Pontus Jäntti Sulkapallokoulu, Ristihaantie 2, Espoo (2020) - Pontus Jäntti Sulkapallokoulu järjestää valmennusta sekä lapsille et
Certest tarjoaa laajan valikoiman kvalitatiivisia immunokromatografisia testejä mahasuolikanavan sairauksien sekä hengitystieinfektioiden diagnoosin…
MKK7 is an essential component of the JNK signal transduction pathway activated by proinflammatory cytokines. Requirement of the JIP1 scaffold protein for stress-induced JNK activation
Following dissemination from a primary tumor, viable cancer cells that lodge at secondary sites (2 sites) can persist for extended periods of time before going on to form clinically detectable disease. It is puzzling why tumor cells that have lost checkpoint control of the cell cycle and evaded death at the 1 tumor site should fail to grow at remote sites in both experimental models and patients. No one knows how such cells ultimately initiate growth and complete the process of metastatic colonization which can ultimately lead to death. Previously we identified a novel function for MKK4/JNKK1, as a metastasis-suppressor gene for prostate cancer. MKK4/JNKK1 is a dual-specificity kinase that activates the JNK and p38 MAP kinases in response to extracellular stimuli. We have recently shown that ectopic expression of MKK4/JNKK1 results in the context-dependent suppression of metastatic colonization, and that MKK4/JNKK1 protein is down-regulated in clinical disease. Our laboratory is now ...
A január 1-jétől alkalmazandó új vagy módosítandó vámfelfüggesztések és vámkontingensek, illetve vámfelfüggesztések meghosszabbítása iránti kérelmek 1. Új kérelmek KN kód TAXUD hivatkozási /Q
MAPK8 [ENSP00000378974]. Stress-activated protein kinase JNK1; Serine/threonine-protein kinase involved in various processes such as cell proliferation, differentiation, migration, transformation and programmed cell death. Extracellular stimuli such as proinflammatory cytokines or physical stress stimulate the stress-activated protein kinase/c-Jun N-terminal kinase (SAP/JNK) signaling pathway. In this cascade, two dual specificity kinases MAP2K4/MKK4 and MAP2K7/MKK7 phosphorylate and activate MAPK8/JNK1. In turn, MAPK8/JNK1 phosphorylates a number of transcription factors, primarily components of AP-1 such as JUN, JDP2 and ATF2 and thus regulates AP-1 transcriptional activity. Phosphorylates the replication licensing factor CDT1, inhibiting the interaction between CDT1 and the histone H4 acetylase HBO1 to replication origins. Loss of this interaction abrogates the acetylation required for replication initiation. Promotes stressed cell apoptosis by phosphorylating key regulatory factors including ...
MK08_HUMAN] Serine/threonine-protein kinase involved in various processes such as cell proliferation, differentiation, migration, transformation and programmed cell death. Extracellular stimuli such as proinflammatory cytokines or physical stress stimulate the stress-activated protein kinase/c-Jun N-terminal kinase (SAP/JNK) signaling pathway. In this cascade, two dual specificity kinases MAP2K4/MKK4 and MAP2K7/MKK7 phosphorylate and activate MAPK8/JNK1. In turn, MAPK8/JNK1 phosphorylates a number of transcription factors, primarily components of AP-1 such as JUN, JDP2 and ATF2 and thus regulates AP-1 transcriptional activity. Phosphorylates the replication licensing factor CDT1, inhibiting the interaction between CDT1 and the histone H4 acetylase HBO1 to replication origins. Loss of this interaction abrogates the acetylation required for replication initiation. Promotes stressed cell apoptosis by phosphorylating key regulatory factors including p53/TP53 and Yes-associates protein YAP1. In ...
