methods. Third, I generalise the phylogenetic model to arbitrary copy-number states. Markov chain Monte Carlo algorithms are presented to perform inference. The models are tested on datasets that include synthetic data, controlled biological data, and clinical data. In particular, the copy-number generalisation is applied to longitudinal circulating tumour DNA samples. Liquid biopsies that leverage circulating tumour DNA require sensitive techniques in order to detect mutations at low allele fractions. One method that allows sensitive mutation calling is the amplicon sequencing strategy TAm-Seq. I present bioinformatic tools to improve both the development of TAm-Seq amplicon panels and the analysis of its sequencing data. Finally, an enhancement of this method is presented and shown to detect mutations de novo and in a multiplexed manner at allele fractions less than 0.1%.
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Cornils, Kerstin, Lars Thielecke, Doreen Winkelmann, Tim Aranyossy, Mathias Lesche, Andreas Dahl, Ingo Roeder, Boris Fehse, and Ingmar Glauche. "Clonal competition in BcrAbl-driven leukemia: how transplantations can accelerate clonal conversion." Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2017. http://nbn-resolving.de/urn:nbn:de:bsz:14-qucosa-230481.

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Background: Clonal competition in cancer describes the process in which the progeny of a cell clone supersedes or succumbs to other competing clones due to differences in their functional characteristics, mostly based on subsequently acquired mutations. Even though the patterns of those mutations are well explored in many tumors, the dynamical process of clonal selection is underexposed. Methods: We studied the dynamics of clonal competition in a BcrAbl-induced leukemia using a γ-retroviral vector library encoding the oncogene in conjunction with genetic barcodes. To this end, we studied the growth dynamics of transduced cells on the clonal level both in vitro and in vivo in transplanted mice. Results: While we detected moderate changes in clonal abundancies in vitro, we observed monoclonal leukemias in 6/30 mice after transplantation, which intriguingly were caused by only two different BcrAbl clones. To analyze the success of these clones, we applied a mathematical model of hematopoietic tissue maintenance, which indicated that a differential engraftment capacity of these two dominant clones provides a possible explanation of our observations. These findings were further supported by additional transplantation experiments and increased BcrAbl transcript levels in both clones. Conclusion: Our findings show that clonal competition is not an absolute process based on mutations, but highly dependent on selection mechanisms in a given environmental context.
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Sikorski, Darek. "Small volume cell culture technology for the analysis of clonal heterogeneity in mammalian cell populations." Thesis, University of British Columbia, 2017. http://hdl.handle.net/2429/61186.

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The ability to culture individual cells provides a unique method to assess the heterogeneity of mammalian cell populations. However, there are many challenges when scaling down culture systems due to the complexity of re-creating a stimulating environment at the clonal level. Small volume culture systems such as integrated microfluidic platforms offer the potential to radically alter the throughput of clonal screening through the use of time-lapse imaging, dynamic stimulus control and economy of scale. In particular, the use of automated fluidic control allows for the characterization of single cells in a dynamic microenvironment similar to large-scale culture. This thesis describes how small volume cell culture practices such as the use of conditioned medium and microfluidic technology can be implemented to isolate large numbers of cells in small volumes and evaluate clonal populations under precise medium conditions. For a Chinese Hamster Ovary (CHO) cell system normal growth kinetics and specific productivity were sustained in small volumes. When exposed to conditioned medium from a parental CHO line, clones cultured at sub-mL scales matched the performance of large-scale cultures. A microfluidic bead assay was developed to detect Immunoglobulin G titers secreted from clones in nL volumes. The combination of microfluidic conditioned medium perfusion with the magnetic bead assay allowed for clonal productivity to be evaluated under simulated fed-batch conditions. Lastly, microfluidic cell culture was demonstrated on a human embryonic stem cell (hESC) system through the robust generation of colonies derived from single cells. hESCs propagated in the microfluidic system were observed to match the growth kinetics, marker expression and colony morphologies of larger cultures, while resolving response heterogeneity during differentiation induction. This thesis demonstrates how high-throughput, small volume culture systems can be used to screen clonal populations for therapeutic applications under complex culture conditions.
Applied Science, Faculty of
Graduate
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Books on the topic "Clonal heterogeneity"

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Straus, Lisa Ann. Heterogeneity of function in human CD4-8-T-cell clones from the periphery. [New Haven: s.n.], 1988.

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Book chapters on the topic "Clonal heterogeneity"

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Fanale, Daniele, Juan Lucio Iovanna, Antonio Giordano, Christian Rolfo, and Antonio Russo. "Cancer Clonal Evolution and Intra-tumor Heterogeneity." In Current Clinical Pathology, 27–39. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-55661-1_3.

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Berger, Marc G., and Céline Bourgne. "Contribution of Chronic Myeloid Leukaemia (CML) as a Disease Model to Define and Study Clonal Heterogeneity." In Stem Cells Heterogeneity in Cancer, 171–85. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-14366-4_10.

