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Artykuły w czasopismach na temat „Two Stage Clonal Expansion Model”

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Data publikacji: 6 września 2023

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1

M Zielinski, R L Kodell, D Krewski, J. "Interaction between two carcinogens in the two-stage clonal expansion model of carcinogenesis." Journal of Epidemiology and Biostatistics 6, no. 2 (2001): 219–28. http://dx.doi.org/10.1080/135952201753172999.

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Kaiser, J. C., and W. F. Heidenreich. "Comparing regression methods for the two-stage clonal expansion model of carcinogenesis." Statistics in Medicine 23, no. 21 (2004): 3333–50. http://dx.doi.org/10.1002/sim.1620.

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Castrén, Olli. "IMPLICATIONS OF A TWO-STAGE CLONAL EXPANSION MODEL TO INDOOR RADON RISK ASSESSMENT." Health Physics 76, no. 4 (1999): 393–97. http://dx.doi.org/10.1097/00004032-199904000-00007.

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Tan, E., N. Warren, A. Darnton, and J. Hodgson. "Modelling mesothelioma mortality in Great Britain using the two-stage clonal expansion model." Occupational and Environmental Medicine 68, Suppl_1 (2011): A60. http://dx.doi.org/10.1136/oemed-2011-100382.194.

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Kaiser, J. C., and W. F. Heidenreich. "Identifying dose dependences of the two-stage clonal expansion model with simulated cohorts." Journal of Radiological Protection 22, no. 3A (2002): A57—A60. http://dx.doi.org/10.1088/0952-4746/22/3a/310.

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Kodell, Ralph L., Daniel Krewski, and Jan M. Zielinski. "Additive and Multiplicative Relative Risk in the Two-Stage Clonal Expansion Model of Carcinogenesis." Risk Analysis 11, no. 3 (1991): 483–90. http://dx.doi.org/10.1111/j.1539-6924.1991.tb00633.x.

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Zeka, A., R. Gore, and D. Kriebel. "The two-stage clonal expansion model in occupational cancer epidemiology: results from three cohort studies." Occupational and Environmental Medicine 68, no. 8 (2010): 618–24. http://dx.doi.org/10.1136/oem.2009.053983.

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Richardson, David B. "Lung cancer in chrysotile asbestos workers: analyses based on the two-stage clonal expansion model." Cancer Causes & Control 20, no. 6 (2009): 917–23. http://dx.doi.org/10.1007/s10552-009-9297-z.

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Heidenreich, W. F., and H. G. Paretzke. "The Two-Stage Clonal Expansion Model as an Example of a Biologically Based Model of Radiation-Induced Cancer." Radiation Research 156, no. 5 (2001): 678–81. http://dx.doi.org/10.1667/0033-7587(2001)156[0678:ttscem]2.0.co;2.

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10

Lensing, Shelly Y., and Ralph L. Kodell. "Fitting the Two-Stage Clonal Expansion Model Based on Exact Hazard to the ED01 Data Using SAS NLIN." Risk Analysis 15, no. 2 (1995): 233–45. http://dx.doi.org/10.1111/j.1539-6924.1995.tb00317.x.

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Curtis, S. B., E. G. Luebeck, W. D. Hazelton, and S. H. Moolgavkar. "A new perspective of carcinogenesis from protracted high-let radiation arises from the two-stage clonal expansion model." Advances in Space Research 30, no. 4 (2002): 937–44. http://dx.doi.org/10.1016/s0273-1177(02)00158-8.

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Negreira, Gabriel H., Pieter Monsieurs, Hideo Imamura, et al. "High throughput single-cell genome sequencing gives insights into the generation and evolution of mosaic aneuploidy in Leishmania donovani." Nucleic Acids Research 50, no. 1 (2021): 293–305. http://dx.doi.org/10.1093/nar/gkab1203.