Cerebral ischemia is associated with the activation of glial cells, infiltration of leukocytes and an increase in inflammatory mediators in the ischemic brain and systemic circulation. How this inflammatory response influences lesion size and neurological outcome remains unclear. D-JNKI1, an inhibitor of the c-Jun N-terminal kinase pathway, is strongly neuroprotective in animal models of stroke. Intriguingly, the protection mediated by D-JNKI1 is high even with intravenous administration at very low doses with undetectable drug levels in the brain, pointing to a systemic mode of action, perhaps on inflammation. We evaluated whether D-JNKI1, administered intravenously 3 h after the onset of middle cerebral artery occlusion (MCAO), modulates secretion of the inflammatory mediators interleukin-6 and keratinocyte-derived chemokine in the plasma and from the spleen and brain at several time points after MCAO. We found an early release of both mediators in the systemic circulation followed by an increase in
The c-Jun NH2-terminal kinases (JNK) are evolutionarily conserved serine/threonine protein kinases that are activated by proinflammatory cytokines, environmental stress, and genotoxic agents. These kinases play key regulatory roles within a cell by coordinating signals from the cell surface to nuclear transcription factors. JNK phosphorylates the amino terminal domain of all three Jun transcription factors (JunB, c-Jun and JunD) all members of the AP-1 family. The activated transcription factors modulate gene expression to generate appropriate biological responses, including cell migration, proliferation, differentiation and cell death. The role of the JNK signaling pathway in cell death/apoptosis is controversial, both pro-apoptotic and pro-survival roles have been attributed to JNK. The mechanism that enables the JNK signaling pathway to mediate both apoptosis and survival is unclear. The aim of this study is to examine the role of TNF-stimulated JNK activation on cell survival. The proinflammatory
PubMed comprises more than 30 million citations for biomedical literature from MEDLINE, life science journals, and online books. Citations may include links to full-text content from PubMed Central and publisher web sites.
Forex momentum trading strategy #### WEB BINARY OPTIONS SIGNALS USD/SEK Non-standard training Forex #### Ctg international trading
Tampereen teknillinen yliopisto on teknologisen kehityksen tiennäyttäjä sekä tutkimusmaailman ja elinkeinoelämän yhteistyökumppani. Yliopistosta valmistuu haluttuja osaajia yhteiskunnan eri aloille.. ...
Ursolic acid (UA), a pentacyclic triterpenoid, is known to have anti-tumor activity in various cancers including human non small cell lung cancer (NSCLC). However, the molecular mechanisms underlying the action of UA remain largely unknown. Cell viability was measured by MTT assays. Apoptosis was analyzed with Annexin V-FITC/PI Apoptosis Detection Kit by Flow cytometry. Western blot analysis was performed to measure the phosphorylation and protein expression of stress-activated protein kinase/c-Jun N-terminal kinase (SAPK/JNK), DNMT1 [DNA (cytosine-5)-methyltransferase 1], enhancer of zeste 2 polycomb repressive complex 2 subunit (EZH2) and SP1. Exogenous expression of SP1 and DNMT1 was carried out by transient transfection assays. We showed that UA inhibited the growth and induced apoptosis of NSCLC cells in the dose- and time-dependent fashion. Furthermore, we found that UA induced phosphorylation of SAPK/JNK and suppressed the protein expression of DNMT1 and EZH2. The inhibitor of SAPK/JNK (SP600125)
3VUM: Seven cysteine-deficient mutants depict the interplay between thermal and chemical stabilities of individual cysteine residues in mitogen-activated protein kinase c-Jun N-terminal kinase 1
3VUM: Seven cysteine-deficient mutants depict the interplay between thermal and chemical stabilities of individual cysteine residues in mitogen-activated protein kinase c-Jun N-terminal kinase 1
Tämä sivusto käyttää evästeitä analytiikkaan sekä mukautetun sisällön ja mainosten näyttämiseen. Jatkamalla sivuston käyttöä hyväksyt tällaisen käytön. Lisätietoja ...
... on luonnontuotealan (luonnonmarjat, -sienet, -yrtit ja erikoisluonnontuotteet) valtakunnallinen toimialajärjestö, joka toiminnallaan edistää luonnontuotteiden talteenottoa, jatkojalostusta ja käyttöä sekä parantaa tuotteiden laatua.
Objective: To explore the effect of minimally invasive hematoma aspiration (MIHA) on the c-Jun NH2-terminal kinase (JNK) signal transduction pathway after intracerebral hemorrhage (ICH). Methods: In this experiment, 300 adult male Wistar rats were randomly and averagely divided into sham-operated group, ICH group and MIHA group. In each group, 60 rats were used in the detection of indexes in this experiment, while the other 40 rats were used to replace rats which reached the exclusion criteria (accidental death or operation failure). In ICH group and MIHA group, ICH was induced by injection of 70 µL of autologous arterial blood into rat brain, while only the rats in MIHA group were treated by MIHA 6 h after ICH. Rats in sham-operated group were injected nothing into brains, and they were not treated either, like rats in ICH group. In each group, six rats were randomly selected to observe their Bedersons scales persistently (6, 24, 48, 72, 96, 120 h after ICH). According to the time they were
AS 602801 | JNK inhibitor | Bentamapimod | AS602801 | AS-602801 | CAS [848344-36-5] | Axon 2002 | Axon Ligand™ with >98% purity available from supplier Axon Medchem, prime source of life science reagents for your research
Erityisesti promo-lahjaksi suunnitellut, Power Bank matkalaturimme, USB autolaturimme sekä Induktiolaturimme ovat loistava tapa esitellä yritystänne seuraavilla messuillanne tai muissa asiakastapahtumissa. Kaikki mallimme ovat yksityiskohtaisesti painatettavissa logollanne tai sloganillanne. ja ovat yhteensopivia lähes kaikkien matkapuhelimien sekä tablettien kanssa.
