11 results on '"Hogenes, Marieke C. H."'
Search Results
2. Molecular subtyping of male breast cancer by immunohistochemistry
- Author
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Kornegoor, Robert, Verschuur-Maes, Anoek H J, Buerger, Horst, Hogenes, Marieke C H, de Bruin, Peter C, Oudejans, Joost J, van der Groep, Petra, Hinrichs, Bernd, and van Diest, Paul J
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- 2012
- Full Text
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3. Oncogene amplification in male breast cancer: analysis by multiplex ligation-dependent probe amplification
- Author
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Kornegoor, Robert, Moelans, Cathy B., Verschuur-Maes, Anoek H. J., Hogenes, Marieke C. H., de Bruin, Peter C., Oudejans, Joost J., Marchionni, Luigi, and van Diest, Paul J.
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- 2012
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4. B cells and regulatory T cells in Graft versus Host Disease: a clinicopathological study in humanized mice
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Hogenes, Marieke C. H., van Diest, Paul J., van Dijk, MR, de Weger, Roel A., and University Utrecht
- Subjects
histology ,B cells ,humanized mice ,Graft-versus-Host-Disease ,chemical and pharmacologic phenomena ,regulatory T cells - Abstract
Morbidity and mortality are major concerns in graft-versus-host disease (GvHD), a response often seen after hematologic cell transplantation. Treatment of GvHD remains difficult and more knowledge is necessary. In this thesis we tried to contribute a small piece to the puzzle of GvHD by analyzing the possible relation between B cells and regulatory T cells (Tregs), from a primarily histological perspective. Humanized mice may serve as promising models in studies to GvHD. Designing the right model for the topic of interest is however subject to many choices. Based on our thorough review of the pearls and pitfalls from different mouse strains, transfer routes and sources of material, we decided that RAG2-/-γc-/- mice with intravenous transfer of huPBMC’s would be a sensible choice for our experiments. A thorough analysis was performed to evaluate the basic kinetics and pathology of our model. The induced GvH response in our model appeared to show many similarities with the sclerotic variant of human GvHD. Our analysis continued with an evaluation of our model with additional modifications: macrophage depletion and early B cell depletion. Macrophage depletion accelerated the induction and morbidity of the clinical GvH response and histologically increased the number of B-cells in the infiltrating cell signature, with only limited changes to the amount of Tregs. In early B cell depletion however, a clear improvement on survival was seen. Despite clinical improvement though, our histology only showed a significant effect on liver fibrosis and human TGF-β production within the liver. Other affected organs did not show signs of improvement or alterations. Our next exploration analyzed the effect of B cell activation on Tregs, using a combination of multiple in vitro studies with an in vivo study. Although based on our in vitro studies additional Tregs should temper the GvH reaction (even after B-cell activation), our in vivo study with myeloma was suprising. Clinical symptoms and survival of our mice did improve with additional Tregs, but no significant improvement was shown on a histological level. This contradiction between clinical symptoms and histology is known from human GvHD, as we continued to show with our last evaluation in this thesis, regarding human cutaneous GvHD. In this last analysis however, we’ve found that nowadays neither clinical grading nor histological grading seems to accurately predict a patients survival. With regard to the aim of these thesis, three major conclusions/considerations come forward. First, B cells and Tregs in GvHD have a complex relation, which is subject to the activation of B cells. Second, the lack of correlation between histology and clinical symptoms in GvHD might be explained by cytokines. Last but not least, we need to consider that Rituximab might serve best as a treatment for GvHD when used as an early B cell depletion therapy. However, since there might be a huge contrast between clinical symptoms and histology, we need to decide on our goal of therapy first: do we treat the patient or the disease? The answer to this, will ultimately decide whether our therapy really works.
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- 2019
5. Modifying Graft-versus-Host Disease in a Humanized Mouse Model by Targeting Macrophages or B-Cells
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Hogenes, Marieke C. H., primary, van Dorp, Suzanne, additional, van Kuik, Joyce, additional, Monteiro, Filipa R. P., additional, ter Hoeve, Natalie, additional, Guedes, Liane, additional, van Dijk, Marijke R., additional, Martens, Anton C., additional, and de Weger, Roel A., additional
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- 2019
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6. A new xenograft model for graft-versus-host disease by intravenous transfer of human peripheral blood mononuclear cells in RAG2-/- γc-/- double-mutant mice
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van Rijn, Rozemarijn S., primary, Simonetti, Elles R., additional, Hagenbeek, Anton, additional, Hogenes, Marieke C. H., additional, de Weger, Roel A., additional, Canninga-van Dijk, Marijke R., additional, Weijer, Kees, additional, Spits, Hergen, additional, Storm, Gert, additional, van Bloois, Louis, additional, Rijkers, Ger, additional, Martens, Anton C. M., additional, and Ebeling, Saskia B., additional
- Published
- 2003
- Full Text
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7. Interobserver Variation in the Assessment of Immunohistochemistry Expression Levels in HER2-Negative Breast Cancer: Can We Improve the Identification of Low Levels of HER2 Expression by Adjusting the Criteria? An International Interobserver Study.
