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At least 289 records · Page 16Linked to original sources
PubMed2007

Impact of tumor spread to the cystic duct on the prognosis of patients with gallbladder carcinoma.

INTRODUCTION: The importance of gallbladder carcinoma spread to the cystic duct has not yet been described. Although the cystic duct is contiguous with the gallbladder, it is located in the hepatoduodenal ligament and differs in structure from the gallbladder. The incidence and prognostic significance of cancer spread to the cystic duct in patients with gallbladder cancer is unclear. METHODS: Surgical specimens from 42 patients who underwent resection for advanced gallbladder carcinoma were examined retrospectively. RESULTS: Altogether, 13 (31%) of the patients had cancer spread to the cystic duct. The incidences of perineural invasion, lymph node metastasis, and venous invasion were significantly higher in these patients than in the other 29 patients without cancer spread to the cystic duct (P = 0.027, 0.034, and 0.034, respectively). The 3- and 5-year survival rates of these 13 patients were significantly lower than those of the other 29 patients (15.4% vs. 51.0% and 7.7% vs. 46.6%, respectively, P < 0.0001 each). Multivariate analysis using the Cox proportional hazard model identified positive cancer spread to the cystic duct and depth of invasion (beyond serosa) as significant independent indicators of a poor prognosis. CONCLUSIONS: Cancer spread to the cystic duct is an indicator of poor prognosis in patients with gallbladder carcinoma. This may be due to the high incidence of concomitant perineural invasion and lymph node metastasis associated with cancer spread.

Adenocarcinoma↗
PubMed1998

Preparation and imaging of nuclear spreads from cells of the zebrafish embryo. Evidence for large degradation intermediates in apoptosis.

We describe a method for preparing nuclear spreads from cells of live, unfixed zebrafish embryos at the late-gastrula (approximately 8000 cell) stage of development. The method consists of a sequence of four steps: (1) a slow, gentle lysis, in low to moderate salt concentration, of cells and then nuclei, to release DNA-containing fibres; (2) spreading of the released fibres by a transverse fluid flow; (3) electrostatic, and possibly also covalent, attachment of the spread fibers to poly(L-lysine)-coated glass microscope slides; and (4) continued incubation to produce periodic cleavage of the DNA within the fibres, apparently through activation of endogenous nucleases. The nuclear spreads are imaged with epifluorescence, at a spatial resolution approaching the Rayleigh limit (approximately 230 nm for blue light). The epifluorescent signal is provided from Hoechst 33,258 bound specifically to the DNA, from a dye-coupled antibody conjugate bound specifically to histone H1 in the fibres, or from a DNA nick end-labelling assay. The spontaneous cleavage of DNA-containing fibres in step (4) of the above procedure can be blocked by the chelating agents EGTA and EDTA, by the caspase-2,3,7 inhibitor N-acetyl-Asp-Glu-Val-Asp-aldehyde, and by the caspase-1,4,5 inhibitors N-acetyl-Tyr-Val-Ala-Asp-aldehyde and N-acetyl-Tyr-Val-Ala-Asp-chloromethyl ketone. These data suggest that the spontaneous cleavage of fibres is catalysed by nucleases that become activated through a caspase-mediated mechanism. The involvement of caspase-dependent nucleases would suggest that an apoptosis pathway is activated in the spreads during their prolonged incubation. If bona fide apoptosis is induced in living zebrafish embryos by treatment with camptothecin (a topoisomerase I poison), and then nuclear spreads are prepared, we observe a similar fragmentation of the spread fibres. However, in this case the fragmentation is more rapid and complete. We hypothesize that, during the early phase of apoptosis, one or more endogenous nucleases are activated by a caspase-mediated mechanism. The nuclease(s) then specifically recognize and cleave a susceptible, periodically repeating feature of interphase chromatin.

Animals↗
PubMed1998

Do occlusal carious lesions spread laterally at the enamel-dentin junction? A histolopathological study.

