The E-cadherin–catenin complex plays an important role in establishing and maintaining intercellular connections and morphogenesis and reduced expression of its constituent molecules is associated with invasion and metastasis. In the present study, we examined E-cadherin and α-, β- and γ-catenin levels in tumour tissues obtained by radical prostatectomy in order to investigate the relationship with histopathological tumour invasion. Immunohistochemical findings for 45 prostate cancer specimens demonstrated aberrant expression of each molecule to be associated with dedifferentiation and, in addition, alteration of staining patterns for the three types of catenin was significantly correlated with capsular but not lymphatic or vascular invasion. The data thus suggest that three types of catenin may be useful predictive markers for biological aggressiveness of prostate cancer. © 1999 Cancer Research Campaign
Lymph node metastasis (LNM) is associated with poor survival in patients with oral squamous cell carcinoma (OSCC). Vascular endothelial growth factor-C (VEGF-C) is thought to be responsible for increased lymphangiogenesis and LNM. Understanding of the mechanism by which VEGF-C expression is regulated in OSCC is thus important to design logic therapeutic interventions. We showed that inoculation of the SAS human OSCC cells expressing the venus GFP (V-SAS cells) into the tongue in nude mice developed LNM. V-SAS cells in LNM were isolated by FACS and re-inoculated into the tongue. This procedure was repeated eight times, establishing V-SAS-LM8 cells. Differential metastasis PCR array between the parental V-SAS and V-SAS-LM8 was performed to identify a molecule responsible for lymphangiogenesis and LNM. Fibronectin 1 (FN1) expression was elevated in V-SAS-LM8 cells compared to V-SAS-cells. V-SAS-LM8 tongue tumor showed increased expression of FN1 and VEGF-C, and promoted lymphangiogenesis and LNM compared with V-SAS tumor. Further, phosphorylation of focal adhesion kinase (FAK), a main downstream signaling molecule of FN1, was up-regulated, and epithelial-mesenchymal transition (EMT) was promoted in V-SAS-LM8 cells. Silencing of FN1 by shRNA in V-SAS-LM8 cells decreased FAK phosphorylation, VEGF-C expression and inhibited lymphangiogenesis and LNM. EMT was also reversed. The FAK phosphorylation inhibitor PF573228 also decreased VEGF-C expression and reversed EMT in V-SAS-LM8 cells. Finally, we detected intense FN1 expression in some clinical specimens obtained from OSCC patients with LNM. These results demonstrate that elevated expression of cellular FN1 and following activation of FAK lead to increased VEGF-C expression, lymphangiogenesis and LNM and promoted EMT in SAS human OSCC cells and suggest that FN1-phosphorylated FAK signaling cascade is a potential therapeutic target in the treatment of LNM in OSCC.
Summary The authors presented the first industry SPE paper on wellbore strengthening, which proposed a new concept for lost-circulation prevention while drilling (Morita et al. 1988; Fuh et al. 1992; Morita et al. 1996). Recently, the authors were invited to present at the 2010 SPE Forum held at Park City, Utah, USA. This presentation focused on wellbore-strengthening methods currently used in the industry, including well cooling, stress cage, and tip screening of induced fractures. During the forum, participants requested a parametric analysis of these methods using rock-mechanics equations and principles. This paper presents a set of analytical equations developed for parametric analysis of three typical wellbore-strengthening methods (Fuh et al. 2007; Alberty and McLean 2004) and provides information about the strengths and limitations of each method. In addition, an updated set of equations developed on the basis of previous work completed by the authors has been provided to make the analysis of wellbore-strengthening methods easier to implement. The equations can be classified by the length of the cracks to be stabilized, as follows: Borehole strengthening by heating to stabilize 0.0- to 0.1-in. cracks. (Not included in this parametric study.)Borehole strengthening to stabilize microcracks (with mudcake or fine particles) for 0.1- to 1-in. cracks.Borehole strengthening to stabilize macrocracks (stress-cage method) for 1-in. to 2-ft cracks.Borehole strengthening to stabilize a large fracture with the tip-screening method for cracks longer than 10 ft.Parametric studies were conducted on three wellbore-strengthening methods, and the following observations were made:Borehole-stabilization method: Water-based mud mixed with 25/40-mesh particles stabilizes the borehole by plugging the microcracks with mudcake. Borehole stability is enhanced by mixing 25/40-mesh crushed nut shells into the mud. Some drilling engineers enhance borehole stability by intentionally returning a proper range of cutting particles from the shale shakers.Stress-cage method: This method is applicable if the formation permeability is not too low. However, if the permeability is low, a high-fluid-loss pill is required to reduce propagation of the induced fracture and adequately place the granular materials. After wellbore strengthening, ultralow-fluid-loss mud is required during drilling to reduce the pressure buildup in the fracture section behind the seal.Tip-screening method: This method does not require the squeezing of particles to induce a fracture. Mixing particles with drilling fluid prevents fracture initiation, and if a fracture is induced, this mixture prevents further fracture propagation by tip screening. Tip screening is effective if a lost-circulation zone has some permeability, but is less effective if the lost-circulation zone has no permeability.
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