Impact of surgery and chemotherapy on von Willebrand factor and vascular endothelial growth factor levels in colorectal cancer

Gil-Bazo, Ignacio; Gonzalez, V.; Gutiérrez, Álvaro Alonso; Rodríguez, Javier; Fernández, J; Gómez, Jesús García; Lizoáin, José Luis Hernández; López, Jesús García

doi:10.1007/bf02708752

Cited by 18 publications

(15 citation statements)

References 26 publications

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“…In the entire cohort, levels of vascular markers soluble E selectin and vWf ( Gil-Bazo et al , 2005 ; Sato et al , 2010 ) both fell after surgery, probably reflecting less vascular perturbation resulting from a reduction in tumour load. However, in each of the three subgroups, differences were not marked, and there was no clear pattern, suggesting overtly damaging effect of standard chemotherapy with or without antiangiogenic therapy on the endothelium.…”

Section: Discussionmentioning

confidence: 93%

“…VEGF is a target of therapy for colorectal and many other forms of cancer ( Koutras et al , 2011 ), whereas raised angiogenin in colorectal cancer is associated with disease stage and outcome after surgery ( Shimoyama et al , 1999 ). Furthermore, there are several other lines of evidence of endothelial activity or perturbation in cancer, such as increased release of endothelial cell-specific molecules von Willebrand factor (vWf) and soluble E selectin into the plasma, as are present in colorectal cancer ( Gil-Bazo et al , 2005 ; Sata et al , 2010) .…”

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confidence: 99%

“…Standard treatment of cytotoxic chemotherapy alone has been challenged by the concurrent use of antiangiogenic therapy ( Hurwitz et al , 2004 ; Gil-Bazo et al , 2005 ; Fürstenberger et al , 2006 ; Koutras et al , 2011 ). We hypothesised that adding antiangiogenic therapy produces different responses in cellular (EPCs, CECs) and plasma (vWf, soluble E selectin) markers of vascular perturbation, and plasma growth factors (VEGF, angiogenin).…”

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confidence: 99%

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Effect of standard chemotherapy and antiangiogenic therapy on plasma markers and endothelial cells in colorectal cancer

et al. 2014

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Introduction:The importance of the endothelium in angiogenesis and cancer is undisputed, and its integrity may be assessed by laboratory markers such as circulating endothelial cells (CECs), endothelial progenitor cells (EPCs), plasma von Willebrand factor (vWf), soluble E selectin, vascular endothelial growth factor (VEGF) and angiogenin. Antiantigenic therapy may be added to standard cytotoxic chemotherapy as a new treatment modality. We hypothesised that additional antiangiogenic therapy acts in a contrasting manner to that of standard chemotherapy on the laboratory markers.Methods:We recruited 68 patients with CRC, of whom 16 were treated with surgery alone, 32 were treated with surgery followed by standard chemotherapy (5-flurouracil), and 20 were treated with surgery followed by standard chemotherapy plus anti-VEGF therapy (Avastin). Peripheral blood was taken before surgery, and again 3 months and 6 months later. CD34+/CD45−/CD146+ CECs and CD34+/CD45−/CD309[KDR]+ EPCs were measured by flow cytometry, plasma markers by ELISA.Results:In each of the three groups, CECs and EPCs fell at 3 months but were back at pre-surgery levels at 6 months (P<0.05). VEGF was lower in both 3-and 6-month samples in the surgery-only and surgery plus standard chemotherapy groups (P<0.05), but in those on surgery followed by standard chemotherapy plus anti-VEGF therapy, low levels at 3 months (P<0.01) increased to pre-surgery levels at 6 months. In those having surgery and standard chemotherapy, soluble E selectin was lower, whereas angiogenin was higher at 6 months than at baseline (both P<0.05).Conclusions:We found disturbances in endotheliod cells regardless of treatment, whereas VEGF returned to levels before surgery in those on antiangiogenic therapy. These observations may have clinical and pathophysiological implications.

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confidence: 93%

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Effect of standard chemotherapy and antiangiogenic therapy on plasma markers and endothelial cells in colorectal cancer

et al. 2014

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“…The plasma level of vWF is therefore a widely used marker for endothelial perturbation and propensity for thrombosis and thromboembolism 20 , 21 . Plasma vWF is significantly elevated in patients with cancer 15 , 22 – 25 . A high level of plasma vWF is associated not only with the development of cancer-associated thrombosis 26 , but also with the degree of malignancy, the rate of metastasis 27 , and cancer prognosis 28 , 29 .…”

Section: Introductionmentioning

confidence: 99%

“…A variable number of dimers then multimerize through N-terminal disulfide bonds 2 , 4 – 6 after the cleavage of a large propeptide 3 , 7 , 8 , 14 . Newly synthesized vWF multimers are either constitutively released or stored in the Weibel–Palade bodies of endothelial cells and in the α-granules of megakaryocytes and platelets 15 , 16 . The stored vWF is enriched in ultra-large multimers 17 and is released in response to inflammatory and ischemic injuries 18 , 19 .…”

Section: Introductionmentioning

confidence: 99%

Cancer cell-derived von Willebrand factor enhanced metastasis of gastric adenocarcinoma

Yang

Wang

et al. 2018

Oncogenesis

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Cancer prognosis is poor for patients with blood-borne metastasis. Platelets are known to assist cancer cells in transmigrating through the endothelium, but ligands for the platelet-mediated cancer metastasis remain poorly defined. von Willebrand factor (vWF) is a major platelet ligand that has been widely used as a biomarker in cancer and associated inflammation. However, its functional role in cancer growth and metastasis is largely unknown. Here we report that gastric cancer cells from patients and cells from two well-established gastric cancer lines express vWF and secrete it into the circulation, upon which it rapidly becomes cell-bound to mediate cancer-cell aggregation and interaction with platelets and endothelial cells. The vWF-mediated homotypic and heterotypic cell–cell interactions promote the pulmonary graft of vWF-overexpressing gastric cancer BGC823 cells in a mouse model. The metastasis-promoting activity of vWF was blocked by antibodies against vWF and its platelet receptor GP Ibα. It was also reduced by an inhibitory siRNA that suppresses vWF expression. These findings demonstrate a causal role of cancer-cell-derived vWF in mediating gastric cancer metastasis and identify vWF as a new therapeutic target.

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5-Fluorouracil-based therapy induces endovascular injury having potential significance to development of clinically overt cardiotoxicity

Jensen

Sørensen

2011

Cancer Chemother Pharmacol

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Impact of surgery and chemotherapy on von Willebrand factor and vascular endothelial growth factor levels in colorectal cancer

Abstract: There was a strong correlation between higher vWf levels and more advanced CRC stage at diagnosis. These levels were elevated post-surgery in patients with locally advanced CRC. Chemotherapy significantly decreased VEGF in metastatic CRC patients before CEA showed any significant change.

Cited by 18 publications

References 26 publications

Effect of standard chemotherapy and antiangiogenic therapy on plasma markers and endothelial cells in colorectal cancer

Effect of standard chemotherapy and antiangiogenic therapy on plasma markers and endothelial cells in colorectal cancer

Cancer cell-derived von Willebrand factor enhanced metastasis of gastric adenocarcinoma

5-Fluorouracil-based therapy induces endovascular injury having potential significance to development of clinically overt cardiotoxicity

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