It is conventionally taught that the carious lesion in dentin undermines the enamel due to lateral spread of the lesion at the enamel-dentin junction (EDJ). The aim of the present study was to challenge this hypothesis by testing an alternative hypothesis, that lateral spread is related to advanced lesions where the dentin is infected. Selected points in the groove-fossa system of 100 unrestored occlusal surfaces were examined and the teeth divided into five groups (scores 0-4) depending on the clinical appearance of the lesion. Teeth were sectioned through these sites and texture of the dentin was assessed by probing. Colour slides of the section face with the more extensive changes in the dentin were projected and the dimensions of the lesions at the EDJ were assessed by three examiners on two separate occasions. Inter- and intra-examiner reproducibility was assessed and found acceptable. Results showed that in 47 teeth demineralisation had not reached the EDJ. In the remaining teeth the presence or absence of lateral spread of the lesion at the EDJ was related to the clinical features of the lesion. Lateral spread was rarely found in lesions with an apparently intact enamel surface (scores 0-2). However, 32% of sites with microcavitation (score 3) and 63% of sites with obvious cavitation (score 4) showed lateral spread. Of those 31 sections which were judged to have soft dentin, 80% had lateral spread. In conclusion, the phenomenon of lateral spread of caries at the FDJ is related to advanced lesions with cavity formation where the dentin is soft and infected.

Bicuspid↗
PubMed2006

Two continuum models for the spreading of myxobacteria swarms.

We analyze the phenomenon of spreading of a Myxococcus xanthus bacterial colony on plates coated with nutrient. The bacteria spread by gliding on the surface. In the first few hours, cell growth is irrelevant to colony spread. In this case, bacteria spread through peninsular protrusions from the edge of the initial colony. We analyze the diffusion through the narrowing reticulum of cells on the surface mathematically and derive formulae for the spreading rates. On the time scale of tens of hours, effective diffusion of the bacteria, combined with cell division and growth, causes a constant linear increase in the colony's radius. Mathematical analysis and numerical solution of reaction-diffusion equations describing the bacterial and nutrient dynamics demonstrate that, in this regime, the spreading rate is proportional to the square root of both the effective diffusion coefficient and the nutrient concentration. The model predictions agree with the data on spreading rate dependence on the type of gliding motility.

Mathematics↗
PubMedDate not supplied

Improved attachment and spreading in primary cell cultures of the eastern oyster, Crassostrea virginica.

At present, establishment of a cell line from bivalve molluscs has been unsuccessful, and in vitro work is limited to primary cell cultures. We sought to improve attachment and spreading of cells of the eastern oyster, Crassostrea virginica, to aid primary cultures and to assist development of a bivalve cell line. Our objectives were to examine the effects of substrate on ventricle cell viability, attachment, and spreading by testing of collagen I, collagen IV, fibronectin, laminin, poly-D-lysine, and two types of uncoated tissue culture plates (Falcon and Corning). Experiments were conducted by incubating cells with the various substrates for 24 h and 5 d. An assay with a tetrazolium compound (MTS) was used to estimate cell numbers based on metabolic activity. Although differences in MTS assay values for substrate effect on cell viability were detected at 24 h and at 5 d (P > 0.0001), these were attributed to variations in metabolic activity due to different levels of attachment and spreading among treatments. Differences among treatments were detected in attachment and spreading at 24 h and 5 d (for all, P > 0.0001). At 24 h, poly-D-lysine induced the highest levels of attachment and spreading; no other factor performed better than the uncoated Falcon substrate, and collagen I performed most poorly. At 5 d, poly-D-lysine and the uncoated Corning substrate induced significantly higher levels of attachment and spreading than did the uncoated Falcons substrate, and collagen I performed most poorly. From these results, poly-D-lysine best promoted cell attachment and spreading. Fibronectin (at 24 h) and laminin (at 5 d) warrant further study. Along with improvements in medium composition, future work should involve screening of other attachment factors and combinations of factors, including those of bivalve origin.

Animals↗
PubMed1989

Adhesion and spreading of cultured endothelial cells on modified and unmodified poly (ethylene terephthalate): a morphological study.

The in vitro adhesion and spreading of human endothelial cells (HEC) on hydrophobic poly(ethylene terephthalate) (PETP) and moderately wettable tissue culture poly(ethylene terephthalate) (TCPETP) were studied with light microscopy and electron microscopy. Numbers of HEC adhering on TCPETP were always higher than those found on PETP. When cells were seeded in the presence of serum, extensive cell spreading on both PETP and TCPETP was observed after the first 30 min. Thereafter, spread cells appeared to withdraw from the PETP surface, resulting in irregularly shaped cells. Complete cell spreading occurred on TCPETP. Complete cell spreading also occurred on PETP and TCPETP when HEC had first been seeded from phosphate buffer solution and serum was supplied after 30 min. Furthermore, HEC spread on both PETP and TCPETP when the surfaces were precoated with protein(s), which promotes cell adhesion. However, when plasma was used for the coating, spread cells did not proliferate in a monolayer pattern. This study shows that TCPETP is, in general, a better surface for adhesion and proliferation of HEC than is PETP, suggesting that vascular prostheses with a TCPETP-like surface will perform better in vivo than prostheses made of PETP.

