Expression of VCAM‐1, ICAM‐1, E‐ and P‐selectin and tumour‐associated macrophages in renal cell carcinoma

Hemmerlein, Bernhard; Scherbening, J; Kugler, A.; Hj, Radzun

doi:10.1046/j.1365-2559.2000.00933.x

Cited by 45 publications

(27 citation statements)

References 12 publications

(23 reference statements)

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“…Subsequently, other studies have reported the direct role of ICAM-1 in the adhesion of myeloid cells to dermal fibroblasts (127). Other authors have linked the increased expression of ICAM-1 with the infiltration of TAMs in renal carcinoma (128). Furthermore, this ICAM-1-mediated infiltration was also augmented in pancreatic cancer and correlated with the formation of precancerous lesions (105).…”

Section: Tumor Cell Extravasation: Opening the Liver's Doors To Invadmentioning

confidence: 95%

Role of liver ICAM-1 in metastasis

2017

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Abstract. Intercellular adhesion molecule (ICAM)-1, is a transmembrane glycoprotein of the immunoglobulin (Ig)-like superfamily, consisting of five extracellular Ig-like domains, a transmembrane domain and a short cytoplasmic tail. ICAM-1 is expressed in various cell types, including endothelial cells and leukocytes, and is involved in several physiological processes. Furthermore, it has additionally been reported to be expressed in various cancer cells, including melanoma, colorectal cancer and lymphoma. The majority of studies to date have focused on the expression of the ICAM-1 on the surface of tumor cells, without research into ICAM-1 expression at sites of metastasis. Cancer cells frequently metastasize to the liver, due to its unique physiology and specialized liver sinusoid capillary network. Liver sinusoidal endothelial cells constitutively express ICAM-1, which is upregulated under inflammatory conditions. Furthermore, liver ICAM-1 may be important during the development of liver metastasis. Therefore, it is necessary to improve the understanding of the mechanisms mediated by this adhesion molecule in order to develop host-directed anticancer therapies.

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Section: Tumor Cell Extravasation: Opening the Liver's Doors To Invadmentioning

confidence: 95%

Role of liver ICAM-1 in metastasis

2017

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“…VCAM-1, which binds ␣ 4 ␤ 1 and members of the ␤ 2 integrin family, is present on endothelium typically upon activation (expression induced by inflammatory cytokines) and is involved in the slow rolling of monocytes and lymphocytes during inflammatory cell recruitment. VCAM-1 has been indicated as an important molecule for the vascularization of tumors, through observation of microvascular density, protein expression, and VCAM-1 serum concentrations in cancer patients (43,60). Additionally, VCAM-1 is essential for activation of B cells, which release many proangiogenic molecules (27).…”

Section: Angiogenic Mediators In Ibd and Experimental Colitismentioning

confidence: 99%

Pathogenic angiogenesis in IBD and experimental colitis: new ideas and therapeutic avenues

Chidlow

Shukla²,

Grisham³

et al. 2007

American Journal of Physiology-Gastrointestinal and Liver Physi

143

114

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Chidlow JH Jr, Shukla D, Grisham MB, Kevil CG. Pathogenic angiogenesis in IBD and experimental colitis: new ideas and therapeutic avenues. Am J Physiol Gastrointest Liver Physiol 293: G5-G18, 2007. First published April 26, 2007; doi:10.1152/ajpgi.00107.2007.-Angiogenesis is now understood to play a major role in the pathology of chronic inflammatory diseases and is indicated to exacerbate disease pathology. Recent evidence shows that angiogenesis is crucial during inflammatory bowel disease (IBD) and in experimental models of colitis. Examination of the relationship between angiogenesis and inflammation in experimental colitis shows that initiating factors for these responses simultaneously increase as disease progresses and correlate in magnitude. Recent studies show that inhibition of the inflammatory response attenuates angiogenesis to a similar degree and, importantly, that inhibition of angiogenesis does the same to inflammation. Recent data provide evidence that differential regulation of the angiogenic mediators involved in IBD-associated chronic inflammation is the root of this pathological angiogenesis. Many factors are involved in this phenomenon, including growth factors/cytokines, chemokines, adhesion molecules, integrins, matrix-associated molecules, and signaling targets. These factors are produced by various vascular, inflammatory, and immune cell types that are involved in IBD pathology. Moreover, recent studies provide evidence that antiangiogenic therapy is a novel and effective approach for IBD treatment. Here we review the role of pathological angiogenesis during IBD and experimental colitis and discuss the therapeutic avenues this recent knowledge has revealed. inflammation; T cells; growth factors; adhesion molecules; antiangiogenesis ANGIOGENESIS PLAYS AN IMPORTANT role in many chronic inflammatory diseases including but not limited to diabetic retinopathy, atherosclerosis, rheumatoid arthritis, hypercholesterolemia, and psoriasis. It has been suggested that the angiogenic components of these diseases contribute to and exacerbate disease conditions (26, 31). Recent findings, both clinical and experimental, indicate that angiogenesis also plays a crucial role in the inflammatory bowel diseases (IBD), consisting of Crohn's disease (CD) and ulcerative colitis (UC) (31,37,58,131,155). Development of new vasculature during chronic inflammation may play a negative "pathological" role by contributing to increased inflammatory responses due to dysfunctional new vessel architecture and increases in the recruitment of inflammatory cell types. Importantly, recent data have shown that angiogenic inhibition during chronic inflammatory diseases attenuates further inflammation and disease pathology (31, 37, 51). As such, expanding our knowledge of how pathological angiogenesis occurs during IBD will further our ability to treat patients with these diseases. IBD PathogenesisCD and UC are idiopathic inflammatory disorders of the intestine and/or colon in which patients suffer from rectal bleeding, severe...

