Metastasis is the most devastating aspect of cancer and it is the main cause of morbidity and mortality in cancer patients. Tumor cell adhesion to the vascular endothelial cell lining is an important step in metastatic progression and is prompted by platelets. Mucin 1 is over-expressed and aberrantly glycosylated in more than 60% of pancreatic ductal adeno-carcinomas, which mediate adhesion of pancreatic cancer cells to platelets via P-selectin. The anticoagulant low molecular weight heparins (LMWHs), which are commonly used in venous Thromboprophylaxis and treatment, appear to have an effect on cancer survival. The aim of this study is to investigate the effect of platelets on human pancreatic cancer MPanc96 cell adhesion to the endothelial cell vessel wall, and to examine the effect of heparin derivatives on MPanc96 adhesion using a novel, in vitro model of human umbilical cord vein. The modified heparin S-NACH (sulfated non-anticoagulant heparin), which is devoid of antithrombin (AT) binding and devoid of inhibition of systemic AT-dependent coagulation factors such as factor Xa and IIa, and the LMWH tinzaparin both potently reduced adhesion and invasion of fluorescence-labeled MPanc96 cancer cells to the endothelial layer of umbilical cord vein in a dose-dependent manner. S-NACH effectively inhibited P-selectin mediated MPanc96 cell adhesion, and inhibited cell adhesion and invasion similar to tinzaparin, indicating that systemic anticoagulation is not a necessary component for heparin attenuation of cancer cell adhesion, invasion, and metastasis. Also, S-NACH and tinzaparin versus unfractionated heparin, heparin derivatives enoxaparin, deltaparin, fraxiparin, and fondaparinux were evaluated for their effect on platelet-cancer cell adhesion. An in vivo anti-metastatic S-NACH-treated nude mouse model of MPanc96 pancreatic cancer cell metastasis demonstrated potent anti-metastasis efficacy as evidenced by IVIS imaging and histological staining.

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Objective This study was aimed to evaluate the prevalence of sonographic markers for placenta accreta spectrum (PAS) in pregnancies at low-risk for PAS. Study Design Pregnant women at low-risk for PAS presenting for routine second trimester ultrasound who enrolled in the study were evaluated prospectively for sonographic markers of PAS during two ultrasounds at 18 to 24 and 28 to 34 weeks. Frequencies of PAS markers were compared between the second and third trimester and between those with and without prior cesarean deliveries (CD). Results Overall, 174 women were included. Several markers were seen frequently in the second trimester: vascular cervical invasion (57%), lacunae (46%), subplacental hypervascularity (37%), and irregularity of the posterior bladder wall (37%). Other markers were seen infrequently or not at all: loss of the retroplacental clear zone, uterovesical interface < 1 mm, bridging vessels, placental bulge or focal exophytic mass. Frequencies of markers did not differ between women with and without prior CD. Lacunae were larger and more numerous in the third trimester. Two or more PAS markers were observed in 98% of second trimester ultrasounds. Conclusion Several PAS sonographic markers occur commonly in low-risk pregnancies. In the absence of risk factors, the independent predictive value of these markers is questionable.

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The new standardized six-step approach to the focused basic obstetric ultrasound examination can be performed successfully and accurately between 18(+0) and 36(+6) weeks of gestation. This standardized approach can be of significant benefit to limited resource settings and in point of care obstetric ultrasound applications.