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Baez-Navarro X, van Bockstal MR, Nawawi D, Broeckx G, Colpaert C, Doebar SC, Hogenes MCH, Koop E, Lambein K, Peeters DJE, Sinke RHJA, Bastiaan van Brakel J, van der Starre-Gaal J, van der Vegt B, van de Vijver K, Vreuls CPH, Vreuls W, Westenend PJ, and van Deurzen CHM
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- Humans, Female, In Situ Hybridization, Fluorescence methods, Observer Variation, Immunohistochemistry, Reproducibility of Results, Receptor, ErbB-2 genetics, Biomarkers, Tumor, Breast Neoplasms pathology
- Abstract
The classification of human epidermal growth factor receptor 2 (HER2) expression is optimized to detect HER2-amplified breast cancer (BC). However, novel HER2-targeting agents are also effective for BCs with low levels of HER2. This raises the question whether the current guidelines for HER2 testing are sufficiently reproducible to identify HER2-low BC. The aim of this multicenter international study was to assess the interobserver agreement of specific HER2 immunohistochemistry scores in cases with negative HER2 results (0, 1+, or 2+/in situ hybridization negative) according to the current American Society of Clinical Oncology/College of American Pathologists (ASCO/CAP) guidelines. Furthermore, we evaluated whether the agreement improved by redefining immunohistochemistry (IHC) scoring criteria or by adding fluorescent in situ hybridization (FISH). We conducted a 2-round study of 105 nonamplified BCs. During the first assessment, 16 pathologists used the latest version of the ASCO/CAP guidelines. After a consensus meeting, the same pathologists scored the same digital slides using modified IHC scoring criteria based on the 2007 ASCO/CAP guidelines, and an extra "ultralow" category was added. Overall, the interobserver agreement was limited (4.7% of cases with 100% agreement) in the first round, but this was improved by clustering IHC categories. In the second round, the highest reproducibility was observed when comparing IHC 0 with the ultralow/1+/2+ grouped cluster (74.3% of cases with 100% agreement). The FISH results were not statistically different between HER2-0 and HER2-low cases, regardless of the IHC criteria used. In conclusion, our study suggests that the modified 2007 ASCO/CAP criteria were more reproducible in distinguishing HER2-0 from HER2-low cases than the 2018 ASCO/CAP criteria. However, the reproducibility was still moderate, which was not improved by adding FISH. This could lead to a suboptimal selection of patients eligible for novel HER2-targeting agents. If the threshold between HER2 IHC 0 and 1+ is to be clinically actionable, there is a need for clearer, more reproducible IHC definitions, training, and/or development of more accurate methods to detect this subtle difference in protein expression levels., (Copyright © 2022 United States & Canadian Academy of Pathology. Published by Elsevier Inc. All rights reserved.)
- Published
- 2023
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8. Quiz page February 2014: swollen kidneys and a pancreatic mass.
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Agterhuis DE, Schuurmans EP, Hogenes MC, and Laverman GD
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- Humans, Immunoglobulin G biosynthesis, Male, Middle Aged, Nephritis complications, Pancreatitis complications, Nephritis blood, Nephritis diagnosis, Pancreatitis blood, Pancreatitis diagnosis
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- 2014
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9. The influence of genetic factors on the osteoinductive potential of calcium phosphate ceramics in mice.
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Barradas AM, Yuan H, van der Stok J, Le Quang B, Fernandes H, Chaterjea A, Hogenes MC, Shultz K, Donahue LR, van Blitterswijk C, and de Boer J
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- Animals, Bone Morphogenetic Protein 2 pharmacology, Cell Line, Mice, Biocompatible Materials pharmacology, Calcium Phosphates pharmacology, Ceramics pharmacology, Mice, Inbred Strains genetics, Osteogenesis drug effects
- Abstract
The efficacy of calcium phosphate (CaP) ceramics in healing large bone defects is, in general, not as high as that of autologous bone grafting. Recently, we reported that CaP ceramics with osteoinductive properties were as efficient in healing an ilium defect of a sheep as autologous bone graft was, which makes this subclass of CaP ceramics a powerful alternative for bone regeneration. Although osteoinduction by CaP ceramics has been shown in several large animal models it is sporadically reported in mice. Because the lack of a robust mouse model has delayed understanding of the mechanism, we screened mice from 11 different inbred mouse strains for their responsiveness to subcutaneous implantation of osteoinductive tricalcium phosphate (TCP). In only two strains (FVB and 129S2) the ceramic induced bone formation, and in particularly, in FVB mice, bone was found in all the tested mice. We also demonstrated that other CaP ceramics induced bone formation at the same magnitude as that observed in other animal models. Furthermore, VEGF did not significantly increase TCP induced bone formation. The mouse model here described can accelerate research of osteoinductive mechanisms triggered by CaP ceramics and potentially the development of therapies for bone regeneration., (Copyright © 2012 Elsevier Ltd. All rights reserved.)
