The fine structure of neoplastic invasion: Invasion of liver, skeletal muscle and lymphatic vessels by the Rd/3 tumour

Carr, Ian; McGinty, F.; Norris, Phillip J.

doi:10.1002/path.1711180205

Cited by 72 publications

(20 citation statements)

References 14 publications

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“…DISCUSSION Tumor cell attachment to and invasion of endothelial monolayers in tissue culture appeared to be similar to blood-borne tumor arrest and extravasation in vivo. Various studies (4,5,35,36) on tumor cell extravasation have suggested that neoplastic cells invade blood vessels at sites near or at endothelial intercellular junctions that are broken and subsequently reseal after tumor cell penetration, in a manner analogous to leukocyte emigration (37). However, in contrast to some reports (38)(39)(40), tumor cells in our studies were never observed to penetrate directly through endothelial cytoplasms.…”

contrasting

confidence: 55%

“…Two critical stages during blood-borne metastatic spread are circulating tumor cell (a) arrest or attachment to the vascular endothelium and (b) extravasation or invasion of the vascular endothelium and underlying basement membrane. Although little is known concerning the mechanism of blood-borne tumor cell arrest (2,3), several theories have been proposed for extravasation: (i) endothelium penetration by breakage of endothelial intercellular junctions (4,5), (ii) cytotoxic or enzymatic destruction of endothelial cells adjacent to tumor cells (6,7), (iii) extension of tumor cell pseudopodia through endothelial cell cytoplasm (8), and (iv) endothelial vessel rupture due to proliferation of tumor cells at the site of arrest (4). Due to the difficulties in studying tumor cell extravasation in vivo we have developed an in vitro model to evaluate malignant tumor cell interactions with vascular endothelial cells.…”

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confidence: 99%

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Interactions of tumor cells with vascular endothelial cell monolayers: a model for metastatic invasion.

Kramer¹,

Nicolson²

1979

Proc. Natl. Acad. Sci. U.S.A.

227

115

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The interactions of tumorigenic and nontumorigenic human and rodent cells with vascular endothelial cells and their underlying extracellular matrix were studied in culture. Gospodarowicz (9)(10)(11). Endothelial cells were used at passage 4-8. BAE cells were routinely cultured in Dulbecco's modified Eagle's medium supplemented with 10% calf bovine serum (Irvine Scientific), and human umbilical cord endothelial cells were cultured in medium 199 plus 20% fetal bovine serum. Fibroblast growth factor was purified as described (11) and added every other day at a concentration of 100-500 ng/ml. At confluency the serum concentration was reduced to 5% and fibroblast growth factor at 5 ng/ml was added every other day.Tumorigenic and nontumorigenic cell lines were obtained and grown as referenced in Table 1. Human foreskin and mouse embryo fibroblasts were obtained from D. Cunningham and cultured in Dulbecco's modified Eagle's medium plus 10% fetal bovine serum.Assays and Electron Microscopy. The adhesion and invasion assays were performed as follows: Completely confluent monolayers of BAE or human umbilical cord endothelial cells were seeded with suspensions of tumorigenic or nontumorigenic cells at 370C in Dulbecco's modified Eagle's medium plus 10% calf serum (or, in the case of human endothelial cells, in medium 199 plus 20% fetal calf serum) at 2-5 X 105 cells per 16-mm culture dish. Single cell suspensions of adherent cell lines were prepared after a 10-to 15-min incubation with 2 mM EDTA in Ca2+,Mg2+-free Dulbecco's phosphate-buffered saline (28). After incubation for various times at 370C, the culture dishes were examined by time-lapse or phase-contrast microscopy (see legend to Table 1). Some of the endothelial monolayers were carefully washed with phosphate buffered saline (28) at 370C by aspiration and fixed in phosphate-buffered saline/1.5% glutaraldehyde for 10 min at 370C and then for 1-3 hr at 220C. The glutaraldehyde-fixed monolayers were prepared for scanning or transmission electron microscopy after postfixation in 1% osmium tetroxide/1 mM CaCl2/0.1 M sodium phosphate, buffer, pH 7.2, for 0.5 hr at room temperature. For scanning electron microscopy, monolayer samples were dehydrated through a graded series of ethanol, transferred to Freon 113, and critical-point dried (29). After they were coated with 50-100 A of gold/palladium (Hummer II, Technics)

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confidence: 99%

Interactions of tumor cells with vascular endothelial cell monolayers: a model for metastatic invasion.

Kramer¹,

Nicolson²

1979

Proc. Natl. Acad. Sci. U.S.A.

