scholarly journals The existence of time global solutions for tumor invasion models with constraints

2011 ◽  
Keyword(s):  
Tumor Invasion ◽  
Global Solutions ◽  
Invasion Models ◽  
Tumor Invasion Models

Comparison Between Different 3D Spheroid Tumor Invasion Models

2020 ◽  
Vol 18 (5) ◽  
pp. 239-242
Author(s):  
Manar Zraikat ◽  
Tasneem Alshelleh
Keyword(s):  
Tumor Invasion ◽  
Invasion Models ◽  
Tumor Invasion Models

scholarly journals NIMG-74. RADIOMICS OF TUMOR INVASION 2.0: COMBINING MECHANISTIC TUMOR INVASION MODELS WITH MACHINE LEARNING MODELS TO ACCURATELY PREDICT TUMOR INVASION IN HUMAN GLIOBLASTOMA PATIENTS

2017 ◽  
Vol 19 (suppl_6) ◽  
pp. vi159-vi159 ◽  
Author(s):  
Kristin R Swanson ◽  
Nathan Gaw ◽  
Andrea Hawkins-Daarud ◽  
Pamela R Jackson ◽  
Kyle W Singleton ◽  
...  
Keyword(s):  
Machine Learning ◽  
Tumor Invasion ◽  
Learning Models ◽  
Human Glioblastoma ◽  
Invasion Models ◽  
Tumor Invasion Models ◽  
Machine Learning Models

775: Cell Culture Proteome Identifies CXCL 1 as a Secreted Marker and Mediator for the Tumor Invasion of Bladder Cancer

2007 ◽  
Vol 177 (4S) ◽  
pp. 260-260 ◽  
Author(s):  
Hiroaki Kawanishi ◽  
Yoshiyuki Matsui ◽  
Toshinari Yamasaki ◽  
Takeshi Takahashi ◽  
Hiroyuki Nishiyama ◽  
...  
Keyword(s):  
Cell Culture ◽  
Bladder Cancer ◽  
Tumor Invasion

Mechanisms of Signaling through Urokinase Receptor and the Cellular Response

1999 ◽  
Vol 82 (08) ◽  
pp. 305-311 ◽  
Author(s):  
Yuri Koshelnick ◽  
Monika Ehart ◽  
Hannes Stockinger ◽  
Bernd Binder
Keyword(s):  
Cell Surface ◽  
Proteolytic Activity ◽  
Tumor Invasion ◽  
Cellular Response ◽  
Transmembrane Protein ◽  
Urokinase Receptor ◽  
Biological Processes ◽  
In Vivo Models ◽  
Proteolytic Activation ◽  
Core Proteins

IntroductionThe urokinase-urokinase receptor (u-PA-u-PAR) system seems to play a crucial role in a number of biological processes, including local fibrinolysis, tumor invasion, angiogenesis, neointima and atherosclerotic plaque formation, inflammation, and matrix remodeling during wound healing and development.1-6 Binding of urokinase to its specific receptor provides cells with a localized proteolytic potential. It stimulates conversion of cell surface-bound plasminogen into active plasmin, which, in turn, is required for proteolytic degradation of basement membrane components, including fibronectin, collagen, laminin, and proteoglycan core proteins.7 Moreover, plasmin activates other matrix-degrading enzymes, such as matrix metalloproteinases.8 Overexpression of u-PA/u-PAR correlates with tumor invasion and metastasis formation,9-13 while reduction of cell-surface bound u-PA and inhibition of u-PAR expression leads to a significant decrease of invasive and metastatic activity.14 Specific antagonists that suppress binding of u-PA to u-PAR have been shown to inhibit cell-surface plasminogen activation, tumor growth, and angiogenesis both in vitro and in vivo models.15,16 Independently of its proteolytic activity, u-PA is implicated in many biological processes that seem to require u-PAR-mediated intracellular signal transduction, such as proliferation, chemotactic movement and adhesion, migration, and differentiation.17 Data obtained in the late 1980s indicated that u-PA not only provides cells with local proteolytic activity, but might also be capable of transducing signals to the cell.18-22 At that time, however, the u-PAR has just been isolated, cloned, and identified as a glycosylphosphatidylinositol (GPI)-linked protein and not a transmembrane protein. Signaling via the u-PAR was, therefore, regarded as being unlikely, and the effects of u-PA on cell proliferation18-22 were thought to be mediated by proteolytic activation of latent growth factors. The assumption of direct signaling via u-PAR was, in fact, considered controversial, until about 10 years later when a physical association between u-PAR and signaling proteins was found.23 From this report on, several proteins associated with u-PAR have been identified. Now, u-PAR seems to be part of a large “signalosome” associated and interacting with several proteins on both the outside and inside of the cell.

Complications of systemic cytomegalovirus infection in therapy refracter Hodgkin’s lymphoma

2012 ◽  
Vol 153 (19) ◽  
pp. 751-755 ◽  
Author(s):  
Gábor Irsai ◽  
Tatjana Tampu-Kiss ◽  
Balázs Dezső ◽  
Zsófia Miltényi ◽  
Árpád Illés ◽  
...  
Keyword(s):  
Hodgkin's Disease ◽  
Tumor Invasion ◽  
Cytomegalovirus Infection ◽  
Hodgkin’S Disease ◽  
Fatal Outcome ◽  
Giant Cells ◽  
Atypical Cell ◽  
Allogenic Stem Cell Transplantation ◽  
Multiple Organs ◽  
Large Atypical Cell

Cytomegalovirus infection related changes frequently remain masked by local symptoms of tumor invasion or therapeutic side effects in cancer patients. The spectrum of cytomegalovirus manifestations, however, can be highly varied and may contribute to the failure of different organs with fatal outcome. The case of a 29-year-old female patient is presented who obtained polychemotherapy and allogenic stem cell transplantation following the diagnosis of classical Hodgkin’s disease. Despite intensified treatment, only partial response could be achieved and the outcome of the disease was death. Postmortem examination revealed regressive lymph node infiltration as well as nodular liver and spleen manifestations of classical Hodgkin’s disease. In addition, parenchymal tissues (lung, kidneys, small intestine, liver, pancreas and ovaries) showed the classical morphology of widespread cytomegalovirus infection. Bilateral enlargement of the ovaries was caused by a partially necrotic giant cell proliferation in the subepithelial cortex. CD30-negativity and cytomegalovirus antigen positivity of the large atypical cell infiltrate supported the diagnosis of cytomegalia oophoritis with morphological overlap between cytomegalovirus-infected giant cells and residual Hodgkin-Reed-Sternberg cells. Further to the cytopathic effect in multiple organs, significant hemophagocytosis was also observed in the spleen, liver and bone marrow. In summary, active cytomegalovirus infection may be a major cause of multi-organ failure in the immunosuppressed oncohematological patient. Careful postmortem analysis demonstrated both the activity of the viral infection and the efficacy of the anti-viral treatment, when applied. Orv. Hetil., 2012, 153, 751–755.

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