Tumor-Cell Homing to Lymph Nodes and Bone Marrow and CXCR4 Expression in Esophageal Cancer

Kaifi, Jussuf T.; Yekebas, Emre F.; Schurr, Paulus; Obonyo, Dennis; Wachowiak, Robin; Busch, Philipp; Heinecke, Antje; Pantel, Klaus; Izbicki, Jakob R.

doi:10.1093/jnci/dji431

Cited by 194 publications

(160 citation statements)

References 37 publications

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“…The CXCR4 protein has multiple essential functions, including homing of stem cells and metastasis of cancer cells (Miki et al, 2007). Several cancers express CXCR4, and a relationship between CXCR4 expression and malignant potentiality has been suggested (Muller et al, 2001;Kaifi et al, 2005). In the present study, 85% of specimens exhibited positive expression of CXCR4.…”

Section: Discussionsupporting

confidence: 50%

CD133 expression is correlated with lymph node metastasis and vascular endothelial growth factor-C expression in pancreatic cancer

et al. 2008

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Although CD133 has been shown to be a marker for cancer stem cells in various tumours, its expression in pancreatic cancer has not yet been clinically reported. In this study, we investigated the relationship between CD133 expression and clinicopathological factors in pancreatic cancer. Pancreatic head carcinoma specimens from 80 patients who underwent surgical resection were immunohistochemically assessed for CD133, vascular endothelial growth factor (VEGF)-C, CXCR4, CD34, Ki-67, and cytokeratin (CK) expressions. Sixty percentage (48/80) of specimens were CD133-positive, with less than 15% cells per specimen expressing the marker. CD133-positive cells were found at the peripheral site of adenocarcinoma glandular structures and were negative for CK. There was a significant correlation between CD133 expression and clinicopathological factors, including histological type, lymphatic invasion, and lymph node metastasis (P ¼ 0.0215, 0.0023, and 0.0024, respectively). Vascular endothelial growth factor-C expression was also significantly correlated with CD133 expression (P ¼ 0.0002). Consequently, the 5-year survival rate of CD133-positive patients was significantly lower than that of CD133-negative patients (P ¼ 0.0002) and multivariate analysis revealed that CD133 expression was an independent prognostic factor (P ¼ 0.0103). These results suggest that CD133 expression in pancreatic cancer was significantly associated with lymphatic metastasis, VEGF-C expression, and prognosis.

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Section: Discussionsupporting

confidence: 50%

CD133 expression is correlated with lymph node metastasis and vascular endothelial growth factor-C expression in pancreatic cancer

et al. 2008

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“…Cabioglu et al [11] reported a positive correlation between the presence of cytokeratinexpressing tumor cells in the bone marrow and CXCR4 expression by primary breast tumors (p ϭ .01). Furthermore, Kaifi et al [10] reported similar results in 136 patients with [20]. Interestingly, the loss of CD24 expression, a heavy glycosylated cell-surface protein, has been found to be associated with greater CXCR4 function, suggesting an important regulatory function in chemotaxis and migration of cancer cells [21].…”

Section: Discussionmentioning

confidence: 77%

“…In preclinical studies, CXCR4 has been shown to mediate lung [6] and bone [8] metastasis. In human models, studies have suggested that CXCR4 expression could correlate with human epidermal growth factor receptor (HER)-2 expression in breast cancer patients [9], and could be associated with the development of lung metastases [9], liver metastases [7], or bone marrow micrometastases [10,11] in both breast and esophageal cancers. In addition to being involved in cell homing, CXCR4 activation by SDF-1 appears to mediate tumor cell proliferation, migration, invasion, and adhesion [9,12].…”

Section: Introductionmentioning

confidence: 99%

CXCR4 Expression in Early Breast Cancer and Risk of Distant Recurrence

et al. 2009

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After completing this course, the reader will be able to:1. Assess CXCR4 expression in the primary tumor for use as an indicator of a higher risk for bone metastasis in early breast cancer.2. Evaluate the relationship between CXCR4 expression and the occurrence of metastases in other SDF-1-producing organs, including the liver and lung.3. Use CXCR4 in different ways in combination with other markers to identify patients to be screened for bony metastases and/or treated preventatively for bone metastasis.This article is available for continuing medical education credit at CME.TheOncologist.com. CME CME ABSTRACTBackground. Chemokine receptor 4 (CXCR4) has been demonstrated to have a critical role in the early metastatic process. The aim of this study was to eval-