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Abstract Leishmania, a unicellular eukaryotic parasite, is a unique model for aneuploidy and cellular heterogeneity, along with their potential role in adaptation to environmental stresses. Somy variation within clonal populations was previously explored in a small subset of chromosomes using fluorescence hybridization methods. This phenomenon, termed mosaic aneuploidy (MA), might have important evolutionary and functional implications but remains under-explored due to technological limitations. Here, we applied and validated a high throughput single-cell genome sequencing method to study for

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13

Schöllnberger, H., R. D. Stewart, and R. E. J. Mitchel. "Low-Let-Induced Radioprotective Mechanisms within a Stochastic Two-Stage Cancer Model." Dose-Response 3, no. 4 (2005): dose—response.0. http://dx.doi.org/10.2203/dose-response.003.04.006.

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A stochastic two-stage cancer model with clonal expansion was used to investigate the potential impact on human lung cancer incidence of some aspects of the hormesis mechanisms suggested by Feinendegen ( Health Phys. 52 663–669, 1987). The model was applied to low doses of low-LET radiation delivered at low dose rates. Non-linear responses arise in the model because radiologically induced adaptations in radical scavenging and DNA repair may reduce the biological consequences of DNA damage formed by endogenous processes and ionizing radiation. Sensitivity studies were conducted to identify crit

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14

Nagah, Ahmed, Asmaa Amer, and Xinan Zhang. "Mathematical modeling of female breast cancer in Japan." International Journal of Biomathematics 13, no. 04 (2020): 2050023. http://dx.doi.org/10.1142/s1793524520500230.

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Cancer incidence rates are significantly different all over the world. Breast cancer is affected by many factors, the most important being genetics and lifestyle. The aim of this paper is to study the mutation mechanisms of breast cancer for Japanese women by fitting the incidence data of three high-quality population areas in Japan from 1985 to 2010. To achieve this goal, we have set up multi-stage models within the mathematical model of Moolgavkar, Venzon, and Knudson. Such models take both mutation rates and clonal expansion rates as parameters in each compartment into consideration. Based

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Hazelton, William D., E. Georg Luebeck, Wolfgang F. Heidenreich, and Suresh H. Moolgavkar. "Analysis of a Historical Cohort of Chinese Tin Miners with Arsenic, Radon, Cigarette Smoke, and Pipe Smoke Exposures Using the Biologically Based Two-Stage Clonal Expansion Model." Radiation Research 156, no. 1 (2001): 78–94. http://dx.doi.org/10.1667/0033-7587(2001)156[0078:aoahco]2.0.co;2.

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Levy, David T., Kenneth Blackman, and Eduard Zaloshnja. "Chapter 10: A Macro-Model of Smoking and Lung Cancer: Examining Aggregate Trends in Lung Cancer Rates Using the CPS-I and CPS-II and Two-Stage Clonal Expansion Models." Risk Analysis 32 (August 2012): S125—S141. http://dx.doi.org/10.1111/j.1539-6924.2012.01795.x.

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Celik, Hamza, Ethan Krug, Hassan Bjeije, et al. "A Novel Humanized Animal Model Reveals Clonal Architecture and Therapeutic Vulnerabilities in Myelofibrosis." Blood 136, Supplement 1 (2020): 17–18. http://dx.doi.org/10.1182/blood-2020-143034.

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Myelofibrosis (MF) is the deadliest subtype of myeloproliferative neoplasm (MPN) with a median survival of approximately 5 years. Ruxolitinib, a front line therapy for JAK2V617F mutant MPN, can alleviate symptoms of the disease, but does not eliminate the malignant clone and has minimal impact on BM fibrosis and overall survival. Current mouse models do not recapitulate the clinical heterogeneity, clonal genetic composition, or morphological features of MF. Most notably, these models do not generate robust reticulin fibrosis in the bone marrow, the most significant MF pathology. This lack of c

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Madas, B. G., and K. Varga. "Biophysical modelling of the effects of inhaled radon progeny on the bronchial epithelium for the estimation of the relationships applied in the two-stage clonal expansion model of carcinogenesis." Radiation Protection Dosimetry 159, no. 1-4 (2014): 237–41. http://dx.doi.org/10.1093/rpd/ncu125.

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Vivian, John, Kimberly Walter, Elliott Drabek, et al. "Abstract P2-01-11: Single-cell sequencing of the blood T cell repertoire before and after trastuzumab treatment in early stage HER2+ breast cancer." Cancer Research 82, no. 4_Supplement (2022): P2–01–11—P2–01–11. http://dx.doi.org/10.1158/1538-7445.sabcs21-p2-01-11.