Blood↗
PubMed1989

Synthesis of calelectrins and calpactin I during cytochalasin mediated cell spreading inhibition.

Mammary epithelial cell spreading on collagen gels has previously been shown to be correlated with the synthesis of a group of calcium-binding proteins (CBPs) which we have identified as the calcium-binding proteins termed calelectrins and calpactin I monomer/p36. To determine whether cell spreading per se is required for CBP synthesis, we examined the effect of cytochalasin D on these two events. Concentrations of cytochalasin D that did not reduce total protein synthesis, caused inhibition of cell spreading in a dose-dependent manner, but did not cause inhibition of CBP synthesis. Synthesis of collagen also continued during cytochalasin inhibition of cell spreading. Removal of the inhibitor from the cultures initiated cell spreading and CBP synthesis continued. Membrane-cytoskeleton complexes from control and CD treated cells were identical in regard to binding CBPs in a calcium-dependent manner. Colchicine, which inhibited cell spreading, was shown to be toxic to general protein synthesis at 75 nM. The data clearly indicate that mere inhibition of epithelial cell spreading does not automatically suppress CBP synthesis.

Animals↗
PubMed2004

The low molecular weight heparan sulfate-mimetic, PI-88, inhibits cell-to-cell spread of herpes simplex virus.

Although a number of sulfated polysaccharides have been shown to inhibit infection of cells by herpes simplex virus (HSV), little is known about their effects on the cell-to-cell spread of the virus. These compounds act by inhibiting the virus binding to cells, and their antiviral potencies usually increase with increasing molecular weight and sulfation density. We report that the low molecular weight HS-mimetic, PI-88, which is a mixture of highly sulfated mannose-containing di- to hexa-saccharides, inhibited HSV infection of cells and cell-to-cell spread of HSV-1 and HSV-2. Compared to a relatively large heparin polysaccharide, PI-88 demonstrated weaker inhibition of HSV infectivity but more efficient reduction of cell-to-cell spread of HSV. A tetrasaccharide fraction of PI-88 was the minimum fragment necessary to inhibit HSV-1 infectivity, while a trisaccharide was sufficient to reduce cell-to-cell spread. A reduction in HSV lateral spread was also observed in cells incubated with another low molecular weight compound, pentosan polysulfate but not with much larger polysaccharide chondroitin sulfate E. Some differences as regards the effects of PI-88, heparin, protamine, poly-L-lysine and sodium chlorate on intercellular spread of HSV-1 and HSV-2 were found. We conclude that structurally different sulfated oligosaccharides are preferred for inhibition of HSV infectivity and the cell-to-cell spread. The latter was efficiently inhibited by a relatively small but densely sulfated PI-88 oligosaccharide, very likely due to the capability of the compound to access the narrow intercellular space.

Alphaherpesvirinae↗
PubMed2004

Effects of electrode density and electrolyte spreading in dense array electroencephalographic recording.

OBJECTIVE: High-density EEG recording offers increased spatial resolution but requires careful consideration of how the density of electrodes affects the potentials being measured. Power differences as a function of electrode density and electrolyte spreading were examined and a method for correcting these differences was tested. METHODS: Separate EEG recordings from 8 participants were made using a high-density electrode net, first with 6 of 128 electrodes active followed by recordings with all electrodes active. For a subset of 4 participants measurements were counterbalanced with recordings made in the reversed order by drying the hair after the high-density recordings and using a fresh dry electrode net of the same size for the low-density recordings. Mean power values over 6 resting eyes open/closed EEG recordings at the 6 active electrodes common to both recording conditions were compared. Evidence for possible electrolyte spreading or bridging between electrodes was acquired by computing Hjorth electrical distances. Spherical spline interpolation was tested for correcting power values at electrodes affected by electrolyte spreading for these participants and for a subset of participants from a larger previous study. RESULTS: For both the complete set and the counterbalanced subset, significant decreases in power at the 6 common electrodes for the high-density recordings were observed across the range of the standard EEG bands (1-44 Hz). The number of bridges or amount of electrolyte spreading towards the reference electrode as evidenced by small Hjorth electrical distances served as a predictor of this power decrease. Spherical spline interpolation increased the power values at electrodes affected by electrolyte spreading and by a significant amount for the larger number of participants in the second group. CONCLUSIONS: Understanding signal effects caused by closely spaced electrodes, detecting electrolyte spreading and correcting its effects are important considerations for high-density EEG recordings. A combination of scalp maps of power density and plots of small Hjorth electrical distances can be used to identify electrodes affected by electrolyte spreading. Interpolation using spherical splines offers a method for correcting the potentials measured at these electrodes.

