Role of Procoagulant Activity in Neoplastic Disease

Author(s):  
Richard L. Edwards ◽  
Frederick R. Rickles
1964 ◽  
Vol 12 (02) ◽  
pp. 484-488
Author(s):  
W. H Seegers ◽  
H Schröer ◽  
D Heene

SummaryThe partial thromboplastin time and purified thrombin were used to demonstrate the procoagulant power of thrombin. Only 0.007 μg of thrombin could be detected in prothrombin activation. Traces of thrombin and autoprothrombin C can fully account for the generation of procoagulant activity in the thromboplastin generation test. Inactivation of these two activities by antithrombin explains the disappearance of the procoagulant power in that test, so that there now remains no valid demonstration of the existence of plasma thromboplastin or of anti-plasma thromboplastin.


1993 ◽  
Vol 70 ◽  
pp. S45
Author(s):  
R.M. Lammel ◽  
M. De Carll ◽  
B. Giusti ◽  
F. Martini ◽  
M. Attanasio ◽  
...  

2009 ◽  
Vol 124 (4) ◽  
pp. 437-440
Author(s):  
S D Shetty ◽  
R J Salib ◽  
S B Nair ◽  
N Mathad ◽  
J Theaker

AbstractIntroduction:Ossifying fibromyxoid tumour is a recently described, rare but morphologically distinctive soft tissue neoplasm characterised by a combination of myxoid and/or fibrous stroma with areas of ossification. Although most authors postulate a neuroectodermal origin for this peculiar tumour, there is no agreement in the literature regarding its histopathogenesis. To our knowledge, this is the first reported case of ossifying fibromyxoid tumour involving the sphenoid sinus.Histological findings:Tumour of low cell density, composed of small, spindle-shaped or stellate cells with small, irregular nuclei set in a fibromyxoid stroma.Management:Following discussion at the skull base multidisciplinary team meeting, a combined surgical team including an otorhinolaryngologist and a neurosurgeon carried out resection of the lesion, using an endoscopic transnasal approach, followed by reconstruction of the defect.Conclusions:An awareness of the distinctive histopathological features of ossifying fibromyxoid tumour, and of its clinical effects, is crucial to establishing a definitive diagnosis and thereby instituting appropriate management. This case report also reinforces the evolving role of the endoscopic transnasal approach in the management of inflammatory and neoplastic disease involving the skull base. This is increasingly being made possible by close collaboration between multiple surgical specialties, including otorhinolaryngology and neurosurgery.


2005 ◽  
Vol 94 (07) ◽  
pp. 107-114 ◽  
Author(s):  
Christelle Lecut ◽  
Martine Jandrot-Perrus ◽  
Marion A. H. Feijge ◽  
Judith M. E. M. Cosemans ◽  
Johan W. M. Heemskerk

SummaryThe role of collagens and collagen receptors was investigated in stimulating platelet-dependent thrombin generation. Fibrillar type-I collagens, including collagen from human heart, were most potent in enhancing thrombin generation, in a way dependent on exposure of phosphatidylserine (PS) at the platelet surface. Soluble, non-fibrillar type-I collagen required pre-activation of integrin α2β1 with Mn2+ for enhancement of thrombin generation. With all preparations, blocking of glycoprotein VI (GPVI) with 9O12 antibody abrogated the collagen-enhanced thrombin generation, regardless of the α2β1 activation state. Blockade of α2β1 alone or antagonism of autocrine thromboxane A2 and ADP were less effective. Blockade of αIIbβ3 with abciximab suppressed thrombin generation in platelet-rich plasma, but this did not abolish the enhancing effect of collagens. The high activity of type-I fibrillar collagens in stimulating GPVI-dependent procoagulant activity was confirmed in whole-blood flow studies, showing that these collagens induced relatively high expression of PS. Together, these results indicate that: i) fibrillar type-I collagen greatly enhances thrombin generation, ii) GPVI-induced platelet activation is principally responsible for the procoagulant activity of fibrillar and non-fibrillar collagens, iii) α2β1 and signaling via autocrine mediators facilitate and amplify this GPVI activity, and iv) αIIbβ3 is not directly involved in the collagen effect.


2020 ◽  
Vol 21 (17) ◽  
pp. 6247
Author(s):  
Yongsheng Ruan ◽  
Hye Na Kim ◽  
Heather Ogana ◽  
Yong-Mi Kim

Leukemia is an aggressive hematologic neoplastic disease. Therapy-resistant leukemic stem cells (LSCs) may contribute to the relapse of the disease. LSCs are thought to be protected in the leukemia microenvironment, mainly consisting of mesenchymal stem/stromal cells (MSC), endothelial cells, and osteoblasts. Canonical and noncanonical Wnt pathways play a critical role in the maintenance of normal hematopoietic stem cells (HSC) and LSCs. In this review, we summarize recent findings on the role of Wnt signaling in leukemia and its microenvironment and provide information on the currently available strategies for targeting Wnt signaling.


2016 ◽  
Vol 213 (9) ◽  
pp. 1723-1740 ◽  
Author(s):  
Srdan Verstovsek ◽  
Taghi Manshouri ◽  
Darrell Pilling ◽  
Carlos E. Bueso-Ramos ◽  
Kate J. Newberry ◽  
...  

Primary myelofibrosis (PMF) is a fatal neoplastic disease characterized by clonal myeloproliferation and progressive bone marrow (BM) fibrosis thought to be induced by mesenchymal stromal cells stimulated by overproduced growth factors. However, tissue fibrosis in other diseases is associated with monocyte-derived fibrocytes. Therefore, we sought to determine whether fibrocytes play a role in the induction of BM fibrosis in PMF. In this study, we show that BM from patients with PMF harbors an abundance of clonal, neoplastic collagen- and fibronectin-producing fibrocytes. Immunodeficient mice transplanted with myelofibrosis patients’ BM cells developed a lethal myelofibrosis-like phenotype. Treatment of the xenograft mice with the fibrocyte inhibitor serum amyloid P (SAP; pentraxin-2) significantly prolonged survival and slowed the development of BM fibrosis. Collectively, our data suggest that neoplastic fibrocytes contribute to the induction of BM fibrosis in PMF, and inhibiting fibrocyte differentiation with SAP may interfere with this process.


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