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Abstract Background: Human epidermal growth factor receptor 2 (HER2) positivity in breast cancer portends an aggressive tumor behavior and poor prognosis and is associated with a positive response to trastuzumab treatment. Prior immunohistochemistry and RNA sequencing of breast tumor tissues suggest that trastuzumab may recruit and activate anti-tumor T cells. Tumor infiltrating lymphocytes have been associated with improved response in patients with HER2+ early breast cancer treated with neoadjuvant trastuzumab plus chemotherapy. However, these cells have not previously been characterized at

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20

Itzykson, Raphael, Olivier Kosmider, Aline Renneville, et al. "Two Distinct Mechanisms Contribute to Granulomonocytic Hyperplasia in Chronic Myelomonocytic Leukemias (CMML)." Blood 120, no. 21 (2012): 309. http://dx.doi.org/10.1182/blood.v120.21.309.309.

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Abstract Abstract 309 Background: The granulomonocytic (GM) hyperplasia of CMML has been attributed to GM-CSF hypersensitivity triggered by mutations in the CBL/RAS pathway according to the prevailing model in juvenile myelomonocytic leukemias (Kotecha Cancer Cell 2008). Recurrent mutations affecting epigenetic (eg TET2 and ASXL1) and splicing (eg SRSF2) machineries, or cytokine signaling (N/KRAS, CBL, JAK2) are present in most CMML cases, but none is specific of CMML. In 224 CMML patients (pts), we found TET2 (58%), SRSF2 (47%) and ASXL1 (38%) to be the most frequently mutated genes; only 66

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Varuzza, Muriele B., Adriane F. Evangelista, Cristiano P. Souza, and Márcia C. Marques. "Abstract P5-13-01: TUMOR PROGRESSION MODEL IN BREAST CANCER WITH BRAIN METASTASIS." Cancer Research 83, no. 5_Supplement (2023): P5–13–01—P5–13–01. http://dx.doi.org/10.1158/1538-7445.sabcs22-p5-13-01.

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Abstract INTRODUCTION: Breast cancer are the main cause of related deaths cancer among women, corresponding to 25% of new cases each year. When diagnosed at early stages, it has an overall five-year survival rate of up to 90%. However, in more advanced stages, survival is reduced to about 24%, with 90% of women in stage IV dying as a result of complications related to metastases. Considering that brain metastasis is an unfavorable prognostic site, and the identification of genetic-molecular profiles in primary tumors and in metastatic sites are a subject poorly described in the literature, we

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22

Kumar, Abhishek, Florian Pecquenard, Martha Baydoun, et al. "An Efficient 5-Aminolevulinic Acid Photodynamic Therapy Treatment for Human Hepatocellular Carcinoma." International Journal of Molecular Sciences 24, no. 13 (2023): 10426. http://dx.doi.org/10.3390/ijms241310426.

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Photodynamic therapy (PDT) is a two-stage treatment relying on cytotoxicity induced by photoexcitation of a nontoxic dye, called photosensitizer (PS). Using 5-aminolevulinic acid (5-ALA), the pro-drug of PS protoporphyrin IX, we investigated the impact of PDT on hepatocellular carcinoma (HCC). Optimal 5-ALA PDT dose was determined on three HCC cell lines by analyzing cell death after treatment with varying doses. HCC-patient-derived tumor hepatocytes and healthy donor liver myofibroblasts were treated with optimal 5-ALA PDT doses. The proliferation of cancer cells and healthy donor immune cell

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23

Simonetto, Cristoforo, Ulrich Mansmann, and Jan Christian Kaiser. "Shape-specific characterization of colorectal adenoma growth and transition to cancer with stochastic cell-based models." PLOS Computational Biology 19, no. 1 (2023): e1010831. http://dx.doi.org/10.1371/journal.pcbi.1010831.