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Ahn, Soyeon, and Haiyan Huang. "Multiregion Sequence Analysis to Predict Intratumor Heterogeneity and Clonal Evolution." In Methods in Molecular Biology, 283–96. New York, NY: Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-1103-6_14.

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De Giovanni, Carla, Pier-Luigi Lollini, Brunella Del Re, Giordano Nicoletti, Giorgio Prodi, Katia Scotlandi, and Patrizia Nanni. "Heterogeneity and Clonal Interactions in the TS/A Murine Mammary Adenocarcinoma." In Advances in Experimental Medicine and Biology, 5–14. Boston, MA: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4899-5037-6_2.

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Scherer, Florian. "Capturing Tumor Heterogeneity and Clonal Evolution by Circulating Tumor DNA Profiling." In Tumor Liquid Biopsies, 213–30. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-26439-0_11.

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Aparicio, Pedro, Dolores Jaraquemada, and José A. López de Castro. "Cellular Allorecognition of HLA-B27: Clonal Heterogeneity and Identification of Immunodominant Sites." In Immunobiology of HLA, 112–13. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-662-39946-0_21.

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Geng, Yu, Zhongmeng Zhao, Jing Xu, Ruoyu Liu, Yi Huang, Xuanping Zhang, Xiao Xiao, Maomao, and Jiayin Wang. "Identifying Heterogeneity Patterns of Allelic Imbalance on Germline Variants to Infer Clonal Architecture." In Intelligent Computing Theories and Application, 286–97. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-63312-1_26.

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Laganà, Alessandro. "Computational Approaches for the Investigation of Intra-tumor Heterogeneity and Clonal Evolution from Bulk Sequencing Data in Precision Oncology Applications." In Advances in Experimental Medicine and Biology, 101–18. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-91836-1_6.

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Biddison, William E., and Stephen Shaw. "SB-Specific CTL Clones Exhibit Functional Heterogeneity in their Susceptibility to Blocking by Anti-T3 and Anti-T4 Antibodies." In Human T Cell Clones, 59–69. Totowa, NJ: Humana Press, 1985. http://dx.doi.org/10.1007/978-1-4612-4998-6_6.

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Mosmann, T. R., N. E. Street, D. F. Fiorentino, M. W. Bond, T. A. T. Fong, J. Schumacher, J. A. Leverah, M. Trounstine, P. Vieira, and K. W. Moore. "Heterogeneity of Mouse Helper T Cells and Cross-Regulation of TH1 and TH2 Clones." In Progress in Immunology, 611–18. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-83755-5_82.

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Conference papers on the topic "Clonal heterogeneity"

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Desai, Rhea, Colin Seymour, and Carmel Mothersill. "Clonal heterogeneity and its relevance to the radiosensitivity of tumours." In RAD Conference. RAD Centre, 2022. http://dx.doi.org/10.21175/rad.sum.abstr.book.2022.25.5.

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Loeb, Lawrence A., Michael W. Schmitt, Mark J. Prindle, and Pamela S. Becker. "Abstract 4890: Duplex sequencing of AML reveals extensive sub clonal heterogeneity." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-4890.

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Laughney, Ashley M., Srinivas Malladi, Danilo Macalinao, and Joan Massagué. "Abstract A01: Investigating clonal heterogeneity and transcriptional vulnerabilities in latent metastasis." In Abstracts: AACR Special Conference on Developmental Biology and Cancer; November 30 - December 3, 2015; Boston, Massachusetts. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1557-3125.devbiolca15-a01.

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Xu, Lixia, Minghui He, Zihao Dai, Sui Peng, and Ming Kuang. "IDDF2018-ABS-0097 Genomic heterogeneity and clonal evolution of multifocal hepatocellular carcinoma." In International Digestive Disease Forum (IDDF) 2018, Best Abstracts, Hong Kong, 9–10 June 2018. BMJ Publishing Group Ltd and British Society of Gastroenterology, 2018. http://dx.doi.org/10.1136/gutjnl-2018-iddfbestabstracts.6.

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Bardelli, Alberto. "Abstract CN02-03: Heterogeneity, drug resistance, and clonal dynamics in colorectal cancers." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics; November 5-9, 2015; Boston, MA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1535-7163.targ-15-cn02-03.

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Liao, Yong, David R. Valdecanas, Shangfeng Liu, David Molkintene, Khalida M. Wani, Nalini B. Patel, Li Wang, Chun Dai, Luka Milas, and Walter N. Hittelman. "Abstract 1161: Visualizing lung cancer heterogeneity by color-coding clonal cell subpopulations." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-1161.

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Bardelli, Alberto. "Abstract PL04-03: Heterogeneity, drug resistance, and clonal evolution in colorectal cancers." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-pl04-03.