Summary Financial overview October 1 - December 31, 2019 Net sales amounted to SEK 0.0 M (0.0) Loss for the period was SEK 244,9 M (loss: 112.0) Loss p...
Nem a v rben l v zs rok, hanem az erek k ls fal nak fert z sei miatti kialakul ell t si zavarok llhatnak a sz vinfarktust is okoz relmeszesed s h tter ben egy n met sz vseb sz kutat sai szerint.
Incihaku.fi on ilmainen yli 19000 hakusanan kosmetiikan sanasto. Incihaku-palvelussa voit hakea tietoa kosmetiikan ainesosista ja niiden INCI-nimistä sekä kosmetiikassa käytettävistä kasveista.
Incihaku.fi on ilmainen yli 19000 hakusanan kosmetiikan sanasto. Incihaku-palvelussa voit hakea tietoa kosmetiikan ainesosista ja niiden INCI-nimistä sekä kosmetiikassa käytettävistä kasveista.
Serine/threonine-protein kinase which acts as an essential component of the MAP kinase signal transduction pathway. Acts as a MAPK kinase kinase kinase (MAP4K) and is an upstream activator of the stress-activated protein kinase/c-Jun N-terminal kinase (SAP/JNK) signaling pathway and to a lesser extent of the p38 MAPKs signaling pathway. Required for the efficient activation of JNKs by TRAF6-dependent stimuli, including pathogen-associated molecular patterns (PAMPs) such as polyinosine-polycytidine (poly(IC)), lipopolysaccharides (LPS), lipid A, peptidoglycan (PGN), or bacterial flagellin. To a lesser degree, IL-1 and engagement of CD40 also stimulate MAP4K2-mediated JNKs activation. The requirement for MAP4K2/GCK is most pronounced for LPS signaling, and extends to LPS stimulation of c-Jun phosphorylation and induction of IL-8. Enhances MAP3K1 oligomerization, which may relieve N-terminal mediated MAP3K1 autoinhibition and lead to activation following autophosphorylation. Mediates also the SAP/JNK
Background/Aims: aberrant c-Jun N-terminal kinase (JNK) activation has been linked to hepatocellular carcinoma (HCC) in mouse models. It remains unclear whether JNK activation plays an important role in human HCC and, if so, how JNK signaling contributes to the initiation or progression of HCC. Methods: the JNK activation, global gene expression, and the status of histone H3 methylations were mea
AEG 3482 | JNK inhibitor | AEG3482 | AEG-3482 | CAS [63735-71-7] | Axon 1291 | Axon Ligand™ with >99% purity available from supplier Axon Medchem, prime source of life science reagents for your research
A bőr az emberi test legnagyobb méretű szerve. A rendkívüli hőnek, sugárzásnak, áramütésnek vagy vegyszereknek kitett bőr megéghet, ami fájdalmat, hól...
The JNK signaling pathway is activated when cells such as neurons are exposed to environmental stress. The JIP proteins are likely to act in this pathway because they bind to JNK, as well as to upstream activators of JNK. A report from Whitmarsh et al. now strengthens the argument that JIPs are scaffolding proteins that coordinate the formation of a JNK-activating module. JIP1 localized to the cell body and to the growth-cone tips of extended neurites in unstimulated murine hippocampal neurons, but upon exposure to various stress stimuli, JIP1 relocalized to the perinuclear region where activated JNK was also found. Neurons from a JIP1-null mouse did not demonstrate stress-induced JNK activation or apoptosis, demonstrating that JIP is required for JNK activation in vivo. Because JIP1 was isolated in a complex with kinesin from mouse brain tissue, the authors speculate that JIP translocation may involve cellular motor proteins. Such a transport mechanism may facilitate signal transduction from ...
c-Jun兔多克隆抗体(ab428)可与鸡, 哺乳动物样本反应并经WB, EMSA实验严格验证,被6篇文献引用。所有产品均提供质保服务,中国75%以上现货。
Helsinki KV V-04 5.12.2004 Tuomarina musta & ruskea; Jukka Kuusisto ja muilla v reill sek valkoisilla Leila K rk s. Ryhm tuomarina toimi Rainer Vuorinen. ...