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Colorectal adenoma are precursor lesions on the pathway to cancer. Their removal in screening colonoscopies has markedly reduced rates of cancer incidence and death. Generic models of adenoma growth and transition to cancer can guide the implementation of screening strategies. But adenoma shape has rarely featured as a relevant risk factor. Against this backdrop we aim to demonstrate that shape influences growth dynamics and cancer risk. Stochastic cell-based models are applied to a data set of 197,347 Bavarian outpatients who had colonoscopies from 2006-2009, 50,649 patients were reported wit

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Rai, Shivam, Nils Hansen, Hui Hao-Shen, Stefan Dirnhofer, Nageswara Rao Tata та Radek C. Skoda. "IL-1β Secreted from Mutant Cells Carrying JAK2-V617Ffavors Early Clonal Expansion and Promotes MPN Disease Initiation and Progression". Blood 134, Supplement_1 (2019): 307. http://dx.doi.org/10.1182/blood-2019-129800.

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JAK2-V617F is the most frequently recurring somatic mutation in patients with myeloproliferative neoplasm (MPN), but it can also be found in healthy individuals with clonal hematopoiesis of indeterminate potential (CHIP) with a frequency much higher than the incidence of MPN. This suggests that the acquisition of the JAK2-V617F is not the rate-limiting step and other factors might be required for the expansion of the JAK2 mutated clone and initiation of MPN disease. Chronic inflammation is a hallmark of advanced MPN and is associated with progression to myelofibrosis and AML. Interleukin-1β (I

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Mylonas, Elena, Kenichi Yoshida, Mareike Frick, et al. "Single-Cell Analysis Based Dissection of Clonality in Myelofibrosis." Blood 134, Supplement_1 (2019): 469. http://dx.doi.org/10.1182/blood-2019-123367.

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Introduction Large-scale sequencing studies have unraveled the mutational landscape of myelofibrosis (MF), demonstrating clonal heterogeneity and importance of genetically defined subgroups in disease prognosis and progression. In order to elucidate the genetics of MF progression and its molecular drivers during JAK inhibition therapy, we performed in-depth genetic studies on longitudinal blood samples from 15 MF patients covering a disease span of 3 to 5 years after initiation of ruxolitinib. Methods Sequential samples from 15 MF patients (PMF n=8; post-ET/PV-MF n=7) accounting for a total of

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Wesseling, Jelle. "Abstract F1-2: Clonal evolution of DCIS to invasion." Cancer Research 83, no. 5_Supplement (2023): F1–2—F1–2. http://dx.doi.org/10.1158/1538-7445.sabcs22-f1-2.

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Abstract Clonal evolution of DCIS to invasion Ductal carcinoma in situ (DCIS) is the most common form of preinvasive breast cancer and, despite treatment, a small fraction (5-10%) of DCIS patients develop subsequent invasive breast cancer (IBC). If not treated, at least 3 out of 4 women with DCIS will not develop IBC1-3. This implies many women with non-progressive, low-risk DCIS are likely to carry the burden of overtreatment. To solve this DCIS dilemma, two fundamental questions need to be answered. The first question is, how the subsequent IBC is related to the initial DCIS lesion. The seco

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DeGregori, James V. "Abstract SY24-01: Changes in adaptive landscapes and somatic evolution as we age." Cancer Research 82, no. 12_Supplement (2022): SY24–01—SY24–01. http://dx.doi.org/10.1158/1538-7445.am2022-sy24-01.

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Abstract Why do we get cancer? Why is cancer highly associated with old age, and why are insults like smoking, obesity, and sunlight associated with increased risk of cancers? Of course, these contexts all cause mutations, and some of these mutations can contribute to malignant phenotypes. But we now understand that carcinogenesis is much more complex than originally appreciated. In particular, there are microenvironmental forces that both impede and promote cancer evolution. Just as organismal evolution is known to be driven by environmental changes, somatic evolution in our bodies is similar

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Kotliar, Michael, Aizhan Surumbayeva, Linara Gabitova, et al. "Abstract PO-068: Cholesterol auxotrophy promotes the expansion of centroacinar cells giving rise to the basal subtype of pancreatic adenocarcinoma." Cancer Research 81, no. 22_Supplement (2021): PO—068—PO—068. http://dx.doi.org/10.1158/1538-7445.panca21-po-068.