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- 2012
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10. Histological assessment of the sclerotic graft-versus-host response in the humanized RAG2-/-γc-/- mouse model.
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Hogenes MC, van Dorp S, van Kuik J, Monteiro FR, ter Hoeve N, van Dijk MR, Martens AC, and de Weger RA
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- Animals, Blood Vessels immunology, Cell Movement immunology, Cytokines biosynthesis, Cytokines immunology, DNA-Binding Proteins deficiency, DNA-Binding Proteins genetics, DNA-Binding Proteins immunology, Disease Models, Animal, Female, Graft vs Host Disease immunology, Humans, Immunohistochemistry, Interleukin Receptor Common gamma Subunit deficiency, Interleukin Receptor Common gamma Subunit genetics, Interleukin Receptor Common gamma Subunit immunology, Leukocytes, Mononuclear immunology, Mice, Mice, Inbred BALB C, Mice, Knockout, Sclerosis, Transplantation, Heterologous, Whole-Body Irradiation, Blood Vessels pathology, Graft vs Host Disease pathology, Hematopoietic Stem Cell Transplantation, Leukocytes, Mononuclear transplantation
- Abstract
Graft-versus-host disease (GVHD) remains a frequently occurring and difficult-to-treat complication in human allogeneic stem cell transplantation. Murine transplantation models are often used to study and understand the complex pathogenesis of GVHD and to explore new treatment strategies. Although GVHD kinetics may differ in murine and human models, adequate models are essential for identification of the crucial factors responsible for the major pathology in GVHD. We present a detailed description of the specific histological features of a graft-versus-host-induced fibrotic response in xenogeneic RAG2(-/-)γc(-/-) mice after total body irradiation and injection with human peripheral blood mononuclear cells. We describe the full morphological features of this reaction, including a detailed analysis of the specific tissue infiltration patterns of the human peripheral blood mononuclear cells. Our data show the development of fibrosis, predominantly near blood vessels, and reveal different cell populations and specific cell migration patterns in the affected organs. The combination of immunohistochemical cell characterization and mRNA expression analysis of both human (donor)- and murine (host)-derived cytokines reveals an interaction between host tissues and donor-derived cells in an entangled cytokine profile, in which both donor- and host-derived cytokines contribute to the formation of fibrosis., (Copyright © 2012 American Society for Blood and Marrow Transplantation. Published by Elsevier Inc. All rights reserved.)
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- 2012
- Full Text
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11. A new xenograft model for graft-versus-host disease by intravenous transfer of human peripheral blood mononuclear cells in RAG2-/- gammac-/- double-mutant mice.
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van Rijn RS, Simonetti ER, Hagenbeek A, Hogenes MC, de Weger RA, Canninga-van Dijk MR, Weijer K, Spits H, Storm G, van Bloois L, Rijkers G, Martens AC, and Ebeling SB
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- Animals, Antimetabolites pharmacology, CD4-CD8 Ratio, Clodronic Acid pharmacology, Cytokines blood, Female, Gene Rearrangement, T-Lymphocyte genetics, Graft vs Host Disease physiopathology, Humans, Immunoglobulin G blood, Immunoglobulin M blood, Injections, Intravenous, Kidney cytology, Liver cytology, Lung cytology, Macrophages cytology, Macrophages drug effects, Male, Mice, Nuclear Proteins, Phenotype, Skin cytology, Spleen cytology, T-Lymphocytes physiology, Titrimetry, Transplantation Chimera, Transplants, DNA-Binding Proteins genetics, Disease Models, Animal, Graft vs Host Disease immunology, Leukocytes, Mononuclear transplantation, Mice, Mutant Strains, Transplantation, Heterologous
- Abstract
The safe application of new strategies for the treatment of graft-versus-host disease (GVHD) is hampered by the lack of a clinically relevant model for preclinical testing. Current models are based on intraperitoneal transfer of human peripheral blood mononuclear cells (huPBMCs) into NOD-SCID (nonobese diabetic-severe combined immunodeficient)/SCID mice. Intravenous transfer would be preferred but this has always been ineffective. We developed a new model for xenogeneic GVHD (X-GVHD) by intravenous transfer of huPBMCs into RAG2-/- gammac-/-mice. Our results show a high human T-cell chimerism of more than 20% (up to 98%) in more than 90% of mice, associated with a consistent development of XGVHD within 14 to 28 days and a total mortality rate of 85% shorter than 2 months. After murine macrophage depletion, engraftment was earlier and equally high with lower doses of huPBMCs. Human macrophages were also absent in these mice. Purified huCD3+ cells showed a similar X-GVH effect with contribution of both CD4 and CD8 phenotypes. Human immunoglobulins and cytokines were produced in diseased mice. One of 30 mice developed chronic X-GVHD with skin histology similar to human GVHD. In conclusion, we present a new model for X-GVHD by intravenous transfer of huPBMCs in RAG2-/- gammac-/- mice. Murine and human macrophages do not seem to be necessary for acute X-GVHD in this model.
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- 2003
- Full Text
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