Adult↗
PubMed2004

Microbial infection causes the appearance of hemocytes with extreme spreading ability in monolayers of the tobacco hornworm Manduca sexta.

The ability to adhere to and spread on a surface is a common property of insect blood cells. Spreading on a glass surface by insect hemocytes is often used as a measure of immune fitness that can be inhibited by some insect pathogens and parasites. Here, we report that upon infection of the tobacco hornworm Manduca sexta with either a fungus (Beauveria bassiana) or a bacterium (Photorhabdus luminescens), a new type of hemocyte, not previously observed in healthy insects, was found in hemocyte monolayers. These cells have a distinctive morphology, characterised by extreme spreading ability. They achieve a diameter of up to 120 microm after 1 h on glass coverslips and are therefore extremely thin. These hyper-spreading cells first appear in fungal-infected insects prior to hyphal growth. Their numbers later fall to zero as the pathogen begins to proliferate. The same hyper-spreading cells are induced after a 24 h delay following an injection of laminarin, a source of the fungal cell wall polymer beta-1,3-glucans. Wounding, on the other hand, did not cause the appearance of hyper-spreading cells. Evidence is presented here that is consistent with these spreading cells having a role in the cellular immune response of nodule formation.

Animals↗
PubMed2005

Spreading of individual toner particles studied using in situ optical microscopy.

This study develops and tests an experimental method to monitor in situ the dynamic spreading of individual toner particles on model substrates during heating, to simulate on laboratory scale the fusing sub-processes occurring in electrophotographic printing of paper. Real toner particles of cyan, magenta, yellow and black are transformed to perfect spheres by a temperature pre-treatment, then applied to the substrate, either high-energy clean glass or low-energy hydrophobised glass, and heated at rates up to 50 degrees C/min. The subsequent spreading as a function of time (and temperature) is recorded by an optical microscope and CCD camera mounted above the substrate, with the measured drop covering area used to calculate the corresponding toner-substrate-air contact angle. On the hydrophobic substrate the spreading is limited and equal for all four colours, while the substantially greater spreading on the hydrophilic substrate is accompanied by significant differences between the toner colours. In particular, the cyan and black toners are found to spread to almost twice the extent of the yellow particles. The dynamic spreading behaviour is interpreted in terms of complementary measurements of substrate and toner surface energy components and bulk toner rheology, and a simple empirical relation is proposed that fits very well the measurements for all toner and substrate types tested. In particular, the spreading relation is found to be determined only by the toner surface energy and its equilibrium contact angle, with no explicit dependence on toner viscosity.

Journal Article↗
PubMed2004

Soluble fibrin augments spreading of fibroblasts by providing RGD sequences of fibrinogen in soluble fibrin.

We previously reported that fibroblasts were found to spread far more avidly on NaBr-solubilized fibrin monomer (FM) monolayers than on immobilized fibrinogen (Fbg), indicating that removal of fibrinopeptides by thrombin is a prerequisite for the fibrin-mediated augmentation of cell spreading [J. Biol. Chem. 272 (1997) 8824-8829]. Soluble fibrin (SF), a 1:2 complex of fibrin-monomer and fibrinogen, is known to be present in the circulating blood under the pathological condition in which blood coagulation is activated. However, its physiological roles are still incompletely known. Fibroblasts spread on immobilized purified soluble fibrin. Cells spreading on immobilized soluble fibrin were blocked by the exogenous addition of soluble fibrin and glycine-arginine-glycine-aspartic acid-serine-phenylalanine (GRGDSP)-synthetic peptide but not by the addition of fibrinogen or fibrin monomer. However, cell spreading activity was decreased in the surfaces coated with fragment X, whose Aalpha-chains lack carboxyl-terminal segments including arginine-glycine-aspartic acid (RGD)-2 domain, fibrin monomer complexes. It suggests that the RGD-2 domain of fibrinogen after being complexed with fibrin monomer plays a pivotal role for soluble fibrin-dependent cell spreading. Soluble fibrin in plasma derived from the patients of disseminated intravascular coagulation (DIC) was immuno-purified using the monoclonal antibody (mAb) which specifically recognizes the Ca(++)-dependent conformer of fibrinogen. The purified soluble fibrin consisted of desAA-fibrin monomer and two fibrinogen molecules and did show the cell spreading activity. Thus, soluble fibrin in plasma plays a role as the modulator of thrombogenic process in vivo.