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Abstract Gene expression analyses established at least two molecular subtypes of pancreatic adenocarcinoma (PDAC), the classical (or glandular), and the basal (or mesenchymal), each of which is associated with distinct prognoses and sensitivity to chemotherapy. It remains unclear, however, whether the basal carcinoma cells arise from a separate cell-of-origin, or are emerging from the pre-existing well-differentiated “classical” PDAC cells. To distinguish these alternatives, we conducted single-cell transcriptome analyses and virtual lineage tracing comparing cellular populations at pre-malign

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Gutierrez, Albert, Renee Tschumper, Tait D. Shanafelt, Jeanette Eckel-Passow, Neil E. Kay, and Diane F. Jelinek. "Aberrant Regulation of the LEF-1 Locus in Monoclonal B Cell Lymphocytosis (MBL) and Chronic Lymphocytic Leukemia (CLL): A Possible Role for Epigenetic Regulation." Blood 114, no. 22 (2009): 669. http://dx.doi.org/10.1182/blood.v114.22.669.669.

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Abstract Abstract 669 Background: Chronic lymphocytic leukemia (CLL) is the most common leukemia in the Western world but its pathogenesis remains largely unknown. More recently, a widely prevalent premalignant condition termed monoclonal B cell lymphocytosis (MBL) has been defined and similarly involves expansion of a CD19+CD5+ population of B cells. MBL has been the focus of a wide number of recent studies in hopes it can provide insight into the early pathological events that lead to clonal expansion of a pre-leukemic CLL-like clone. Previously, we and others identified the transcription fa

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Shehata, Medhat, Rainer Hubmann, Martin Hilgarth, et al. "Partial Characterization and In Vitro Expansion of Putative CLL Precursor/Stem Cells Which Are Dependent on Bone Marrow Microenvironment for Survival." Blood 116, no. 21 (2010): 2433. http://dx.doi.org/10.1182/blood.v116.21.2433.2433.

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Abstract Abstract 2433 Chronic lymphocytic leukemia (CLL) is characterized by the clonal expansion of B lymphocytes which typically express CD19 and CD5. The disease remains incurable and recurrence often occurs after current standard therapies due to residual disease or probably due to the presence of therapy-resistant CLL precursors. Based on the growing evidence for the existence of leukemia stem cells, this study was designed to search for putative CLL precursors/stem cells based on the co-expression of CLL cell markers (CD19/CD5) with the hematopoietic stem cell marker (CD34). Forty seven

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Passamonti, Francesco, Elisa Rumi, Daniela Pietra, et al. "Sequential Evaluation of the Proportion of Granulocyte JAK2 (V617F) Mutant Alleles in Chronic Myeloproliferative Disorders." Blood 108, no. 11 (2006): 2682. http://dx.doi.org/10.1182/blood.v108.11.2682.2682.

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Abstract A somatic gain-of-function mutation of the Janus kinase 2 (JAK2) gene is found in most patients with polycythemia vera (PV) and in about half of those with essential thrombocythemia (ET) or chronic idiopathic myelofibrosis (CIMF). In this study, we investigated the time course of the proportion of mutant alleles during the clinical course of the disease, and its relationship with clinical phenotype and treatment. Using a quantitative real-time polymerase chain reaction (qRT-PCR)-based allelic discrimination assay for the detection of the V617F mutation, we studied 522 patients diagnos

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Tamplin, Owen J., Jonathan E. Henninger, Hunter L. Elliott, Douglas S. Richardson, and Leonard I. Zon. "A Zebrafish Model of Fetal Bone Marrow Provides a Dynamic View of Hematopoietic Stem Cell Niche Colonization." Blood 128, no. 22 (2016): 170. http://dx.doi.org/10.1182/blood.v128.22.170.170.

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Abstract The entire blood system is supported throughout life by a small number of hematopoietic stem and progenitor cells (HSPCs) that are produced exclusively during embryonic development. These stem cells are generated from the hemogenic endothelium of the dorsal aorta, then migrate to the fetal liver where they expand, before making a final migration to the fetal bone marrow. After seeding the bone marrow, the stem cell pool stabilizes and the total number of HSPCs remains relatively constant. Very little is known about this early stage of bone marrow niche colonization. A better understan

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Cox, Charlotte V., Roger S. Evely, and Allison Blair. "A Model System for Proliferation and Characterisation of Stem Cells in Childhood T-ALL." Blood 106, no. 11 (2005): 1370. http://dx.doi.org/10.1182/blood.v106.11.1370.1370.

