Publications by authors named "Paul S Stonelake"

Background: Circulating endothelial cells (CECs), endothelial progenitor cells (EPCs), Willebrand factor (vWf), soluble E-selectin, vascular endothelial growth factor (VEGF) and angiogenin are of interest in cancer vascular biology. However, few studies have looked at more than one in combination. We set out to determine which would be best in predicting the Dukes' and American Joint Committee on Cancer (AJCC) scores in colorectal cancer patients.

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As the importance of the endothelium is becoming increasingly recognised, additional tools are needed to assess its functions. Separate studies have looked at different aspects of vascular biology primarily focusing on the central role of the endothelium, i.e.

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Background: Seromas constitute a common complication following surgery for breast cancer, and closed drainage is used routinely to reduce its incidence. The aim of this study was to evaluate the influence of number of drains on patient discomfort, seroma formation, and hospital stay during the immediate postoperative period after mastectomy for breast cancer.

Patients And Methods: Based on a retrospective review of our clinical database, 110 consecutive patients from January 2004 through January 2006 who had undergone a mastectomy and axillary clearance for breast cancer were sent a simple postal questionnaire for collection of data.

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Background And Methods: Abnormal circulating endothelial cell (CEC) and circulating progenitor cell (CPC) numbers are present in cancer, but their relationship with angiogenesis, apoptosis, vascular biology, and prognosis is unclear. We prospectively studied 160 patients with breast cancer and 63 age-matched controls free of breast cancer, measuring CECs (CD45(-)/CD146(+)/CD34(+)) and CPCs (CD45(-)/CD133(+)/CD34(+)) by flow cytometry and plasma markers of endothelial damage/dysfunction (von Willebrand factor), apoptosis (Fas/Fas-L) and angiogenesis (vascular endothelial growth factor [VEGF], angiogenin) by ELISA. These were compared with clinicopathophysiologic features and the Nottingham Prognostic Index (NPI).

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Background: Over-expression of angiogenic growth factors and their receptors, and high levels of these molecules in the blood, are a common feature of cancer although the relationships between cell expression and plasma levels are unknown. We hypothesized a significant correlation between the expression and cellular distribution of vascular endothelial growth factor (VEGF), its receptor Flt-1, and the angiopoietin receptor Tie-2 with levels of these molecules in the plasma.

Methods: The tissue expression of VEGF, Flt-1, and Tie-2 were investigated by immunohistochemistry, and plasma levels assessed by enzyme-linked immunosorbent assay in 36 patients with breast cancer and 15 with benign breast disease.

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The link between cancer, hypertension and anti-hypertensive drug treatment is controversial. Despite numerous studies looking either directly or indirectly at cancer and hypertension, the results are often conflicting and do little to answer the dominant questions of cause and effect. Also, the treatment of hypertension has continued to evolve, with newer therapies being made available including angiotensin-converting enzyme inhibitors.

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Background: Vascular endothelial growth factor (VEGF), a major angiogenic growth factor, is involved in the pathogenesis of cancer. Plasma VEGF is raised in breast cancer and falls after successful surgery. Less is known about angiopoietins 1 and 2 (Ang-1, Ang-2).

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Mature circulating endothelial cells (CECs) are novel cellular markers of endothelial damage/dysfunction. The two main techniques of CEC enumeration are flow cytometry (FC) and immunomagnetic bead (IB) isolation. Both quantify CECs accurately, but a direct comparison of both methods has not been reported.

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Cancer is a disease largely dependent on neoangiogenesis. Cancer neoangiogenesis is often disordered and abnormal, with evidence of coexisting vascular endothelial dysfunction. A novel method of assessing vascular endothelial function in cancer is via the quantification of circulating endothelial cells (CEC).

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The increased risk of thromboembolism in cancer may be related to a prothrombotic or hypercoagulable state, with abnormalities of haemostasis and platelet activation. To further investigate the role of platelets in this disease, we developed and applied a new assay to detect and quantify platelet adhesion to the well-defined subendothelial substrate, fibrinogen. Platelet-rich plasma was obtained from 31 females with breast cancer (13 metastatic, 18 benign), and 30 healthy female controls, re-suspended to 2 x 10(8) cells/ml and 100 microl and incubated for 1 h in microtitre plates pre-coated with fibrinogen (5 mg/ml).

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In health, haemostasis and angiogenesis are tightly regulated processes, but may become deregulated in cancer. Recent evidence suggests that platelet activation may link these processes as platelets can release angiogenic factors such as vascular endothelial growth factor (VEGF). Furthermore, inflammation has also been implicated in regulating both coagulation and angiogenesis, possibly by activating platelets directly and increasing, for example, plasma fibrinogen.

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Patients with cancer are highly susceptible to thromboembolic complications, which account for a significant percentage of the morbidity and mortality of the disease. Up to 15% of patients with clinically overt cancer present with venous thromboembolism during the course of their disease. Moreover, patients with cancer represent 20% of all patients in whom deep venous thrombosis and pulmonary embolism are diagnosed.

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A hypercoagulable or prothrombotic state of malignancy occurs due to the ability of tumor cells to activate the coagulation system. It has been estimated that hypercoagulation accounts for a significant percentage of mortality and morbidity in cancer patients. Prothrombotic factors in cancer include the ability of tumor cells to produce and secrete procoagulant/fibrinolytic substances and inflammatory cytokines, and the physical interaction between tumor cell and blood (monocytes, platelets, neutrophils) or vascular cells.

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