Studies on platelet function in patients with prostatic cancer

Yazaki, Tsunetada; Inage, H; Iizumi, Takashi; Kôyama, Akio; Kanoh, Shori; Koiso, Kenkichi; Narita, Mitsuharu; Tojo, Shizuo

doi:10.1016/0090-4295(87)90574-7

Cited by 14 publications

(6 citation statements)

References 8 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: 98%

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

147

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: 98%

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

147

109

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“…Several studies have suggested an increase in platelet activation in the blood of patients with cancer [13–19]. Both tumor secretion of activators and direct contact with tumors have been related to this platelet activation [20–22].…”

Section: Platelet Structure and Functionmentioning

confidence: 99%

The platelet contribution to cancer progression

Bambace

Holmes

2011

Journal of Thrombosis and Haemostasis

579

487

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Summary. Traditionally viewed as major cellular components in hemostasis and thrombosis, the contribution of platelets to the progression of cancer is an emerging area of research interest. Complex interactions between tumor cells and circulating platelets play an important role in cancer growth and dissemination, and a growing body of evidence supports a role for physiologic platelet receptors and platelet agonists in cancer metastases and angiogenesis. Platelets provide a procoagulant surface facilitating amplification of cancer-related coagulation, and can be recruited to shroud tumor cells, thereby shielding them from immune responses, and facilitate cancer growth and dissemination. Experimental blockade of key platelet receptors, such as GP1b/IX/V, GPIIbIIIa and GPVI, has been shown to attenuate metastases. Platelets are also recognized as dynamic reservoirs of proangiogenic and anti-angiogenic proteins that can be manipulated pharmacologically. A bidirectional relationship between platelets and tumors is also seen, with evidence of Ôtumor conditioningÕ of platelets. The platelet as a reporter of malignancy and a targeted delivery system for anticancer therapy has also been proposed. The development of platelet inhibitors that influence malignancy progression and clinical testing of currently available antiplatelet drugs represents a promising area of targeted cancer therapy.

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“…Platelet activation was also increased in cancer patients. Several clinical studies investigated the levels of biomarkers of platelet activation, such as soluble P-selectin, CD40 ligand, PF4, TSP-1 and β-thromboglobulin (β-TG) in the blood of cancer patients [144] [145].…”

Section: A) Thrombocytosis and Platelet Activation Markers During Cancermentioning

confidence: 99%

Role of platelets in cancer and cancer-associated thrombosis: Experimental and clinical evidences

Mezouar

Frère

Darbousset

et al. 2016

Thrombosis Research

173

167

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The primary hemostatic function of platelets has been recognized for more than a century, but increasing experimental and clinical evidences suggest that platelets are also important mediators of cancer. Cancer indeed influences platelet physiology, and activated platelets participate in each step of cancer development by promoting tumor growth, angiogenesis, metastasis, and cancer-associated thrombosis. Based on both the results of numerous experimental models addressing the involvement of platelets in cancer progression and the results of epidemiologic studies on the use of anti-platelet drugs to prevent cancer, platelets have been proposed as a potential target to reduce the short-term risk of cancer, cancer dissemination and cancer mortality. However, the cancer-associated thrombosis and the risk of bleeding due to anti-platelet drugs are not enough evaluated in experimental models. Therefore, the interesting contribution of platelets to cancer and cancer-associated thrombosis requires the standardization of preclinical and clinical models.

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Studies on platelet function in patients with prostatic cancer

Cited by 14 publications

References 8 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

The platelet contribution to cancer progression

Role of platelets in cancer and cancer-associated thrombosis: Experimental and clinical evidences

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