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Abstract T cell acute lymphoblastic leukaemias (T-ALL) are highly aggressive malignancies representing 10–15% of paediatric and 25% adult ALLs. T-ALL was considered to arise as a consequence of clonal expansion of early thymocytes. However, progress towards increasing our understanding of the biology of this disease has been hampered by lack of appropriate culture systems to study primary cells and use of murine model systems that often do not accurately reflect human disease. Traditional xenograft models of leukaemia have involved implantation of malignant cells or immortalised leukaemic cell

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Wu, Song, Zongdong Li, Dmitri V. Gnatenko, et al. "Blvrb Mutation Induces Thrombocytosis Via Redox Dysregulation in the Heme Degradation Pathway." Blood 126, no. 23 (2015): 74. http://dx.doi.org/10.1182/blood.v126.23.74.74.

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Abstract Known genetic loci influencing blood cell production account for <10% of platelet and red blood cell variability, and thrombopoietin (Tpo)/c-MPL liganding is dispensable for definitive thrombopoiesis establishing that fundamentally important modifier loci remain unelucidated. We completed RNASeq of highly-purified platelets from 7 essential thrombocythemia (ET) subjects [4 harbored the JAK2V617F mutation and 3 were genotypically normal] and 5 healthy controls, and developed an iterative algorithm to identify 33 non-synonymous SNVs that are putatively linked to the ET phenotype. Tra

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Fu, Xiao, Yue Zhao, Jose I. Lopez, et al. "Spatial patterns of tumour growth impact clonal diversification in a computational model and the TRACERx Renal study." Nature Ecology & Evolution 6, no. 1 (2021): 88–102. http://dx.doi.org/10.1038/s41559-021-01586-x.

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AbstractGenetic intra-tumour heterogeneity fuels clonal evolution, but our understanding of clinically relevant clonal dynamics remain limited. We investigated spatial and temporal features of clonal diversification in clear cell renal cell carcinoma through a combination of modelling and real tumour analysis. We observe that the mode of tumour growth, surface or volume, impacts the extent of subclonal diversification, enabling interpretation of clonal diversity in patient tumours. Specific patterns of proliferation and necrosis explain clonal expansion and emergence of parallel evolution and

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Stevens, Aaron D., Davey B. Daniel, Jerome H. Goldschmidt, et al. "Effects of trilaciclib prior to chemotherapy ± atezolizumab on T-cell activation in patients with newly diagnosed extensive-stage small cell lung cancer." Journal of Clinical Oncology 39, no. 15_suppl (2021): e20582-e20582. http://dx.doi.org/10.1200/jco.2021.39.15_suppl.e20582.

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e20582 Background: Chemotherapy ± immunotherapy has demonstrated meaningful clinical benefit to patients (pts) with extensive-stage small cell lung cancer (ES-SCLC); however, chemotherapy-induced damage to the immune system can potentially diminish treatment efficacy. Trilaciclib (T) is an intravenous cyclin-dependent kinase 4/6 inhibitor that protects hematopoietic stem and progenitor cells from chemotherapy-induced damage (myeloprotection) and may directly enhance antitumor immunity. Here, we evaluated the immune effects of T in pts with ES-SCLC receiving T or placebo (P) prior to first-line

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Heidenreich, Wolfgang F., E. Georg Luebeck, and Suresh H. Moolgavkar. "Some Properties of the Hazard Function of the Two-Mutation Clonal Expansion Model." Risk Analysis 17, no. 3 (1997): 391–99. http://dx.doi.org/10.1111/j.1539-6924.1997.tb00878.x.

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Goldberg, Liat, Rachel M. Pierce, Masahiro Onozawa, et al. "Co-Expression of NUP98-HOXD13 and Mutant IDH2 Triggers an Early T-Cell Precursor-like Leukemia in Mice." Blood 126, no. 23 (2015): 904. http://dx.doi.org/10.1182/blood.v126.23.904.904.