227

115

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“…This cessation was not an artefact of our perfused-liver model, since it also occurred in vivo. The extension of protrusions has often been seen as an initial step in infiltration by both tumour cells (Fisher and Fisher, 1961;Babai and Tremblay, 1972;Dingemans, 1973;Fasske et al, 1975;Carr et al, 1976;Chew et al, 1976;Roos et al, 1977) and leucocytes (Dingemans, 1978). The ballooning of these protrusions, which then become globular invasive processes, is apparently also important.…”

Section: Discussionmentioning

confidence: 99%

Mammary-carcinoma cells in mouse liver: infiltration of liver tissue and interaction with Kupffer cells

Roos¹,

Dingemans²,

Pavert³

et al. 1978

Br J Cancer

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“…2) Interacción transcelular, reportada por Babaï (1976), y 3) Invasión intrasarcoplásmica, es la interacción más rara y con peor pronóstico en pacientes que la presentaron, se caracteriza por la invasión de las células cancerosas al interior de las fibras del músculo esquelético, con la aparición de agregados de células tumorales en el sarcoplasma (Carr et al, 1976;Slatkin & Pearson, 1976;Stratton et al, 1982).…”

Section: Introductionunclassified

Las Células TC-1 Implantadas Invaden a las Fibras Musculares Esqueléticas Adyacentes en un Modelo Murino de Cáncer

et al. 2013

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RESUMEN:La línea celular TC-1 se ha utilizado en la evaluación de la inmunoterapia antitumoral. No existen reportes sobre el efecto de las células TC-1 en tejidos adyacentes cuando se implantan en ratones C57BL/6. El objetivo de este trabajo fue evaluar la interacción entre las células TC-1 implantadas y las fibras musculares adyacentes. Se emplearon 8 ratones con células TC-1 implantadas y 3 ratones sin células. Se colectó el sitio del implante de las células tumorales a 10 días, las muestras se procesaron para microscopia de luz y electrónica de transmisión. Se realizaron tinciones con HyE y tricrómico de Masson, histoquímica con PAS, e inmunohistoquímica para identificar citoqueratinas, actina específica de músculo y metaloproteinasa de la matriz-9 (MMP-9). También se comparó el diámetro de las fibras musculares en ambos grupos de estudio. En el análisis histológico se observaron masas de células TC-1 que infiltran el tejido muscular y separan a las fibras entre sí. Las fibras musculares mostraron variaciones en la intensidad de la tinción y disminución de su diámetro. Se observaron masas de células tumorales TC-1 que invaden la fibra hacia el interior y logran atravesar la lámina externa y el sarcolema que las rodea. Se observó positividad a MMP-9 en el citoplasma de las células TC-1, y en el espacio entre las células tumorales y las fibras musculares. En el análisis ultraestructural se observó fragmentación y variaciones en el grosor de la lámina externa y vesículas subsarcolemales en el sitio en donde las células TC-1 invaden las fibras.Ahí, las células TC1 emiten proyecciones de membrana similares a pseudópodos. Existió diferencia estadística significativa en el diámetro de las fibras del grupo experimental vs el grupo control. Estos hallazgos deben tomarse en cuenta cuando se utiliza este modelo murino de cáncer para valorar la respuesta de inmunoterapia antitumoral.PALABRAS CLAVE: Células TC-1; Invasión intrasarcoplásmica; Modelo murino de cáncer. INTRODUCCIÓNLos pacientes afectados de enfermedad neoplásica maligna cursan con caquexia severa, atribuible principalmente a una atrofia importante y progresiva de la masa muscular corporal (Argilés et al., 2006). A la fecha, la invasión de célu-las cancerosas al interior de las fibras musculares esqueléticas ha sido reportada con poca frecuencia (Sridhar et al., 1987;Ueyama et al., 1998;Mathis et al., 2010), y en la práctica clínica han sido raramente reportados los casos de tumores metastásicos desarrollados en músculo (Luo et al., 2002). Cuando se presentan, las metástasis a músculo esquelético se han asociado con un mal pronóstico, que se traduce en una menor esperanza de vida para el paciente (Ferrandina et al., 2006;Albiruni et al., 2007;Mathis et al.).Tanto en modelos animales experimentales como en reportes histopatológicos de pacientes, se han descrito tres formas histológicas de interacción de las células cancerosas con las fibras musculares esqueléticas: 1) Infiltración (Brandes et al., 1967;Gabbert et al., 1987;Lamura et al., 2003). 2) Interacción ...

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The fine structure of neoplastic invasion: Invasion of liver, skeletal muscle and lymphatic vessels by the Rd/3 tumour

Cited by 72 publications

References 14 publications

Interactions of tumor cells with vascular endothelial cell monolayers: a model for metastatic invasion.

Interactions of tumor cells with vascular endothelial cell monolayers: a model for metastatic invasion.

Mammary-carcinoma cells in mouse liver: infiltration of liver tissue and interaction with Kupffer cells

Las Células TC-1 Implantadas Invaden a las Fibras Musculares Esqueléticas Adyacentes en un Modelo Murino de Cáncer

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