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

Roos, E.; Dingemans, K. P.; Pavert, I. V. van de; Bergh-Weerman, M A Van den

doi:10.1038/bjc.1978.167

Cited by 73 publications

(42 citation statements)

References 16 publications

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“…This is an in situ confirmation of previous in vitro findings concerning tumor cell binding prior to cytoxocity and phagocytosis. 14 -16 The presence of a single large DiO-filled phagosome in KCs indicates whole tumor cell phagocytosis and degradation in vivo, in concordance with the literature, 7,15,35,52 and parallel to the lysosomal localization of fluorescein in KCs 24 hr after injection of fluorescein-labeled colon cancer cells. 53 Lysosomal degradation of the ingested tumor cells was demonstrated by the subsequent appearance of smaller DiO-filled vacuoles resembling lysosomes at the electron microscopy level and the complete disappearance of the phagosome after 24 hr.…”

Section: Discussionsupporting

confidence: 74%

“…Others have reported only 40% similar contact for mammary carcinoma cells. 35 While the difference may be due in part to the different types of tumor cells used, our observation of a higher efficiency of contact may also be attributed to the use of intramesenteric injections, as opposed to liver perfusion, which may provide a more appropriate model for metastasis, and the more powerful CLSM to study KC-tumor cell interactions in 3 dimensions in large volumes.…”

Section: Discussionmentioning

confidence: 93%

“…There was a rapid response by macrophages to the newly arrived cancer cells, which were observed lying against and protruding through the endothelial lining as described in a model for mouse mammary carcinoma metastasis. 35 Within 1 hr of their arrival in the liver, 72% of the CC531s cancer cells were already in contact with KCs, and even higher frequencies of contact were observed as more cancer cells arrived in the following hours. Others have reported only 40% similar contact for mammary carcinoma cells.…”

Section: Discussionmentioning

confidence: 93%

“…Synergism between KCs and NK cells in the elimination of tumor cells has been postulated in vivo 34 and illustrated in vitro. 12 However, most studies describing the in situ KC-tumor cell interactions focused on events occurring 2-3 weeks after tumor cell inoculation, 20,22,34,35 and only a few studies examined the early stages of hepatic metastases (Ͻ 24 hr). 36,37 Routine microscopic methods are not optimal for studying early hepatic metastasis because they require thin sections, low sampling volumes, complicated preparation methods and immunohistochemical procedures.…”

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confidence: 99%

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Interactions between rat colon carcinoma cells and Kupffer cells during the onset of hepatic metastasis

Timmers

Vekemans

Vermijlen³

et al. 2004

Intl Journal of Cancer

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Liver sinusoids harbor populations of 2 important types of immunocompetent cells, Kupffer cells (KCsColon cancer is one of the most common cancers in the Western world. 1 Metastases to the liver, a common event in cancer patients, is an important cause of death, and the rate of metastasis generally determines survival time. 2,3 The growth and development of metastasis involve a cascade of tumor-host cell interactions.The first vascular bed encountered by blood-borne tumor cells from the gastrointestinal tract is in the liver, in the sinusoids of which they encounter 2 immunocompetent cells, Kupffer cells (KCs) and natural killer (NK) cells. 4,5 KCs represent the largest macrophage population in the body. 5 They move along sinusoids, scavenge degenerated cells, macromolecules and microorganisms and function as antigen-presenting cells. 4,6,7 By virtue of these capacities and their privileged location within the circulation, KCs form the first line of defense against disseminating colorectal tumor cells. 8 Their role in controlling hepatic metastasis in vivo has been demonstrated by their capacity to kill tumor cells in vitro. 9 -13 It has been shown that binding to tumor cells is necessary for effective killing in vitro, 14 -16 which is accomplished by a variety of mechanisms, including phagocytosis and the release of proteinases, tumor necrosis factor and oxygen metabolites. 4,17,18 The role of KCs in controlling metastasis has been demonstrated at late stages of metastasis (3 weeks); metastasis is enhanced by selectively eliminating KCs and reduced by stimulating them. 8,19 -22 Whether or not this effect can also be observed during the early stages of metastasis has not been reported yet.Liver 32 and the receptor-mediated pathway (members of the TNF family). 33 Both KCs and liver NK cells belong to the innate immune system and are often observed in close contact with each other. 24,27 It is supposed that these cells affect the growth of liver metastases only if they interact with incoming tumor cells shortly after their arrival in the liver (ϳ 24 hr) because later on the natural host defenses may be incapable of limiting metastasis due to the rapid proliferation of the cancer cell population, angiogenesis and weakened host defenses. Synergism between KCs and NK cells in the elimination of tumor cells has been postulated in vivo 34 and illustrated in vitro. 12 However, most studies describing the in situ KC-tumor cell interactions focused on events occurring 2-3 weeks after tumor cell inoculation, 20,22,34,35 and only a few studies examined the early stages of hepatic metastases (Ͻ 24 hr). 36,37 Routine microscopic methods are not optimal for studying early hepatic metastasis because they require thin sections, low sampling volumes, complicated preparation methods and immunohistochemical procedures. 38 In contrast, confocal laser scanning microscopy (CLSM) enables the study of large sample volumes and sections 50 -100 m thick, facilitating investigation of rare cellular events such as the occurrence of tumor...

