BioModelsapplication/xmlhttps://www.ebi.ac.uk/biomodels/model/download/BIOMD0000000759?filename=denBreems2015.xmlhttps://www.ebi.ac.uk/biomodels/model/download/BIOMD0000000759?filename=den%20Breems2015.omexhttps://www.ebi.ac.uk/biomodels/model/download/BIOMD0000000759?filename=denBreems2015.sedmlhttps://www.ebi.ac.uk/biomodels/model/download/BIOMD0000000759?filename=denBreems2015.cpsprimaryOK200Jinghao MenManually curatedordinary differential equation model*Immuno-oncologyhttps://www.ebi.ac.uk/biomodels/BIOMD000000075926551154falseBioModelsModelsSBMLden Breems2015 macrophage in cancer2016MODEL1907240004den Breems NYden Breems NY, Eftimie R26551154,
The anti-tumour and pro-tumour roles of Th1/Th2 immune cells and M1/M2 macrophages have been documented by numerous experimental studies. However, it is still unknown how these immune cells interact with each other to control tumour dynamics. Here, we use a mathematical model for the interactions between mouse melanoma cells, Th2/Th1 cells and M2/M1 macrophages, to investigate the unknown role of the re-polarisation between M1 and M2 macrophages on tumour growth. The results show that tumour growth is associated with a type-II immune response described by large numbers of Th2 and M2 cells. Moreover, we show that (i) the ratio k of the transition rates k12 (for the re-polarisation M1→M2) and k21 (for the re-polarisation M2→M1) is important in reducing tumour population, and (ii) the particular values of these transition rates control the delay in tumour growth and the final tumour size. We also perform a sensitivity analysis to investigate the effect of various model parameters on changes in the tumour cell population, and confirm that the ratio k alone and the ratio of M2 and M1 macrophage populations at earlier times (e.g., day 7) cannot always predict the final tumour size.. , 390.
Centre for Advanced Computational Solutions (C-fACS), Lincoln University, Lincoln 7476, New Zealand; Division of Mathematics, University of Dundee, Dundee DD1 4HN, United Kingdom; Division of Cancer Research, University of Dundee, Dundee DD1 9SY, United Kingdom. Electronic address: nicoline.vanloenen@lincolnuni.ac.nz.jm2187@cam.ac.ukUniversity of CambridgeBIOMD0000000759The anti-tumour and pro-tumour roles of Th1/Th2 immune cells and M1/M2 macrophages have been documented by numerous experimental studies. However, it is still unknown how these immune cells interact with each other to control tumour dynamics. Here, we use a mathematical model for the interactions between mouse melanoma cells, Th2/Th1 cells and M2/M1 macrophages, to investigate the unknown role of the re-polarisation between M1 and M2 macrophages on tumour growth. The results show that tumour growth is associated with a type-II immune response described by large numbers of Th2 and M2 cells. Moreover, we show that (i) the ratio k of the transition rates k12 (for the re-polarisation M1→M2) and k21 (for the re-polarisation M2→M1) is important in reducing tumour population, and (ii) the particular values of these transition rates control the delay in tumour growth and the final tumour size. We also perform a sensitivity analysis to investigate the effect of various model parameters on changes in the tumour cell population, and confirm that the ratio k alone and the ratio of M2 and M1 macrophage populations at earlier times (e.g., day 7) cannot always predict the final tumour size.The re-polarisation of M2 and M1 macrophages and its role on cancer outcomes.den Breems Nicoline Y NY, Eftimie Raluca Rmacrophagocyte, malignant Growth, malignancy, primary cancer, N-ethyl-N-nitrosoethanamine, N-diethylnitrosamine, typical plasmatocyte, malignant, N, cell type cancer, neoplasm (disease), CA., Diethylnitrosamine, monocyte-derived macrophage, 1-diethyl-2-oxohydrazine, Pl, malignant tumor, MT, macrophage, lamellocyte, malignant neoplasm, malignant neoplastic