The hepatic sinusoidal endothelial lining and colorectal liver metastases

Braet, Filip; Nagatsuma, Keissuke; Saito, Masaya; Soon, Lilian; Wisse, Eddie; Matsuura, Tomokazu

doi:10.3748/wjg.v13.i6.821

Cited by 38 publications

(27 citation statements)

References 27 publications

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“…These findings could be decisive for future investigations regarding the surgical resection options of the colorectal hepatic metastasis [3]. Furthermore, tumour cells metastasized to the liver have certainly crossed the hepatic sinusoidal endothelial barrier and completed steps of metastatic cascade [2]. Accordingly, further studies exploring the earlier stages of colorectal metastasis, proliferation and new vessel formation as well as mechanisms to disturb cell survival are needed [5].…”

Section: Discussionmentioning

confidence: 99%

Peritumoural, but not intratumoural, lymphatic vessel density and invasion correlate with colorectal carcinoma poor-outcome markers

et al. 2007

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To evaluate whether lymphatic vessel density (LVD) and lymphatic vessel invasion (LVI) are useful markers of worse outcome in colorectal carcinoma and if LVD and LVI correlate to the classical clinical-pathological parameters, we analysed 120 cases of colorectal carcinomas selected from the files of Division of Pathology, Hospital das Clinicas, São Paulo University, Brazil. Assessment of LVD and LVI was performed by immunohistochemical detection of lymphatic vessels, using the monoclonal antibody D2-40. Higher LVD was found in the intratumoural area, when comparing with normal and peritumoural areas (p < 0.001). However, peritumoural LVD, but not intratumoural, correlated with both colonic-wall-invasion depth (p = 0.037) and liver metastasis (p = 0.012). Remarkably, LVI was found associated with local invasion (p = 0.016), nodal metastasis (p = 0.022) and hepatic metastasis (p < 0.001). Peritumoural LVD and LVI are directly related to histopathological variables indicative of poor outcome such as lymph-node status and liver metastasis.

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Section: Discussionmentioning

confidence: 99%

Peritumoural, but not intratumoural, lymphatic vessel density and invasion correlate with colorectal carcinoma poor-outcome markers

et al. 2007

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“…Once in the liver microvasculature, cancer cells encounter diverse cell types including liver sinusoid endothelial cells (LSEC), KC and hepatic natural killer cells (pit cells, NK) (21) (Figures 1 and 2). They may be rapidly eliminated through KC-mediated phagocytosis and NK-derived perforin and granzymes or through apoptosis induced by reactive oxygen species (ROS), nitric oxide (NO) interferon-γ (IFNγ) and tumor necrosis factor-α (TNFα).…”

Section: B Clinical-translational Advancesmentioning

confidence: 99%

Molecular Pathways: Targeting the Microenvironment of Liver Metastases

Milette

Sicklick

Lowy

et al. 2017

Clinical Cancer Research

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Curative treatment for metastatic solid cancers remains elusive. The liver, which is nourished by a rich blood supply from both the arterial and portal venous systems is the most common site of visceral metastases, particularly from cancers arising in the gastrointestinal (GI) tract, with colorectal cancer (CRC) being the predominant primary site in Western countries. A mounting body of evidence suggests that the liver microenvironment (LME) provides autocrine and paracrine signals originating from both parenchymal and non-parenchymal cells, that collectively create both pre-and pro-metastatic niches for the development of hepatic metastases. These resident cells and their molecular mediators represent potential therapeutic targets for the prevention and/or treatment of liver metastases (LM). This review summarizes: 1) the current therapeutic options for treating LM with a particular focus on CRC LM (CRCLM); 2) the role of the LME in LM at each of its phases 3) potential targets in the LME identified through pre-clinical and clinical investigations and 4) potential therapeutic approaches for targeting elements of the LME before and/or after the onset of LM, as the basis for future clinical trials.

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“…This can lead to further tumor cell damage and death due to the local release of nitric oxide (NO) and reactive oxygen species by HSEC and Kupffer cells (10,11). The release of NO and IFN-g by HSEC upon contact with metastasizing tumor cells can result in upregulation of FasL and subsequent apoptosis of an estimated 95% of tumor cells entering the sinusoids (12). The release of TNF-a in response to tumor infiltration can also cause tumor cells in the sinusoidal vessels to undergo apoptosis (13,14).…”

Section: Cells Of the Hepatic Sinusoid Can Kill Tumor Cellsmentioning

confidence: 99%

The Multifaceted Role of the Microenvironment in Liver Metastasis: Biology and Clinical Implications

et al. 2013

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The liver is host to many metastatic cancers, particularly colorectal cancer, for which the last 2 decades have seen major advances in diagnosis and treatment. The liver is a vital organ, and the extent of its involvement with metastatic disease is a major determinant of survival. Metastatic cells arriving in the liver via the bloodstream encounter the microenvironment of the hepatic sinusoid. The interactions of the tumor cells with hepatic sinusoidal and extrasinusoidal cells (endothelial, Kupffer, stellate, and inflammatory cells) determine their fate. The sinusoidal cells can have a dual role, sometimes fatal to the tumor cells but also facilitatory to their survival and growth. Adhesion molecules participate in these interactions and may affect their outcome. Bone marrowderived cells and chemokines also play a part in the early battle for survival of the metastases. Once the tumor cells have arrested and survived the initial onslaught, tumors can grow within the liver in 3 distinct patterns, reflecting differing host responses, mechanisms of vascularization, and proteolytic activity. This review aims to present current knowledge of the interactions between the host liver cells and the invading metastases that has implications for the clinical course of the disease and the response to treatment. Cancer Res; 73(7); 2031-43. Ó2013 AACR.

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The hepatic sinusoidal endothelial lining and colorectal liver metastases

Cited by 38 publications

References 27 publications

Peritumoural, but not intratumoural, lymphatic vessel density and invasion correlate with colorectal carcinoma poor-outcome markers

Peritumoural, but not intratumoural, lymphatic vessel density and invasion correlate with colorectal carcinoma poor-outcome markers

Molecular Pathways: Targeting the Microenvironment of Liver Metastases

The Multifaceted Role of the Microenvironment in Liver Metastasis: Biology and Clinical Implications

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