Cell Adhesion↗
PubMed2005

An in vitro system to study trans-neuronal spread of pseudorabies virus infection.

The neuronal spread of infection of alpha herpesviruses is controlled by unknown mechanisms. In the natural host, primary infection always leads to invasion of the peripheral nervous system, but rarely results in extensive invasion of the central nervous system. After reactivation of latent infection in the peripheral nervous system, virions are produced and shed from epithelial surfaces, but rarely invade the central nervous system. We have been studying two aspects of the general problem. First, using GFP and mRFP fusion proteins, we have used video confocal microscopy to assess mechanisms that influence spread of pseudorabies (PRV) virion components within axons. Second, and the subject of this report, is the development of a new in vitro cell culture system that enables the study of trans-neuronal spread of infection from neurons to non-neuronal cells similar to what happens after reactivation and spread to epithelial surfaces. We have developed a tissue culture system involving tri-chamber Teflon rings that enables facile analysis of trans-neuronal spread. The system duplicates all the known in vivo correlates of trans-neuronal spread and provides the opportunity to do both quantitative and qualitative assessment of spread of PRV infection from infected neurons to non-neuronal cells.

Animals↗
PubMed1998

A spreading technique for forming film in a captive bubble.

Mechanisms underlying the surface properties of lung surfactant are extensively studied in in vitro systems such as the captive-bubble surfactometer (CBS), the pulsating-bubble surfactometer, and the Wilhelmy balance. Among these systems, the CBS is advantageous when a leakproof system and high cycling rates are required. However, widespread application of the CBS to mechanistic studies of dynamic surfactant protein-phospholipid interactions of spread film and to comparative studies between spread and adsorbed film is hampered because spreading of film is difficult. In addition, when film is formed by adsorption, the amount of material required is fairly large. We have developed an easy spreading technique that allows routine formation of film by spreading of small amounts of surfactant components at the air-water interface of an air bubble in a CBS. The technique is reliable, precise, and accurate, and the biophysical activity of film formed by spreading is similar to that of film formed by adsorption. This method will be useful for mechanistic studies of surfactant components under dynamic conditions and for comparative studies of spread films and adsorbed films.

1,2-Dipalmitoylphosphatidylcholine↗
PubMed2003

Spreading of non-Newtonian liquids over solid substrates.

The spreading of drops of a non-Newtonian liquid (Ostwald-de Waele liquid) over horizontal solid substrates is theoretically investigated in the case of complete wetting and small dynamic contact angles. Both gravitational and capillary regimes of spreading are considered. The evolution equation deduced for the shape of the spreading drops has self-similar solutions, which allows obtaining spreading laws for both gravitational and capillary regimes of spreading. In the gravitational regime case of spreading the profile of the spreading drop is provided.

Journal Article↗
PubMedDate not supplied

Integrin-like RGD-dependent binding mechanism involved in the spreading response of circulating molluscan phagocytes.

Circulating phagocytic cells (hemocytes) of the snail Biomphalaria glabrata, intermediate host of the human blood fluke Schistosoma mansoni, were treated with the tetrapeptide, arg-gly-asp-ser (RGDS), an integrin-specific adhesion inhibitor, and assessed for their ability to adhere and spread on uncoated and snail plasma protein-coated glass slides. Although cells were capable of adherence, RGDS significantly inhibited the spreading ability of hemocytes in both a time and RGDS concentration-dependent fashion regardless of plasma protein coating. The inhibition of hemocyte spreading by RGDS was a specific response, since treatment of cells with a glutamic acid-substituted control peptide (RGES) did not exert the same inhibitory effect. A comparison of RGDS-responses between hemocytes of two strains of B. glabrata, one resistant (R; 13-16-R1 strain) and the other susceptible (S; NMRI strain) to infection by S. mansoni, revealed several snail strain-specific differences. At concentrations of 0.5 mM RGDS, R snail hemocyte spreading was unaffected, whereas a significant depression of spreading was seen in cells of the S snail. Moreover, we observed that R strain hemocytes spread more rapidly on homologous plasma-coated surfaces than the S snail strain following peptide pretreatment and removal. These data suggest that hemocytes from S and R snails may differ either in the number of RGDS-binding receptors or in their affinity for the RGDS peptide. In order to identify the type(s) of integrin-like RGD-binding receptors that may be present on the surface of snail immunocytes, washed hemocytes were placed on various mammalian extracellular matrix proteins and evaluated for their spreading function in the presence of specific or non-specific peptides. Hemocyte aggregation or clumping was observed on all test protein substrates, and this aggregation behavior was specifically inhibited by RGDS. Thus, RGD-binding receptors appear to play a critical role in cellular motility on matrix-coated surfaces and/or cell-cell binding. Our data provide functional evidence for an integrin-like receptor on circulating phagocytes of snails, and for an RGD-binding mechanism involved in cell-substrate interactions.