disease, diethylnitrosoamine, DEN, Den, malignant neoplasm (disease), DANA, organ system cancer, granulocyte, 1, NDEA, histiocyte, podocyte, N-diethylnitrosoamine, agranular plasmatocyte, neoplasm, cancer, malignant tumour, N-NitrosodiethylamineUnknown if Another form of Birth Control was Used, Unknown/Not Stated, Unknown if Chief Complaint Caused by Trauma, A1, Not Known if MET Mutation Analysis Was Performed, A4, growth and development, Unknown Tamoxifen Use, sci, CG17228, Th1, Th2, 1135/09, 1135/07, Treatment Effect, 0451/09, HOW, How, Importance Rating Score 0, Not Known if ROS1 Rearrangement Analysis Was Performed, myd, Not Known if Fluorescence In Situ Hybridization Was Performed, Documentation Unknown, Not Known if PTEN Mutation Analysis Was Performed, Tumor Progression Unknown After Initial Treatment, 0244/09, Theoretical Study, TH-1 Cells, DROPROSA, stru, bHLHa26, Unknown Clark Level, Mbp-1, U, l(3)S053606, 932, Not Known if BRAF Rearrangement Analysis Was Performed, Not Known if NF1 Mutation Analysis Was Performed, 671/2, allergic reaction, Not Known if KRAS Mutation Analysis Was Performed, Thing2, Sectm1, Role Concepts, Unknown Molecular Analysis, Unknown Procedure Type for New Tumor Event, Unknown Age When Started using Smokeless Tobacco after Regular Use, AI661148, Not Known if 1p/19q Deletion Analysis Was Performed, Unknown History of Gestational Complication, Final Study Report, Unknown if Interferon Gamma Treatment was Administered Prior to Specimen Resection, Th1/Th2 Ratio Measurement, Adjuvant Post-operative Chemotherapy Administration Unknown, Mouse Melanoma, New Tumor Event After Initial Treatment Unknown, Experimental, Role Concept, 1810003C24Rik, mKIAA0609, 1316/02, Role, BcDNA:HL08040, Unknown History of Other Muscular Dystrophy or Glycogen Storage Disorder, Not Known if Mutation Analysis Was Performed, Unknown if Routine Cytogenetics were Completed, Monocyte-Derived Macrophages, fg, Regular Smokeless Tobacco Use for Six Weeks or More Unknown, Unknown History of Congenital Heart Disease, 1167/13, proportionality, expanded, UNK, rate, First Course Treatment Completion Measure of Success of Outcome Unknown, experimental procedures, Theoretical Models, Th1/Th2, Not Known if Additional Molecular Studies Were Performed, MDC1D, enr, Treatment Outcome, Cells, l(1)16Fg, School-Age Population, Final., 0989/01, Mathematical Model, pds, big, Molecular Abnormalities Unknown, Unknown Number of Full Term Pregnancies, Chemical/Occupational Exposure History Unknown, Experimental Models, Effects, Evidence of Disease Unknown after Completion of Therapy, treatment effect, Not Known if BRAF Mutation Analysis Was Performed, 0763/13, Therapy Effect, Theoretical, Not Known if ERBB2 Mutation Analysis Was Performed, Documented, large, Not Known if IDH Family Mutation Analysis Was Performed, DmelCG17228, sensitive, Adjuvant Post-operative Immunological Therapy Administration Unknown, Prosp, MAM, Additional Surgery for New Tumor Event Unknown, School-Age Populations, F15E12_6, proportion, M1 macrophage, Unknown Use of Menopausal Hormone Therapy, MDDGB6, Unknown if Targeted Molecular Therapy Was Administered as an Additional Treatment for a New Tumor Event, Not Known if 10q23/PTEN Locus Deletion Analysis Was Performed, Not Known if Lymph Node Dissection Was Performed, Bone Marrow-Derived Macrophage, Theoretic, Population, Final, l(3)rH013, Bone Marrow-Derived, Study, Usage, Unknown Daily Salt Intake, Prodos, Unknown if Immunotherapy Was Administered as an Additional Treatment for a New Tumor Event, {Unknown}, PERFORMED, Use, tumour cell, Mathematical, Appearance, AI835216, Unknown Oral Contraceptive Use, Unknown History of Myopathy, Follow-Up Form Completion Outcome Measure of Success Unknown, 0671/02, Adjuvant Post-operative Targeted Molecular Therapy Administration Unknown, l(3)j12C8, Not Known if NRAS Mutation Analysis Was Performed, Perform, Unknown