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Section: Discussionsupporting

confidence: 74%

Section: Discussionmentioning

confidence: 93%

Section: Discussionmentioning

confidence: 93%

mentioning

confidence: 99%

See 2 more Smart Citations

Interactions between rat colon carcinoma cells and Kupffer cells during the onset of hepatic metastasis

Timmers

Vekemans

Vermijlen³

et al. 2004

Intl Journal of Cancer

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“…Various studies have shown that interactions between these ECM components within the liver and tumor cells appear to be crucial to the formation of hepatic metastases (19)(20)(21). The liver is furthermore unique, since it lacks a basement membrane under the sinusoidal endothelium (22). This unique nature of the hepatic ECM is predicted by its special configuration and apparent continuity with the extraparenchymal areas of the connective tissue (23).…”

Section: Regulation By Circulation Patterns and Microvessels In Livermentioning

confidence: 99%

Mechanisms regulating colorectal cancer cell metastasis into liver (Review)

Jin¹,

Weili

Lu³

et al. 2011

Oncology Letters

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Abstract. The metastatic spread of tumor cells is one of the most common causes of mortality in cancer patients. The elucidation of the molecular mechanisms that underlie the formation of metastatic colonies has been one of the major objectives of cancer research. Organ-specific colonization of cancer cells is a significant and noteworthy feature of metastasis. Colorectal cancer (CRC) is one of the most common causes of cancerrelated mortality. The liver is commonly the sole site of metastasis for CRC and represents a major cause of mortality in CRC patients. However, what regulates CRC cell metastasis into liver and the reasons for the liver-specific metastasis of CRC have yet to be adequately elucidated. Recent progress provides indications and a conceptual framework with which to investigate this issue. This review evaluated experimental and clinical evidence to support a mechanistic role for circulation patterns and microvessels in liver, metastasis-related genes, chemokines and their receptors, and cellular adhesion molecules in the process of CRC liver metastasis.

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Liver‐associated macrophage precursors as natural cytotoxic effectors against Candida albicans and Yac‐1 cells

1986

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Liver nonparenchymal cells of maleic anhydride divinyl ether or cyclophosphamide-treated mice were assayed for cytotoxic activity against the yeast form of Candida albicans. A strong increase in this activity was observed after both in vivo treatments, as compared to untreated control mice. The effector cell was enriched by nylon wool passage and separation of nonadherent liver nonparenchymal cells on a discontinuous Percoll gradient. By means of direct and indirect rosetting techniques, based on the presence of Fc receptors and the F4/80 and M143 macrophage surface markers, we could separate a nearly homogeneous effector cell population. It displayed, besides the candidacidal activity, Fc receptors and the M143 and F4/80 antigens, also strong natural cytotoxicity against Yac-1 lymphoma cells. When cultured in medium containing colony-stimulating factor-1, this effector population reacted with a strong proliferative response as measured through incorporation of tritiated thymidine. The data presented show that nonadherent, nonphagocytic macrophage precursors, which we characterized previously from in vitro bone marrow cultures, occur in vivo as organ-associated effector cells in the liver after elicitation with maleic anhydride divinyl ether or cyclophosphamide. These macrophage precursors have prior to their maturation the ability to serve as a microbicidal and tumoricidal natural killer cell.

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

Abstract: Summary.-Interactions between TA3 mammary-carcinoma cells and liver cells were studied with the electron microscope in mouse livers that had been perfused with a defined medium containing the tumour cells.

Cited by 73 publications

References 16 publications

Interactions between rat colon carcinoma cells and Kupffer cells during the onset of hepatic metastasis

Interactions between rat colon carcinoma cells and Kupffer cells during the onset of hepatic metastasis

Mechanisms regulating colorectal cancer cell metastasis into liver (Review)

Liver‐associated macrophage precursors as natural cytotoxic effectors against Candida albicans and Yac‐1 cells

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