MyHeritagen käyttäjäehdot. MyHeritage on verkkopalvelu, joka antaa jäsenten luoda verkossa profiileja ja yhteisösivustoja perheen ja ystävien kanssa kommunikoimiseen sekä mahdollistaa jurrein tutkimisen ja kasvojen tunnistamisen eri välineillä.
Tämä sivusto käyttää evästeitä analytiikkaan sekä mukautetun sisällön ja mainosten näyttämiseen. Jatkamalla sivuston käyttöä hyväksyt tällaisen käytön. Lisätietoja ...
Background: Alzheimers Disease (AD) is a neuron related brain disorder leading to reasoning and memory loss. There is no specific cure identified for AD. JNK3 (c-Jun N-terminal kinase /stress-activated protein kinase) are highly revealed within the central nervous system, particularly neurons, playing vital role in functioning of brain. JNK3 hyper phosphorylation is a very common conclusion in neurodegenerative diseases. JNK3 in turn hyper phosphorylates Amyloid Precursor Protein (APP) which leads to the formation of Amyloid β peptides (an inductive agent of Alzheimers disease). Methods: Protein JNK-3 (PDB ID: 3KVX) was retrieved from protein data bank and later we docked a library of compounds against it. These were further validated by ADMET studies. Results: Thus, docking inhibitors of JNK3 may provide a promising sanitive approach. Based on best docking score and glide score a potential lead is identified against JNK3. Conclusion: Inhibiting JNK-3 may lead to less production of amyloidβ ...
Several studies have described abnormalities in the expression, distribution, and regulation of ventricular connexins in CHF. Absolute Cx43 expression is generally reduced in CHF ventricles,9,20,23-25 likely related to the activation of the mitogen-activated protein kinase c-Jun N-terminal kinase.26 Recent work suggests an important role for defects in Cx43 phosphorylation in CHF-induced ventricular cardiomyocyte uncoupling,9,10,20 thought to be attributable to increased dephosphorylating activity of protein phosphatase-2A colocalized with Cx43.20 Connexin dephosphorylation plays significant roles in targeting connexins to intercalated disks and in regulating connexin conductance.8,10 One study showed ventricular Cx40 upregulation in CHF,23 possibly as a compensation for Cx43 downregulation; however, the functional importance of this alteration is uncertain in view of low level ventricular Cx40 expression.. Clinical and experimental studies of gap junctional remodeling in the atria have produced ...
We have identified a novel serine/threonine kinase, NIK, that interacts with the SH3 domains of Nck. Overexpression of NIK constitutively activated the JNK/SAPK pathway. NIK interacts with MEKK1 in cells and likely signals through MEKK1 to activate JNK, suggesting that NIK directly regulates MEKK1 activity. We found that NIK contains a regulatory domain in its C‐terminus that is conserved in two other members of this kinase family. This domain mediates the association of NIK with MEKK1 and is critical for NIK activation of the SAPK pathway, suggesting that the C‐terminal domain of these proteins encodes a new protein domain family that couples these kinases to the SAPK pathway, possibly by interacting with MEKK1. Our finding that NIK also interacts with Nck suggests that SH2/SH3 adaptor proteins couple NIK and related kinases to activation of the SAPK/JNK pathway by different receptors.. Studies in Saccharomyces cerevisiae have shown that a serine/threonine kinase, Ste20, acts upstream of ...
TY - JOUR. T1 - Cytosolic-DNA-mediated, STING-dependent proinflammatory gene induction necessitates canonical NF-kB activation through TBK1. AU - Abe, Takayuki. AU - Barber, Glen N.. PY - 2014. Y1 - 2014. N2 - STING (stimulator of interferon genes) is known to control the induction of innate immune genes in response to the recognition of cytosolic DNA species, including the genomes of viruses such as herpes simplex virus 1 (HSV-1). However, while STING is essential for protection of the host against numerous DNA pathogens, sustained STING activity can lead to lethal inflammatory disease. It is known that STING utilizes interferon regulatory factor 3 (IRF3) and nuclear factor kB (NF-kB) pathways to exert its effects, although the signal transduction mechanisms remain to be clarified fully. Here we demonstrate that in addition to the activation of these pathways, potent induction of the Jun N-terminal protein kinase/stress-activated protein kinase (JNK/SAPK) pathway was similarly observed in ...