History of Kawasaki Disease, Use of Smokeless Tobacco at Time of Diagnosis Unknown, Model (Theoretical), Not Known if ATRX Mutation Analysis Was Performed, qkr, l(3)S090417, Cell, Concept, l(3)rL433, Monocyte-Derived, l(3)rI160, 0441/16, Have, Cytokeratin-12, KH93F, chemical analysis, Performance Status Scale Timing Unknown, Unknown if Hormone Therapy Was Administered as an Additional Treatment for a New Tumor Event, Intercurrent Illness is Unknown at Onset of Chief Complaint, ATCMPG1, MET, ATCMPG2, Macrophage, Hypertension Unknown, hypersensitivity, Unknown Dosage Form Category, Paraneoplastic Syndrome Status is Unknown, Unknown if Patient Has Genetic Syndrome Associated with Congenital Heart Defect, Not Known, Unknown Data Entry Method, DMDA1, CDISC Final Standard, Macrophages, postnatal growth, Not Known if Bone Marrow Aspirate Immunophenotyping and Cytochemistry Were Performed, School Age Populations, l(3)rK204, Tumor Laterality Unknown, Models (Theoretical), Type 1 Helper T Cells, Not Known if SDH Complex Mutation Analysis Was Performed, Outcome of Therapy, AI225906, Bone Marrow-Derived Macrophages, Multiple Known Primary Tumors Unknown at Initial Melanoma Diagnosis, quotient, UNKNOWN, T Helper 1 Cells, Unknown History of Non-Cardiac Surgery, l(3)rK137, determination, Theoretical Model, postnatal development, Mbp1, Unknown, inflammatory macrophage, Mathematical Models, School-Age, Roles, treatment outcome, Monocyte-Derived Macrophage, Concepts, Unknown Daily Fluid Intake, Effect, l(3)j5D5, Unknown Site of New Tumor Event, 24B, Chemotherapy Status Unknown, tumor cell, reference sample, MUB3_18, Not Known if EGFR Mutation Analysis Was Performed, TH-1 Cell, Not Known if PDGFRA Mutation Analysis Was Performed, Krt-12, MUB3.18, l(3)j6E2, CG10293, Employ, Unknown if Medication Taken, l(3)j5B5, reaction, 0320/10, Unknown: Could not be determined or unsure, DMPROSPER, Immune, Had, CK-12, associated, Has, Importance Score 0, Th1 Cell/Th2 Cell Ratio Measurement, ratio, 0904/17, l(3)rO534, Cancer History Unknown, gyltl1b-b, PRO, Pro, Unknown Daily Caloric Intake, Delay, Not Known if Immunohistochemistry Was Performed, Importance 0, CYS, results, Tumor Location Unknown, Not Known if ALK Rearrangement Analysis Was Performed, PROS-1, PROS-2, Not Known if RET Rearrangement Analysis Was Performed, Type 1 T Helper Cell/Type 2 T Helper Cell Ratio Measurement, FINAL, SZ1, pro, MDDGA6, School Age, Theoretical Studies, Not Known if TP53 Mutation Analysis Was Performed, Type I keratin Ka12, Unknown if Radiation Was Administered as an Additional Treatment for a New Tumor Event, Unknown if Chemotherapy Was Administered as an Additional Treatment for a New Tumor Event, and GLY protein 2, 1p/19q Codeletion Status Unknown, Unknown Family History Cardiovascular Disease or Cardiovascular Disease Risk Factors, Populations, and GLY protein 1, Not Known if Peripheral Blood Immunophenotyping and Cytochemistry Were Performed, gyltl1b, Voila, Unknown if Caffeine Consumption is Routine, growth pattern, non-developmental growth, 0664/07, mdc1d, Unknown History of Alcohol Use, Unknown GENC, AX1, TAF[[II]], TH 1 Cells, Adjuvant Post-operative Pharmaceutical Therapy Administration Unknown, Delayed, Unknown if Chief Complaint was Witnessed, Hed, DMDA, enlarged, hypersensitivity reaction disease, anon-EST:Liang-2.39, History of Medical Treatment Unknown, Unknown if New Disease is Multifocal, Krt1-12, Additional Surgery for New Loco-Regional Tumor Event Unknown, Important, experimental, Monocyte Derived Macrophages, P62, Unknown Route of Administration, Importance, Not Known if MGMT Promoter Methylation Testing Was Performed, TYPE, froggy, Gyltl1a, l(3)10419, DAGA4, dmTAF8, Unknown Transformation, Therapy Outcome, Adjuvant Post-operative Radiation Therapy Administration Unknown, Unknown if Subsequent Known Primary Melanoma(s) Found During the