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“…It is interesting that, in clear cell RCC, increased VCAM1 protein is observed primarily in cancer cells rather than in vascular endothelial cells by immunohistochemistry (13,35,36). In renal proximal tubular epithelial cells, which are considered to be a precursor to clear cell and papillary RCCs, VCAM1 remains at almost undetectable levels under normal conditions (13,35,36), although it has been induced in these cells under various pathologic conditions, such as acute renal allograft rejection, systemic lupus erythematosus, and glomerulonephritides (37 -39). VCAM1 binds to a 4 h 1 and a 4 h 7 integrins constitutively expressing on lymphocytes and macrophages and is responsible for adhering and recruiting these leukocytes to sites of active inflammation (40).…”

Section: Vcam1 As a Prognosticmentioning

confidence: 99%

Vascular Cell Adhesion Molecule 1 Predicts Cancer-Free Survival in Clear Cell Renal Carcinoma Patients

Shioi

Komiya

Hattori

et al. 2006

Clinical Cancer Research

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Purpose: Vascular cell adhesion molecule 1 (VCAM1) is a cell surface glycoprotein implicated in various pathophysiologic conditions.We measured VCAM1 expression levels in tumor tissues and evaluated its significance and prognostic use in renal cell carcinoma (RCC). Experimental Design: We used real-time quantitative PCR to examine the VCAM1 expression levels of a total of 485 sporadic renal tumors, including 429 clear cell, 21 papillary, 17 chromophobe, 11 oncocytomas, and 7 collecting duct carcinomas. We retrospectively examined the relationship of this expression to various clinicopathologic variables and the von Hippel-Lindau alteration status. We evaluated its significance with respect to patient survival rates using the Cox regression model combined with the split-sample method. Results: Compared with normal kidney samples (n = 43),VCAM1 was significantly up-regulated in clear cell RCC and papillary RCC, whereas it was down-regulated in chromophobe RCC and oncocytoma. In clear cell RCC, VCAM1 expression levels were apparently high in patients asymptomatic at presentation and in patients with small tumor size, low-stage, low-grade, microvascular invasion^negative, and von Hippel-Lindau alteration-positive tumors. Univariate analyses showed that VCAM1 high expression is strongly associated with better outcomes in clear cell and papillary RCCs. Further, Cox multivariate analysis models combined with the split-sample method revealed that this association is significant only in cancer-free survival for patients with clear cell RCC after curative surgical resection. Conclusions: VCAM1 expression levels were found to be histologically subtype specific in renal tumors. Determination of theVCAM1 expression level as a biomarker can provide useful prognostic information for patients with clear cell RCC.

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Expression of VCAM‐1, ICAM‐1, E‐ and P‐selectin and tumour‐associated macrophages in renal cell carcinoma

Cited by 45 publications

References 12 publications

Role of liver ICAM-1 in metastasis

Role of liver ICAM-1 in metastasis

Pathogenic angiogenesis in IBD and experimental colitis: new ideas and therapeutic avenues

Vascular Cell Adhesion Molecule 1 Predicts Cancer-Free Survival in Clear Cell Renal Carcinoma Patients

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