Neoplastic vessels

One of the most important and difficult steps in pancreatic neoplasm staging is to evaluate the relationship between the neoplasm and the surrounding major peripancreatic vessels a number of studies have been conducted in order to establish a correct grading in neoplastic vessel infiltration (Lu et al. 1997 Mazzeo et al. 2007), being this one of the most important key points in determining patient resectablity (Allema et al. 1995). 

Ethanol ablation is used widely due to its ease of treatment, minimal and inexpensive therapeutic equipment required, and good cHnical results. Following percutaneous instillation, ethanol causes dehydration of thecy-toplasm and subsequent co-agulation necrosis, followed by fibrous reaction. Within neoplastic vessels, ethanol induces necrosis of endothehal cells and platelet aggregation, thus causing thrombosis and tissue ischemia. 

Blood vessels penetrating tumors provide malignant cells with another point at which to enter the circulation. Evidence exists that in situation where cancers disseminate predominantly by the blood, the extent of metastasis depends upon the vasculature of the primary tumor. Thin-walled capillaries, especially those newly formed, provide poor resistance to invading cancer cells. Also, data from microscopy studies show that the endothelium of tumor vessels, particularly in areas of poor oxygenation, is often abnormal (Kl). These abnormalities may permit invasion by neoplastic cells (P3). Finally, tumors can spread by direct extension into body cavities such as pleural and peritoneal spaces. An example of this is the formation of peritoneal metastases from ovarian carcinoma. 

In addition, very recent work indicates that COX-2 may play a vital role in the regulation of angiogenesis associated with neoplastic tumor cells, hence COX-2 inhibitors may block the growth of blood vessels into developing tumors (56). Thus, according to epidemiological, clinical, and experimental data, COX-2 appears to be intimately related to the development and growth of some types of cancer, especially of colorectal cancer. 

Plasma contains protease inhibitors that rapidly inactivate the coagulation proteins as they escape from the site of vessel injury. The most important proteins of this system are -anti protease, 2-macroglobulin, -antiplasmin, and antithrombin. If this system is overwhelmed, generalized intravascular clotting may occur. This process is called disseminated intravascular coagulation (DIC) and may follow massive tissue injury, cell lysis in malignant neoplastic disease, obstetric emergencies such as abruptio placentae, or bacterial sepsis. 

Folkman, J. (1986). How is blood vessel growth regulated in normal and neoplastic tissue Cancer Res. 46, 467-473. 

Fibronectin. Fibronectin is expressed in and around neoplastic blood vessels during tumor growth and angiogenesis. Fibronectin is an extracellular adhesion glycoprotein that binds to integrin receptors and mediates interactions between cells and extracellular matrix components. Antibodies against fibronectin have been studied for targeting. " ... 

In animals, HCl is a severe irritant of the eyes and respiratory system. The 30 min LC50 values in rats and mice are 4701 and 2644 ppm, respectively. Animals exposed to high concentrations of HCl gas developed necrosis of the tracheal and bronchial epithelium, pulmonary edema, atelectasis, emphysema, and damage to the pulmonary blood vessels and liver. Chronic exposure to 10 ppm for 6hday for life did not cause neoplastic lesions or serious irritant effects in the nasal epithelium of rats. In experimental animals, exposure to a concentration of 1350 ppm hydrogen chloride gas caused clouding of the cornea after 1.5 h and exposure to 3000 ppm for 6 h caused slight erosion of the corneal epithelium. 

TothB. 1973a. 1,1-Dimethylhydrazine (unsymmetrical) carcinogenesis in mice. Light microscopic and ultrastructural studies on neoplastic blood vessels. J Natl Cancer Inst 50 181-194. 

VEGFR3 is a transmembrane protein that is also known as tyrosine-protein kinase receptor FLT4 it is encoded by a gene at chromosomal locus 5q33-qter and is expressed exclusively by lymphatic endothelial cells. In similarity to PPN, VEGFR3 is seen in non-neoplastic lymphatic vessels and in many vascular neoplasms. However, it is more selective than PPN. 

Some epithelial mesotheliomas are composed of small cysts formed by uniform cuboidal mesothelial cells and associated numerous blood vessels (Fig. 12.68). This type of mesothelioma may be difficult to differentiate from a vascular neoplasm. The epithelial mesothelial cells may contain intracytoplasmic hemosiderin (Fig. 12.69). The immunophenotype of such neoplasms is identical to that of other epithelial mesotheliomas. The vascular proliferation may be related to an endothelial growth factor produced by neoplastic mesothelial cells.Adenomatoid tumors are localized benign mesothelial proliferations that most frequently occur in the epididymus and cornua of the uterus.Adenomatoid tumors have been identified in the adrenal gland and pancreas. These tumors are formed by uniform small cuboidal cells and can appear invasive. They express keratin and other markers of mesothelial cells and have the characteristic ultrastruc-tural features of mesothelial cells. Adenomatoid tumors have also been reported in the pleura. Hyperplastic... 

INTRAVASCULAR LYMPHOMA The CNS is One of the sites of predilection for intravascular lymphoma, a large B-cell lymphoma. The neoplastic cells fill the blood vessel lumina. The clinical presentation mimics vasculitis. Neoplastic cells are positive for CD20. 

Demyelination may be confused with neoplastic disease because it produces abundant gliosis. Large cells with short chromosomes spread apart in their cytoplasm mimic mitotic activity in a glioma.If numerous lipidladen KPl-positive macrophages are encountered within parenchyma and around vessels, demyelinating disease should be considered. Appropriate stains for myelin, NF stain for axons (see Box 20.2), and features described in this section should be considered in the interpretation (see Figs. 20.3A, 20.11 A and B, and 20.60). 

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