Follow-Up, HL-VIII, Studies, anon-WO0140519.15, Experimental Model, F15E12.6, Models, SCG3, sensitivity, TH-1, PROS, 0585/13, methods, l(3)s2612, experimental section, Th1 Cell, CG7128, Unknown if Patient was Previously Evaluated for Current Chief Complaint, BPFD#36, prod, Device Status Unknown, great, DmelCG10293, dHAND, hypersensitivity reaction, Average Daily Use Smokeless Tobacco after Use for Six Weeks Unknown, School Age Population, TAF, 0563/18, Model, treatment_outcome, Unknown History of Illicit Drug Use, Controlled, Possess, Unknown History of Rheumatic Fever, Controlling, Tumor Reoccurrence Unknown After Initial Treatment, clone 2.39, Monocyte Derived, Immunotherapy Status Unknown, l(3)rJ806, LGMD2C, Pros, Unknown when Chief Complaint Present, development, K12, TFIID, Unknown Release Mechanism of Action, effect, Not Known if Additional Immunohistochemistry Was Performed, who, Performed, Not Known if KIT Mutation Analysis Was Performed, Chemical/Occupational Exposure Type Unknown, Physician Diagnosed Diabetes Unknown, hypersensitive, Keratin-12, Bone Marrow Derived Macrophages, Not Known if Additional Testing Was Performed, Unknown History of Neonatal Complication, Who/How, Interferon Gamma Treatment Administration 90 Days Prior to Specimen Resection Unknown, Ehand2, DmelCG7128, SCARMD2, classically activated macrophage, qkr[93F], assay, TAF8, Additional Surgery for New Metastatic Tumor Event Unknown, Not Known if EGFR Amplification Analysis Was Performed, growthextent, malignant Growth, l(3)rK137, Public Sectors, determination, Thing-1, neoplasia, postnatal development, Helix-loop-helix transcription factor expressed in extraembryonic mesoderm and trophoblast, Mbp1, A4, inflammatory macrophage, growth and development, sci, CG17228, Th1, Th2, 1135/09, 1135/07, School-Age, Roles, Monocyte-Derived Macrophage, 0451/09, Concepts, 1, HOW, How, Public Enterprise, myd, TH1, l(3)j5D5, 24B, 0244/09, tumor cell, reference sample, MUB3_18, TH-1 Cell, cell process disease, tumor disease, N, neoplasm (disease), TH-1 Cells, Public Domains, DROPROSA, stru, bHLHa26, bHLHa27, Mbp-1, Krt-12, l(3)S053606, MUB3.18, l(3)j6E2, CG10293, CA, 671/2, Thing1, allergic reaction, l(3)j5B5, reaction, 0320/10, DmelCG9984, DMPROSPER, Thing2, Sectm1, malignant neoplasm, Role Concepts, CK-12, tumor, house mouse, associated, ratio, malignancy, AI661148, 0904/17, Papers, l(3)rO534, N-diethylnitrosamine, gyltl1b-b, completeness, PRO, Pro, mouse, neoplastic disease, Malignant Melanomas, CYS, results, PROS-1, Role Concept, PROS-2, Melanoma, 1810003C24Rik, SZ1, Public Domain, pro, MDDGA6, School Age, mKIAA0609, 1316/02, organ system cancer, Role, Domains, Type I keratin Ka12, BcDNA:HL08040, and GLY protein 2, Domain, Monocyte-Derived Macrophages, fg, Populations, and GLY protein 1, N-ethyl-N-nitrosoethanamine, gyltl1b, Voila, growth pattern, mice, non-developmental growth, 0664/07, 1167/13, mdc1d, proportionality, expanded, rate, CG9984, TAF[[II]], TH 1 Cells, experimental procedures, tumour disease, MDC1D, Hed, DMDA, Sector, enr, enlarged, Cells, hypersensitivity reaction disease, DANA, autonomic nervous system and neural crest derivatives-expressed protein 1, anon-EST:Liang-2.39, l(1)16Fg, Mouse, School-Age Population, NDEA, other neoplasm, 0989/01, cancer, pds, Krt1-12, big, Sectors, Phages, experimental, Monocyte Derived Macrophages, Bacteriophage, P62, cell type cancer, number, Copyrights, 0763/13, Malignant, 1-diethyl-2-oxohydrazine, presence, TYPE, froggy, Gyltl1a, l(3)10419, DAGA4, dmTAF8, large, DmelCG17228, C77797, sensitive, HL-VIII, anon-WO0140519.15, F15E12.6, Prosp, MAM, neoplasm, SCG3, Enterprises, sensitivity, malignant tumour, TH-1, School-Age Populations, PROS, F15E12_6, Extraembryonic tissues, proportion, Hxt, M1 macrophage, 0585/13, methods, l(3)s2612, experimental section, MDDGB6, Th1 Cell, Naevocarcinoma, CG7128, NELF, Bone Marrow-Derived