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Abstract Background and hypothesis: Acute lymphoblastic leukemia (ALL) is the most common pediatric malignancy, comprising of B lineage ALL and T-cell lineage ALL (about 85% and 15%, respectively). In most cases, treatment regimens for ALL patients have proved efficient and prognosis is usually encouraging. However, a recently described subgroup of T-cell ALL patients have been found to have a poor prognosis when treated with conventional therapy. These higher risk T-cell leukemias have a cell of origin thought to resemble an early T-cell precursor (ETP), which retains the capability to differ

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Roulland, Sandrine, Jean-marc Navarro, Pierre Grenot, et al. "Follicular Lymphoma-Like B-Cells in Healthy Individuals: A Novel Intermediate Step in Early Lymphomagenesis." Blood 108, no. 11 (2006): 821. http://dx.doi.org/10.1182/blood.v108.11.821.821.

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Abstract Follicular lymphoma (FL) is one of the most common B-cell lymphoma, and remains virtually incurable despite its relatively indolent nature. T(14;18)(q32;q21), the genetic hallmark and early initiating event of FL pathogenesis, is also present at low frequency (10−5–10−7) in blood from healthy individuals (HI), indicating that t(14;18) and the ensuing BCL2 overexpression is necessary but not sufficient for malignant transformation. It has long been assumed that in HI, t(14;18) is carried by circulating quiescent naïve B-cells, where its oncogenic potential would be restrained. Yet, se

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Rajagopalan, Adhithi, Zhi Wen, Quinlan Furumo, et al. "Mice Expressing MYC and NrasQ61R in Germinal Center B Cells Develop Highly Aggressive Multiple Myeloma." Blood 132, Supplement 1 (2018): 1006. http://dx.doi.org/10.1182/blood-2018-99-116757.

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Abstract Multiple myeloma (MM) is characterized by clonal expansion of malignant plasma cells (PCs) and aberrant production of monoclonal immunoglobulin detected as an M spike using serum protein electrophoresis. In the United States, MM represents ~15% of hematologic malignancies and is one of the few cancers increasing in incidence (e.g., 14,400 in 1996 to 30,770 in 2018, from SEER). Previously, a Vk*MYC mouse model was described, in which AID-dependent activation of MYC transgene in germinal center (GC) B cells catalyzes a highly penetrant, indolent MM after a prolonged latency, suggesting

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Heidenreich, Wolfgang F., and Rudolf Hoogenveen. "Limits of Applicability for the Deterministic Approximation of the Two-Step Clonal Expansion Model." Risk Analysis 21, no. 1 (2001): 103–6. http://dx.doi.org/10.1111/0272-4332.211093.

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Zhang, Pei, and Azmy S. Ackleh. "A discrete stage-structured two-species competition model with sexual and clonal reproduction." Journal of Biological Dynamics 6, no. 1 (2012): 2–16. http://dx.doi.org/10.1080/17513758.2011.623188.

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Hoogenveen, Rudolf T., Harvey J. Clewell, Melvin E. Andemen, and Wout Slob. "An Alternative Exact Solution of the Two-Stage Clonal Growth Model of Cancer." Risk Analysis 19, no. 1 (1999): 9–14. http://dx.doi.org/10.1111/j.1539-6924.1999.tb00381.x.

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Brisou, Gabriel, Laurent Jallades, Alexandra Traverse-Glehen, et al. "Expression of a Dysfunctional Activation Induced Cytidine Deaminase Is Correlated with Disease Progression in Splenic Marginal Zone Lymphoma." Blood 120, no. 21 (2012): 2397. http://dx.doi.org/10.1182/blood.v120.21.2397.2397.

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Abstract Abstract 2397 B cells can undergo at least two differentiation pathways, dependent of T cells or not, starting from follicular or marginal zone B cells respectively. The T-independent response, less understood than the germinal center reaction, is triggered by specific antigens and arises from marginal zone B cells. During this development, some B cells undergo somatic hypermutation (SHM) and class switch recombination (CSR), triggered by the same DNA editing enzyme called Activation Induced Cytidine Deaminase (AID). The splenic marginal zone lymphoma (SMZL) is a rare lymphoproliferat

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Markov, Andrey A. "Model of SPS Two-Stadium Synthesis and Densification Reactor Applied for Ultrafine Zirconium Nitride Powder." Materials Science Forum 1085 (April 20, 2023): 113–18. http://dx.doi.org/10.4028/p-5i02r0.