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Krook, Melanie A., Russell Bonneville, Hui-Zi Chen, Julie W. Reeser, Michele R. Wing, Jharna Miya, Amy M. Smith, et al. "Abstract 2909: Rapid autopsy of metastatic cholangiocarcinoma demonstrates diverse patterns of clonal heterogeneity." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-2909.

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Krook, Melanie A., Russell Bonneville, Hui-Zi Chen, Julie W. Reeser, Michele R. Wing, Jharna Miya, Amy M. Smith, et al. "Abstract 2909: Rapid autopsy of metastatic cholangiocarcinoma demonstrates diverse patterns of clonal heterogeneity." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-2909.

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Tshering, Lara F., Fu Luo, Nam D. Nguyen, James G. Rail, Ting Jin, Daifeng Wang, and Flaminia Talos. "Abstract 3126: Intratumor heterogeneity and clonal dynamics underlying treatment resistance in prostate cancer." In Proceedings: AACR Annual Meeting 2021; April 10-15, 2021 and May 17-21, 2021; Philadelphia, PA. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.am2021-3126.

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Reports on the topic "Clonal heterogeneity"

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Applebaum, Shalom W., Lawrence I. Gilbert, and Daniel Segal. Biochemical and Molecular Analysis of Juvenile Hormone Synthesis and its Regulation in the Mediterranean Fruit Fly (Ceratitis capitata). United States Department of Agriculture, 1995. http://dx.doi.org/10.32747/1995.7570564.bard.

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Abstract:
Original Objectives and revisions: (1) "To determine the biosynthetic pathway of JHB3 in the adult C. capitata CA in order to establish parameters for the future choice and synthesis of suitable inhibitors". Modified: to determine the pattern of FR-7 biosynthesis during normal reproductive maturation, and identify enzymes potentially involved in its synthesis. (2) "To correlate allatal epoxidase activity to the biosynthesis of JHB3 at different stages of reproductive maturation/vitellogenesis and evaluate the hypothesis that a specific JH-epoxidase may be rate limiting". Modified: to study the effects of epoxidase inhibitors on the pattern of allatal JH biosynthesis in vitro and on female reproduction in vive. (3) "To probe and clone the gene homologous to ap from C. capitata, determine its exon-intron organization, sequence it and demonstrate its spatial and temporal expression in larvae, pupae and adults." The "Medfly" (Ceratitis capitata) is a serious polyphagous fruit pest, widely distributed in subtropical regions. Damage is caused by oviposition and subsequent development of larvae. JH's are dominant gonadotropic factors in insects. In the higher Diptera, to which the Medfly belongs, JHB3 is a major homolog. It comprises 95% of the total JH produced in vitro in D. melanogaster, with JH-III found as a minor component. The biosynthesis of both JH-III and JHB3 is dependent on epoxidation of double bonds in the JH molecule. The specificity of such epoxidases is unknown. The male accessory gland D. melanogaster produces a Sex Peptide, transferred to the female during copulation. SP reduces female receptivity while activating specific JH biosynthesis in vitro and inducing oviposition in vive. It also reduces pheromone production and activates CA of the moth Helicoverpa armigera. In a previous study, mutants of the apterous (ap) gene of D. melanogaster were analyzed. This gene induces previteilogenic arrest which can be rescued by external application of JH. Considerable progress has been made in recombinant DNA technology of the Medfly. When fully operative, it might be possible to effectively transfer D. melanogaster endocrine gene-lesions into the Medfly as a strategy for their genetic control. A marked heterogeneity in the pattern of JH homologs produced by Medfly CA was observed. Contrary to the anticipated biosynthesis of JHB;, significant amounts of an unknown JH-like compound, of unknown structure and provisionally termed FR-7, were produced, in addition to significant amounts of JH-III and JHB3. Inhibitors of monooxygenases, devised for their effects on ecdysteroid biosynthesis, affect Medfly JH biosynthesis but do not reduce egg deposition. FR-7 was isolated from incubation media of Medfly CA and examined by various MS procedures, but its structure is not yet resolved. MS analysis is being done in collaboration with Professor R.R.W. Rickards of the Australian National University in Canberra, Australia. A homologue of the ap gene of D. melanogaster exists in the Medfly. LIM domains and the homeo-domain, important for the function of the D. melanogaster ap gene, are conserved here too. Attempts to clone the complete gene were unsuccessful. Due to the complexity of JH homologs, presence of related FR-7 in the biosynthetic products of Medfly CA and lack of reduction in eggs deposited in the presence of monooxygenase inhibitors, inhibition of epoxidases is not a feasible alternative to control Medfly reproduction, and raises questions which cannot be resolved within the current dogma of hormonal control of reproduction in Diptera. The Medfly ap gene has similar domains to the D. melanogaster ap gene. Although mutant ap genes are involved in JH deficiency, ap is a questionable candidate for an endocrine lesion, especially since the D. melanogoster gene functions is a transcription factor.
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