scholarly journals Biomechanical modelling of spinal tumour anisotropic growth

Author(s):  
Ioanna Katsamba ◽  
Pavlos Evangelidis ◽  
Chrysovalantis Voutouri ◽  
Alkiviadis Tsamis ◽  
Vasileios Vavourakis ◽  
...  

Biomechanical abnormalities of solid tumours involve stiffening of the tissue and accumulation of mechanical stresses. Both abnormalities affect cancer cell proliferation and invasiveness and thus, play a crucial role in tumour morphology and metastasis. Even though, it has been known for more than two decades that high mechanical stresses reduce cancer cell proliferation rates driving growth towards low-stress regions, most biomechanical models of tumour growth account for isotropic growth. This cannot be valid, however, in tumours that grow within multiple host tissues of different mechanical properties, such as the spine. In these cases, structural heterogeneity would result in anisotropic growth of tumours. To this end, we present a biomechanical, biphasic model for anisotropic growth of spinal tumours. The model that accounts for both the fluid and the solid phase of the tumour was used to predict the evolution of solid stress and interstitial fluid pressure in intramedullary spinal tumours and highlight the differences between isotropic and anisotropic growth. Varying the degree of anisotropy, we found considerable differences in the shape of the tumours, leading to tumours of more realistic ellipsoidal shapes.

2001 ◽  
Vol 120 (5) ◽  
pp. A615-A615
Author(s):  
S KUWADA ◽  
C SCAIFE ◽  
J KUANG ◽  
R DAYNES

Planta Medica ◽  
2012 ◽  
Vol 78 (11) ◽  
Author(s):  
S Sun ◽  
M Zhang ◽  
M Li ◽  
F Guan ◽  
F Wu ◽  
...  

Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 1957-P
Author(s):  
TAKAKO KAWANAMI ◽  
TAKASHI NOMIYAMA ◽  
YURIKO HAMAGUCHI ◽  
TOMOKO TANAKA ◽  
TOSHIHIKO YANASE

2020 ◽  
Author(s):  
Lungwani Muungo

ADP ribosylation factor GTPase-activating protein 3 (ARFGAP3) is a GTPase-activating protein that associates with the Golgiapparatus and regulates the vesicular trafficking pathway. In the present study, we examined the contribution of ARFGAP3 toprostate cancer cell biology. We showed that ARFGAP3 expression was induced by 100 nM of dihydrotestosterone (DHT) atboth the mRNA and protein levels in androgen-sensitive LNCaP cells. We generated stable transfectants of LNCaP cells withFLAG-tagged ARFGAP3 or a control empty vector and showed that ARFGAP3 overexpression promoted cell proliferation andmigration compared with control cells. We found that ARFGAP3 interacted with paxillin, a focal adhesion adaptor protein thatis important for cell mobility and migration. Small interfering RNA (siRNA)-mediated knockdown of ARFGAP3 showed thatARFGAP3 siRNA markedly reduced LNCaP cell growth. Androgen receptor (AR)-dependent transactivation activity on prostatespecificantigen (PSA) enhancer was synergistically promoted by exogenous ARFGAP3 and paxillin expression, as shown byluciferase assay in LNCaP cells. Thus, our results suggest that ARFGAP3 is a novel androgen-regulated gene that can promoteprostate cancer cell proliferation and migration in collaboration with paxillin.


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