β‐thromboglobulin in patents with breast cancer

Ferriere, J. P.; Bernard, Dominique; Legros, Michel; Chassagne, J; Chollet, Philippe; Gaillard, G; Plagne, R

doi:10.1002/ajh.2830190107

Cited by 20 publications

(13 citation statements)

References 18 publications

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“…Levels of β-thromboglobulin were significantly elevated, e.g. in prostatic cancer (Yazaki et al, 1987), in breast cancer (Ferriere et al, 1985) and in small-cell lung cancer (Milroy et al, 1988), compared with those of healthy individuals. VEGF appears to be released by activated platelets together with β-thromboglobulin, suggesting that VEGF is located in the α-granules of platelets (Möhle et al, 1997;Wartiovaara et al, 1998).…”

Section: Discussionmentioning

confidence: 91%

Platelet number and interleukin-6 correlate with VEGF but not with bFGF serum levels of advanced cancer patients

Salgado¹,

Vermeulen

Benoy³

et al. 1999

Br J Cancer

149

109

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SummaryWe have compared the platelet number and the serum concentration of vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF) and interleukin-6 (IL-6) in 80 blood samples of 50 patients with advanced cancer. We have also measured the mitogenic effect of patient sera on endothelial cells in vitro in order to estimate the biological activity of serum VEGF. Serum VEGF concentration correlated with platelet number (r = 0.61; P < 10 -4 ). Serum IL-6 levels correlated with platelet count (r = 0.36; P < 10 -3 ), with serum VEGF levels (r = 0.55; P < 10 -4 ) and with the calculated load of VEGF per platelet (r = 0.4; P = 3 × 10 -4 ). Patients with thrombocytosis had a median VEGF serum concentration which was 3.2 times higher (P < 10 -4 ) and a median IL-6 serum level which was 5.8 times higher (P = 0.03) than in other patients. Serum bFGF did not show an association with any of the other parameters. Patient sera with high VEGF and bFGF content stimulated endothelial cell proliferation significantly more than other sera (P = 4 × 10 -3 ). These results support the role of platelets in the storage of biologically active VEGF. Platelets seem to prevent circulating VEGF from inducing the development of new blood vessels except at sites where coagulation takes place. IL-6, besides its thrombopoietic effect, also seems to affect the amount of VEGF stored in the platelets. This is in accordance with the indirect angiogenic action of IL-6 reported previously. The interaction of IL-6 with the angiogenic pathways in cancer might explain the stimulation of tumour growth occasionally observed during IL-6 administration. It also conforms to the worse outcome associated with high IL-6 levels and with thrombocytosis in several tumour types and benign angiogenic diseases.

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Section: Discussionmentioning

confidence: 91%

Platelet number and interleukin-6 correlate with VEGF but not with bFGF serum levels of advanced cancer patients

Salgado¹,

Vermeulen

Benoy³

et al. 1999

Br J Cancer

149

109

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“…Since that time, numerous studies have contributed to our understanding of the role of platelets in multiple steps in breast cancer progression. Platelet roles in breast cancer progression, including increased survival of disseminated cancer cells within the circulation, tumor cell adhesion to the endothelium, extravasation into the parenchyma of distant tissues, and ultimately the growth of tumor cells at meta-static sites, are reviewed below [5,9,12-17]. …”

Section: Platelets and Breast Cancermentioning

confidence: 99%

“…At least two markers of platelet activation - B-thromboglobulin and P-selectin - are increased in the blood of patients with breast cancer, suggesting that ongoing platelet activation occurs in these patients [5,16]. One mechanism of platelet activation is tumor cell-induced platelet aggregation (TCIPA).…”

Section: Platelet Activationmentioning

confidence: 99%

Platelets, coagulation and fibrinolysis in breast cancer progression

2013

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The progression of breast cancer from early-stage to metastatic disease results from a series of events during which malignant cells invade and travel within the bloodstream to distant sites, leading to a clonogenic accumulation of tumor cells in non-breast tissue. While mechanistically complex, an emerging literature supports hemostatic elements as an important patient factor that facilitates the metastatic potential of breast cancer. Hemostatic elements involved include platelets, coagulation, and fibrinolysis. Key steps in breast tumor progression, including cellular transformation, proliferation, tumor cell survival, and angiogenesis, can be mediated by components of the hemostatic system. Thus, the hemostatic system provides potential targets for novel therapeutic approaches to breast cancer therapy with drugs in current use and in development. The present article provides a comprehensive overview of the evidence and mechanisms supporting the roles played by platelets, coagulation activation, and the fibrinolytic system in breast cancer progression.

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“…However, cardioembolic strokes were no more common in our case patients than would be expected in the general population, making this explanation unlikely. Chemotherapy agents may accelerate development of atherosclerotic disease as a result of altered coagulation, vasospasm, and endothelial damage (20,(22)(23)(24). Furthermore, agents used in conjunction with chemotherapy, such as erythropoietin, might somehow increase stroke risk (25).…”

Section: ) (5)mentioning

confidence: 99%

Stroke Risk and Tamoxifen Therapy for Breast Cancer

Geiger¹,

Fischberg²,

Chen³

et al. 2004

JNCI Journal of the National Cancer Institute

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Background: Tamoxifen, which is used widely to treat, and increasingly to prevent, breast cancer, has been associated with increased risk of stroke. We assessed the impact of tamoxifen treatment for breast cancer on the risk of stroke, considering dose, duration, and recency of use of tamoxifen and known stroke risk factors. Methods: We conducted a nested case-control study of stroke after breast cancer among female Los Angeles County residents enrolled in a large health maintenance organization when diagnosed with breast cancer between January 1, 1980, and July 1, 2000. We obtained information on breast cancer treatment and stroke risk factors through medical record review and telephone interviews. The association (odds ratio [OR] and 95% confidence interval [CI]) between tamoxifen and stroke risk was determined by using a conditional logistic regression model, adjusting for menopausal status and history of hypertension and diabetes. All statistical tests were two-sided. Results: Of 11 045 women with breast cancer, 179 met stroke eligibility criteria and were individually matched to two stroke-free control subjects with breast cancer on age and year of breast cancer diagnosis. The mean age at breast cancer diagnosis was 66.6 years (standard deviation [SD] ‫؍‬ 12.3 years), and the mean at-risk period (i.e., the time between breast cancer diagnosis and first stroke or comparable time period for control subjects) was 5.7 years (SD ‫؍‬ 4.5 years). Tamoxifen use was not associated with risk of stroke, either overall (OR ‫؍‬ 1.0, 95% CI ‫؍‬ 0.6 to 1.6) or in subgroups defined by duration, dose, or recency of use. Chemotherapy, but not a specific chemotherapy regimen, was associated with an increased risk of stroke, regardless of tamoxifen use (no tamoxifen use, OR ‫؍‬ 2.8, 95% CI ‫؍‬

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β‐thromboglobulin in patents with breast cancer

Cited by 20 publications

References 18 publications

Platelet number and interleukin-6 correlate with VEGF but not with bFGF serum levels of advanced cancer patients

Platelet number and interleukin-6 correlate with VEGF but not with bFGF serum levels of advanced cancer patients

Platelets, coagulation and fibrinolysis in breast cancer progression

Stroke Risk and Tamoxifen Therapy for Breast Cancer

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