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“…For example, the chemokine receptor CXCR4 and its ligand CXCL12 are important for cell movement in both homeostatic and disease states 63 . CXCR4 is frequently expressed by malignant cells 16 , and the amount of CXCR4 expressed by primary human tumours correlates with the extent to which metastasis to the lymph nodes occurs in colorectal, breast, liver and oesophageal cancer [64][65][66] . Other functional chemokine receptors (including CX 3 Cchemokine receptor 1 (CX 3 CR1), CC-chemokine receptor 1 (CCR1), CCR7, CCR9, CCR10, CXCR1, CXCR2, CXCR3, CXCR5 and CXCR7) are also expressed by malignant cells from a variety of tissues and are implicated in organ-specific metastasis [67][68][69][70][71][72] ; for example, the expression of CCR7 correlates with lymph-node metastasis, and expression of CCR9 with metastasis of melanoma to the small intestine.…”

Section: Inflammatory Pathways In Invasion and Metastasismentioning

confidence: 99%

Cancer-related inflammation

Mantovani

Allavena

Sica

et al. 2008

Nature

9,943

112

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Links between cancer and inflammation were first made in the nineteenth century, on the basis of observations that tumours often arose at sites of chronic inflammation and that inflammatory cells were present in biopsied samples from tumours 1 . The idea that these processes are connected was out of favour for more than a century, but there has been a recent resurgence in interest. Several lines of evidence 1-4 (Box 1) -based on a range of findings, from epidemiological studies of patients to molecular studies of genetically modified mice -have led to a general acceptance that inflammation and cancer are linked.Epidemiological studies have shown that chronic inflammation predisposes individuals to various types of cancer. It is estimated that underlying infections and inflammatory responses are linked to 15-20% of all deaths from cancer worldwide 1 . There are many triggers of chronic inflammation that increase the risk of developing cancer. Such triggers include microbial infections (for example, infection with Helicobacter pylori is associated with gastric cancer and gastric mucosal lymphoma), autoimmune diseases (for example, inflammatory bowel disease is associated with colon cancer) and inflammatory conditions of unknown origin (for example, prostatitis is associated with prostate cancer). Accordingly, treatment with non-steroidal anti-inflammatory agents decreases the incidence of, and the mortality that results from, several tumour types [5][6][7] .The hallmarks of cancer-related inflammation include the presence of inflammatory cells and inflammatory mediators (for example, chemokines, cytokines and prostaglandins) in tumour tissues, tissue remodelling and angiogenesis similar to that seen in chronic inflammatory responses, and tissue repair. These signs of 'smouldering' inflammation 2 are also present in tumours for which a firm causal relationship to inflammation has not been established (for example, breast tumours). Indeed, inflammatory cells and mediators are present in the microenvironment of most, if not all, tumours, irrespective of the trigger for development.Studies of genetically modified mice, adoptive-transfer experiments in mice, and analyses of human tumours have allowed researchers to begin to unravel the molecular pathways that link inflammation and cancer. Here we review current knowledge of the molecular and cellular pathways that link inflammation and cancer, and we describe how these pathways suppress effective antitumour immunity during tumour progression. We also discuss how cancer-related inflammation affects many aspects of malignancy, including the proliferation and survival of malignant cells, angiogenesis (which is required for the survival of cells within tumours of a certain size), tumour metastasis, and tumour response to chemotherapeutic drugs and hormones.Advances in understanding the genetic pathways involved in cancer have led to the development of a range of therapies that target malignant cells. Understanding the pathways involved in cancer-related inflammation could ...

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Tumor-Cell Homing to Lymph Nodes and Bone Marrow and CXCR4 Expression in Esophageal Cancer

Cited by 194 publications

References 37 publications

CD133 expression is correlated with lymph node metastasis and vascular endothelial growth factor-C expression in pancreatic cancer

CD133 expression is correlated with lymph node metastasis and vascular endothelial growth factor-C expression in pancreatic cancer

CXCR4 Expression in Early Breast Cancer and Risk of Distant Recurrence

Cancer-related inflammation

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