10 The importance of blood cell-vessel wall interactions in tumour metastasis

Poggi, Andreina; Stella, Manuela; Donati, Maria Benedetta

doi:10.1016/s0950-3536(05)80196-9

Cited by 27 publications

(12 citation statements)

References 97 publications

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“…Platelets may play a role in promoting metastasis through the selective release of key growth factors (e.g., vascular endothelium growth factor (VEGF; TGF β ; PDGF) and metalloproteases (MMPs)) at sites of CTC adhesion to the endothelium (56–58). Once released from platelet α-granules, MMPs will degrade specific components of the extracellular matrix (ECM), increasing vascular permeability and the extravasation of CTCs, as well as the release of growth factors sequestered in the ECM (59).…”

Section: The Cross-talk Between the Hemostatic And The Malignant Smentioning

confidence: 99%

The prothrombotic activity of cancer cells in the circulation

et al. 2016

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The hemostatic system is often subverted in patients with cancer, resulting in life-threatening venous thrombotic events. Despite the multifactorial and complex etiology of cancer-associated thrombosis, changes in the expression and activity of cancer-derived tissue factor (TF) – the principle initiator of the coagulation cascade – are considered key to malignant hypercoagulopathy and to the pathophysiology of thrombosis. However, many of the molecular and cellular mechanisms coupling the hemostatic degeneration to malignancy remain largely uncharacterized. In this review we discuss some of the tumor-intrinsic and tumor-extrinsic mechanisms that may contribute to the prothrombotic state of cancer, and we bring into focus the potential for circulating tumor cells (CTCs) in advancing our understanding of the field. We also summarize the current status of anti-coagulant therapy for the treatment of thrombosis in patients with cancer.

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Section: The Cross-talk Between the Hemostatic And The Malignant Smentioning

confidence: 99%

The prothrombotic activity of cancer cells in the circulation

et al. 2016

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“…The disintegrin function probably relates to cell-to-cell and cell-toextracellular matrix (ECM) adhesive interactions and transduction of signals from the ECM to the cell interior and vice versa. It may be involved in cell migration, invasion, intra-and extravasation and platelet interaction (Poggi et al, 1993;Mizejewski, 1999).…”

Section: Adam9 Expression In Pancreatic Cancermentioning

confidence: 99%

ADAM9 expression in pancreatic cancer is associated with tumour type and is a prognostic factor in ductal adenocarcinoma

et al. 2004

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Gene expression profiling revealed ADAM9 to be distinctly overexpressed in pancreatic ductal adenocarcinoma (PDAC). We examined the relevance of ADAM9 expression in PDAC diagnosis and prognosis. A total of 59 infiltrating PDACs, 32 specimens from patients with chronic pancreatitis, 11 endocrine tumours and 24 acinar cell carcinomas were immunohistochemically analysed for ADAM9 expression. Staining for ADAM9 was detected in 58 out of 59 (98.3%) PDACs and in two out of 24 (8.3%) acinar cell carcinomas, but not in endocrine tumours. In the non-neoplastic pancreas, whether normal or chronically inflamed, ADAM9 was expressed in centroacinar and intralobular duct cells, but not in interlobular duct cells and their hyperplastic lesions. Pancreatic ductal adenocarcinomas showing cytoplasmic ADAM9 expression correlated with poor tumour differentiation and also with shorter overall survival than in cases showing only an apical membranous staining pattern (P ¼ 0.001). Multivariate analysis identified cytoplasmic ADAM9 expression as an independent marker of shortened survival in a set of 42 curatively (R0) resected PDAC (Po0.05, hazard ratio 2.85, 95% confidence interval: 1.21 -6.71). The results show that ADAM9 expression distinguishes PDACs from other solid pancreatic tumours. In addition, cytoplasmic ADAM9 overexpression is associated with poor differentiation and shortened survival. Therefore, ADAM9 overexpression might contribute to the aggressiveness of PDACs.

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“…The changes induced by cytokines on the vascular wall do not only lead to a prothrombotic state, but they may also contribute to the enhancement of the metastatic potential through changes in the adhesion molecules of endothelial cells which become more capable of attracting tumor cells and supporting their extravasation [74, 75]. …”

Section: Pathogenetic Mechanismsmentioning

confidence: 99%

Pathogenetic Mechanisms of Thrombosis in Malignancy

Donati¹,

Falanga

2001

Acta Haematol

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The interactions between components of the hemostatic system and cancer cells are multifaceted. Strong clinical evidence is accumulating on the prothrombotic tendency of cancer patients, which is enhanced by anticancer therapy, such as surgery and chemotherapy. The mechanisms of thrombus promotion in malignancy include some general responses of the host to the tumor (acute phase, inflammation, angiogenesis) and specific interactions of tumor cells with the clotting/fibrinolysis systems and with blood (leukocytes, platelets) or vascular cells. It is at present difficult to rank the relative weight of these multiple interactions on the basis of the well-recognized clinical evidence of enhanced thrombotic episodes in tumor patients. In any case, the mechanisms explored so far offer a sound experimental basis for prevention/treatment of thrombosis in tumor patients and leave open the possibility that some antithrombotic strategies may also affect the processes of tumor growth and dissemination.

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10 The importance of blood cell-vessel wall interactions in tumour metastasis

Cited by 27 publications

References 97 publications

The prothrombotic activity of cancer cells in the circulation

The prothrombotic activity of cancer cells in the circulation

ADAM9 expression in pancreatic cancer is associated with tumour type and is a prognostic factor in ductal adenocarcinoma

Pathogenetic Mechanisms of Thrombosis in Malignancy

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