The structure-based design and synthesis of a novel series of c-Jun N-terminal kinase (JNK) inhibitors with selectivity against p38 is reported. The unique structure of 3,5-disubstituted quinolines (2) was developed from the previously reported 4-(2,7-phenanthrolin-9-yl)phenol (1). The X-ray crystal structure of 16a in JNK3 reveals an unexpected binding mode for this new scaffold with protein ...
387518839 - EP 1027429 A4 2002-11-20 - JNK3 MODULATORS AND METHODS OF USE - [origin: WO9918193A1] The c-Jun NH2-terminal kinase (JNK) group of MAP kinases are activated by exposure of cells to environmental stress. The role of JNK in the brain was examined by targeted disruption of the gene that encodes the neuronal isoform JNK3. It was found that JNK3 is required for the normal response to seizure activity. Methods of screening for molecules and compounds that decrease JNK3 expression or activity are described. Such molecules or compounds are useful for treating disorders involving excitotoxicity such as seizure disorders, Alzheimer s disease, Huntington disease, Parkinson s disease, and ischaemia.[origin: WO9918193A1] The c-Jun NH2-terminal kinase (JNK) group of MAP kinases are activated by exposure of cells to environmental stress. The role of JNK in the brain was examined by targeted disruption of the gene that encodes the neuronal isoform JNK3. It was found that JNK3 is required for the normal
Der diesjährige Schwerpunkt des Kongresses liegt auf den Themen Trauma und Tumor in der Wirbelsäulenchirurgie. Wichtige wissenschaftliche Beiträge zu Tumorerkrankungen, degenerativen Erkrankungen, entzündlichen und metabolischen Erkrankungen, Verletzungen und Deformitäten aber auch zu innovativen Techniken erwarten die Besucherinnen und Besucher. Dabei steht ein fächerübergreifender Ansatz im Vordergrund, denn auch auf dem Gebiet der Wirbelsäulenheilkunde gilt es, Bewährtes zu erhalten und gleichzeitig neuen Behandlungsmethoden gegenüber offen zu sein. Dass die Deutsche Wirbelsäulengesellschaft diesen Anspruch ernst nimmt, zeigt auch die Zentren-Zertifizierung, die in diesem Jahr gestartet wurde. (Mehr in: Veranstaltungen - idw - Informationsdienst Wissenschaft). - Weiterlesen ...
Virginia tech housing options #### NOW FOREX BINARY OPTIONS EUR/SEK Forex currency futures #### NOW Binary Options Demo Accounts CTOption
Venue: Edificio Povo 2, via Sommarive nr. 9, Povo (Tn) - Room B102 Time: 12.15 p.m. Speaker: Serras Rigalt Florencio - University of Barcelona Oxidative stress initiated by dying or damaged cells propagates to neighboring undamaged cells, activating the MAP kinases JNK and p38 for cytokine-dependent regenerative growth. However, the stress sensing mechanism by which
CaseM-ratkaisulle myönnettiin Partner Innovation Award innovatiivisesta sovelluskehityksestä sekä edistyksellisestä käyttöliittymästä ja käyttöönoton suunnittelusta.
Cage Riders Show on mahtava ja henkeä salpaava surmanajo - näytös jossa voit kokea jännityksen ja vaaran, sekä mahtavat efektit ja kommentit ihan pallon vieressä.
TY - JOUR. T1 - Stimulation of Jun N-terminal kinase (JNK) by gonadotropin-releasing hormone in pituitary αt3-1 cell line is mediated by protein kinase C, c-Src, and CDC42. AU - Levi, N. L.. AU - Hanoch, T.. AU - Benard, Outhiriaradjou. AU - Rozenblat, M.. AU - Harris, D.. AU - Reiss, N.. AU - Naor, Z.. AU - Seger, R.. PY - 1998. Y1 - 1998. N2 - The signaling of ligands operating via heterotrimeric G proteins is mediated by a complex network that involves sequential phosphorylation events. Signaling by the G protein-coupled receptor GnRH was shown to include elevation of Ca2+ and activation of phospholipases, protein kinase C (PKC) and extracellular signal-regulated kinase (ERK). In this study, GnRH was shown to activate Jun N-Terminal Kinase (JNK)/SAPK in αT3-1 cells in a PKC- and tyrosine kinase-dependent manner. GnRH as well as tumor-promoting agent (TPA) also increased c-Src activity, which peaked at 2 min after GnRH stimulation and was sensitive both to PKC and to tyrosine kinase ...