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The volumetric changes and variable porosity due to the concentration expansion of the solid phase in the synthesis of zirconium nitride (ZrN) are studied. The model of two-stage reactor based on spark plasma sintering (SPS) is proposed. At the first stage the synthesis for the given kinetics is simulated. At the second stage the densification of ZrN using the Olevsky’s sintering model [1-5] is applied. The synthesis and densification processes using the prescribed heat sources, at the given positions inside the reactor is simulated. The generalization of the two-temperature model [6] and the

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Spencer, David A., Eva Bengtèn, and Melanie Wilson. "Expansion and exhaustion of alloantigen-specific cytotoxic T lymphocytes (CTL) in channel catfish, Ictalurus punctatus." Journal of Immunology 200, no. 1_Supplement (2018): 59.3. http://dx.doi.org/10.4049/jimmunol.200.supp.59.3.

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Abstract CTL are well studied in mammals, however less is known about the dynamics of memory CTL expansion and exhaustion in teleost fish. Here we provide insights into teleost CTL dynamics using our model alloantigen-specific catfish clonal CTL cell line called TS32.15. Briefly, TS32.15 was cloned from peripheral blood leukocytes isolated from fish immunized with allogenic 3B11 B cells. This clonal line is not synchronized and consists of small resting T cells and larger granular effectors. TS32.15 cells exhibit strict target specificity for 3B11s and they require stimulation with irradiated

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Richardson, David B. "Multistage Modeling of Leukemia in Benzene Workers: A Simple Approach to Fitting the 2-Stage Clonal Expansion Model." American Journal of Epidemiology 169, no. 1 (2008): 78–85. http://dx.doi.org/10.1093/aje/kwn284.

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Manser, T. "Evolution of antibody structure during the immune response. The differentiative potential of a single B lymphocyte." Journal of Experimental Medicine 170, no. 4 (1989): 1211–30. http://dx.doi.org/10.1084/jem.170.4.1211.

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Changes in the structure and function of antibodies occur during the course of an immune response due to variable (V) region gene somatic mutation and isotype switch recombination. While the end products of both these processes are now well documented, their mechanisms, timing, and regulation during clonal expansion remain unclear. Here I describe the characterization of antibodies expressed by a large number of hybridomas derived from single B cell clones at an intermediate stage of an immune response. These data provide new insights into the mechanism, relative timing, and potential of V gen

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Niida, Atsushi, Koshi Mimori, Tatsuhiro Shibata, and Satoru Miyano. "Modeling colorectal cancer evolution." Journal of Human Genetics 66, no. 9 (2021): 869–78. http://dx.doi.org/10.1038/s10038-021-00930-0.

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AbstractUnderstanding cancer evolution provides a clue to tackle therapeutic difficulties in colorectal cancer. In this review, together with related works, we will introduce a series of our studies, in which we constructed an evolutionary model of colorectal cancer by combining genomic analysis and mathematical modeling. In our model, multiple subclones were generated by driver mutation acquisition and subsequent clonal expansion in early-stage tumors. Among the subclones, the one obtaining driver copy number alterations is endowed with malignant potentials to constitute a late-stage tumor in

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Panov, V. F., O. V. Sandakova, E. V. Kuvshinova, and D. M. Yanishevsky. "Evolution of the Universe with two rotating fluids." International Journal of Modern Physics A 35, no. 02n03 (2020): 2040042. http://dx.doi.org/10.1142/s0217751x20400424.

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An anisotropic cosmological model with expansion and rotation and the Bianchi type IX metric has been constructed within the framework of general relativity theory. The first inflation stage of the Universe filled with a scalar field and an anisotropic fluid is considered. The model describes the Friedman stage of cosmological evolution with subsequent transition to accelerated exponential expansion observed in the present epoch. The model has two rotating fluids: the anisotropic fluid and dust-like fluid. In the approach realized in the model, the anisotropic fluid describes the rotating dark

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