Animals↗
PubMed1999

Effects of nitric oxide inhibition on the spread of biotinylated dextran and on extracellular space parameters in the neostriatum of the male rat.

Volume transmission in the brain is mediated by the diffusion of neurotransmitters, modulators and other neuroactive substances in the extracellular space. The effects of nitric oxide synthase inhibition on extracellular space diffusion properties were studied using two different approaches, the histological dextran method and the real-time iontophoretic tetramethylammonium method. The spread of biotinylated dextran (mol. wt 3000) in the extracellular space was measured morphometrically following microinjection into the neostriatum of male rats. Two parameters were used to describe the spread of biotinylated dextran in brain tissue, namely, total volume of spread and the mean grey value. The nonspecific nitric oxide synthase inhibitors NG-nitro-L-arginine methyl ester (10-100 mg/kg) and NG-monomethyl-L-arginine acetate (30-200 mg/kg) decreased the total volume of spread of dextran in a dose-dependent manner. 7-Nitroindazole monosodium salt (50-100 mg/kg), a specific neuronal nitric oxide synthase inhibitor, did not change the total volume of spread of dextran. Using the tetramethylammonium method, the extracellular space diffusion properties can be described by the volume fraction (alpha = extracellular space volume/total tissue volume), tortuosity lambda (lambda2 = free diffusion coefficient/apparent diffusion coefficient in tissue), and non-specific uptake kappa' [Nicholson C. and Syková E. (1998) Trends Neurosci. 21, 207-215]. Nitric oxide synthase inhibition by NG-nitro-L-arginine methyl ester (50 mg/kg) had relatively little effect on volume fraction and tortuosity, and no changes were observed after NG-monomethyl-L-arginine acetate (20 mg/kg) or 7-nitroindazole monosodium salt (100 mg/kg) treatment. A substantial increase was found only in non-specific uptake, by 13% after NG-nitro-L-arginine methyl ester and by 16% after NG-monomethyl-L-arginine acetate, which correlates with the decreased total volume of spread of dextran observed with the dextran method. NG-Nitro-L-arginine methyl ester treatment (100 mg/kg) decreased striatal blood flow and increased mean arterial blood pressure. The changes in dextran spread and non-specific uptake can be explained by an increased capillary clearance following the inhibition of endothelial nitric oxide synthase, as neuronal nitric oxide synthase inhibition had no effect. The observed changes after non-specific nitric oxide synthase inhibition may affect the extracellular space concentration of neurotransmitters and modulators, and influence volume transmission pathways in the central nervous system by increased capillary and/or cellular clearance rather than by changes in extracellular space diffusion.

Animals↗
PubMed2003

Cervical lymph node metastasis in oral cancer: the importance of even microscopic extracapsular spread.

The prognostic significance of extracapsular spread of cervical metastases in oral cancer is still controversial. To investigate the importance of extent of extracapsular spread; the relationship between extracapsular spread and both traditional measures of metastatic disease and clinical/histological features of the primary tumour, and to determine their relative prognostic significance. The survival of 173 patients undergoing radical surgery and simultaneous neck dissection for oral/oropharyngeal squamous cell carcinoma with histologically confirmed nodal metastasis and followed for 2.2-12.3 years is reported and related to pathological features. The most predictive clinical/histopathological features were determined by Cox regression modelling. The 3-year survival probability was similar for patients with macroscopic and only microscopic extracapsular spread (33 and 36%, respectively, compared with 72% for patients with intranodal metastasis). The Cox model showed the most predictive factor was extracapsular spread followed by status of resection margins. Extracapsular spread should be incorporated into pathological staging systems. Even microscopic extracapsular spread is of critical importance and must be sought especially in small-volume metastatic disease.

Adult↗