Apoptosis signal-regulating kinase I (ASK1, also called MAP3K5) is a mitogen-activated kinase kinase kinase (MAP3K) that plays pivotal roles in cellular stress and immune response. Active ASK1 can directly phosphorylate downstream mitogen-activated kinase kinases (MKKs) from both stress-activated protein kinase (SAPK) pathways: c-jun N-terminal kinase (JNK). The structural of these three kinase complexes (JNK, MKK4, and ASK1) remains still unknown. For this reason, the present study has been designed to find out the assembly of ASK1-MKK4-JNK3 firstly using computational docking based on the Protein Frustratometer combined with the sequence identity calculations of Evolutionary Trace forms along with rigid docking (Cluspro) followed by experimental design. To verify the proposed computational model of ASK1-MKK4-JNK3 complex, we designed a series of maltose binding protein (MBP) fusion peptides, which contains different peptide fragments derived from MKK4: MBP-P1, MBP-P2, MBP-P3, MBP-P4 and ...
Accumulated evidence shows that many cancers including prostate cancer disseminate to metastatic sites early in the natural history of disease and can remain undetected and quiescent for extended periods of time.3, 4, 10 In one recent report, disseminated prostate cancer cells (DTCs) can be detected in the bone marrow of 57% men who are without evidence of disease after prostatectomy. With a median follow-up of 42 months, 52% of those with DTCs have not recurred, including patients who still have DTCs 12 years after surgery.5 Thus, in the context of prostate cancer recurrence, metastatic colonization, or the progressive outgrowth of disseminated cancer cells within a secondary site into clinically manifested metastases, is a particularly critical aspect to the multistep metastatic process.7, 35 The molecular factors that control the survival and eventual growth of these disseminated cells are largely unknown.. Experimental modulation of metastasis suppressor genes preclinically affords the ...
Abstract : To improve our understanding of the biology of the metastatic colonization process, we conducted a modelling study based on multi-modal data from an orthotopic murine experimental system of metastatic renal cell carcinoma. The standard theory of metastatic colonization usually assumes that secondary tumours, once established at a distant site, grow independently from each other and from the primary tumour. Using a mathematical model describing the metastatic population dynamics under this assumption, we challenged the theory against our data that included: 1) dynamics of primary tumour cells in the kidney and metastatic cells in the lungs, retrieved by green fluorescent protein tracking, and 2) magnetic resonance images (MRI) informing on the number and size of macroscopic lesions. While the model could fit the primary tumour and total metastatic burden, the predicted size distribution was not in agreement with the MRI observations. Moreover, the model was incompatible with the growth ...
Abstract : To improve our understanding of the biology of the metastatic colonization process, we conducted a modelling study based on multi-modal data from an orthotopic murine experimental system of metastatic renal cell carcinoma. The standard theory of metastatic colonization usually assumes that secondary tumours, once established at a distant site, grow independently from each other and from the primary tumour. Using a mathematical model describing the metastatic population dynamics under this assumption, we challenged the theory against our data that included: 1) dynamics of primary tumour cells in the kidney and metastatic cells in the lungs, retrieved by green fluorescent protein tracking, and 2) magnetic resonance images (MRI) informing on the number and size of macroscopic lesions. While the model could fit the primary tumour and total metastatic burden, the predicted size distribution was not in agreement with the MRI observations. Moreover, the model was incompatible with the growth ...
Abstract : To improve our understanding of the biology of the metastatic colonization process, we conducted a modelling study based on multi-modal data from an orthotopic murine experimental system of metastatic renal cell carcinoma. The standard theory of metastatic colonization usually assumes that secondary tumours, once established at a distant site, grow independently from each other and from the primary tumour. Using a mathematical model describing the metastatic population dynamics under this assumption, we challenged the theory against our data that included: 1) dynamics of primary tumour cells in the kidney and metastatic cells in the lungs, retrieved by green fluorescent protein tracking, and 2) magnetic resonance images (MRI) informing on the number and size of macroscopic lesions. While the model could fit the primary tumour and total metastatic burden, the predicted size distribution was not in agreement with the MRI observations. Moreover, the model was incompatible with the growth ...