Macrophage, Diethylnitrosamine, tumour, Population, Public Enterprises, l(3)rH013, Bone Marrow-Derived, BPFD#36, prod, Prodos, Abstract, tumour cell, great, DmelCG10293, AI835216, dHAND, hypersensitivity reaction, School Age Population, TAF, 0563/18, Enterprise, Controlled, 0671/02, Phage, l(3)j12C8, Controlling, TH1L, clone 2.39, malignant, Monocyte Derived, qkr, l(3)S090417, Cell, l(3)rJ806, LGMD2C, Concept, Pros, development, l(3)rL433, Melanomas, count in organism, Monocyte-Derived, neoplastic growth, MT, l(3)rI160, 0441/16, Mus, Public, diethylnitrosoamine, Cytokeratin-12, malignant neoplasm (disease), KH93F, Malignant Melanoma, K12, heart, chemical analysis, TFIID, N-diethylnitrosoamine, ATCMPG1, MET, Data Base, ATCMPG2, Macrophage, who, hypersensitivity, primary cancer, hypersensitive, Th1l, DMDA1, Macrophages, Keratin-12, postnatal growth, Bone Marrow Derived Macrophages, Who/How, Ehand1, disease of cellular proliferation, Ehand2, malignant tumor, School Age Populations, l(3)rK204, NELF-D, eHAND, Type 1 Helper T Cells, DmelCG7128, malignant neoplastic disease, 2410003I03Rik, DEN, Den, AI225906, NELF-C, SCARMD2, Bone Marrow-Derived Macrophages, quotient, classically activated macrophage, qkr[93F], malignant melanoma, Public., assay, quantitative, TAF8, growth, T Helper 1 Cells, N-Nitrosodiethylamine, presence or absence in organismmalignant Growth, malignancy, primary cancer, Monocyte Derived Macrophages, Macrophages, malignant, cell type cancer, neoplasm (disease), CA., Bone Marrow Derived Macrophages, Bone Marrow-Derived Macrophage, Monocyte Derived, malignant tumor, Concept, Bone Marrow-Derived, Monocyte-Derived, Role Concept, MT, Roles, malignant neoplasm, malignant neoplastic disease, malignant neoplasm (disease), Role Concepts, Bone Marrow-Derived Macrophages, Monocyte-Derived Macrophage, organ system cancer, Role, Concepts, neoplasm, cancer, malignant tumour, Monocyte-Derived Macrophages, Macrophagefalseden Breems2015 - macrophage in cancerThe paper describes a model of re-polarisation of M2 and M1 macrophages and its role on cancer outcomes.
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This model is described in the article:
The re-polarisation of M2 and M1 macrophages and its role on cancer outcomes
den Breems, Nicoline Y.; Eftimie, Raluca
Journal of Theoretical Biology, 390, 23-39
Abstract:
The anti-tumour and pro-tumour roles of Th1/Th2 immune cells and M1/M2 macrophages have been documented by numerous experimental studies. How- ever, it is still unknown how these immune cells interact with each other to control tumour dynamics. Here, we use a mathematical model for the inter- actions between mouse melanoma cells, Th2/Th1 cells and M2/M1 macro- phages, to investigate the unknown role of the re-polarisation between M1 and M2 macrophages on tumour growth. The results show that tumour growth is associated with a type-II immune response described by large num- bers of Th2 and M2 cells. Moreover, we show that: (i) the ratio k of the transition rates k12 (for the re-polarisation M1→M2) and k21 (for the re- polarisation M2→M1) is important in reducing tumour population, and (ii) the particular values of these transition rates control the delay in tumour growth and the final tumour size. We also perform a sensitivity analysis to investigate the effect of various model parameters on changes in the tumour cell population, and confirm that the ratio k alone and the ratio of M2 and M1 macrophage populations at earlier times (e.g., day 7), cannot always predict the final tumour size.
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Please refer to CC0 Public Domain Dedication for more information.2021-03-052021-03-052019-07-24BIOMD0000000759SBO:0000610SBO:0000661SBO:0000393SBO:000017926551154C94498C156004C123783C25636C75958BIOMD0000000759MODEL1907240004GO:0002418GO:0008283GO:0006909GO:0002419GO:0008219CL:0001064CL:0000545CL:00005469606