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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pharmacokinetics of chemoembolization with a fibrous collagen carrier was studied in rabbit kidney and porcine liver models. Cisplatin (1 mg/ml) chemoembolization of liver and kidney was compared with i.v. and intraarterial cisplatin infusion. Tissue platinum concentration [Pt] was measured at 2.5 h by atomic absorption spectrometry. Renal platinum retention and Angiostat (collagen for embolization) concentration were linearly related (r = 0.87, p less than 0.001). At 10 mg/ml collagen for embolization, chemoembolized kidney [Pt] was 220 +/- 50 (SE; n = 4) times contralateral kidney [Pt], and 62 and 23 times renal [Pt] by i.v. and intraarterial infusion, respectively. At 10 mg/ml collagen for embolization, chemoembolized liver [Pt] was 2 times hepatic [Pt] by i.v. and intraarterial infusion. Since hepatic tumor vasculature is end arterial, chemoembolization should yield high [Pt] in tumor (as in kidney) but lower levels in normal liver.
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PMID:Collagen chemoembolization: pharmacokinetics and tissue tolerance of cis-diamminedichloroplatinum(II) in porcine liver and rabbit kidney. 335 8

The effects of hyperthermia on murine tumor vasculature were studied by microangiography and histological examination. The tumors used were SCC VII carcinoma and mammary adenocarcinoma of syngeneic C3H/He mice. For the quantitative analysis of microangiographic changes, the percent (%) vascular area, which was defined as the percentage of opacified tumor vessel area to the entire tumor area, was determined in each microangiogram. The % vascular area after heating in a water bath at 44 degrees C for 30 min was minimized 24 hr after heating in both types of tumors. The histologic study revealed that the initial decrease of the % vascular area was due to congestion, thrombosis, and rupture of tumor vessels, and its subsequent increase was due to angiogenesis. SCC VII was more heat sensitive than mammary adenocarcinoma in terms of tumor growth delay, and tumor vessels of SCC VII were more vulnerable to heat than those of mammary adenocarcinoma. Histological examinations showed a marked difference in the architecture of vessels between the two types of tumors. Tumor vessels of mammary adenocarcinoma were supported by a connective tissue band, whereas those of SCC VII consisted of a single endothelial cell layer. Our findings suggest that the tumor vessels supported by a connective tissue band are less sensitive to heat than those without such support. The vascular damage of SCC VII was temperature dependent, and the critical temperature at which dramatic vascular damage appeared was between 42.7 degrees C and 43.7 degrees C.
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PMID:Microangiographic and histologic analysis of the effects of hyperthermia on murine tumor vasculature. 340 22

In search for an index of endothelial injury that would provide an early diagnosis of radiation pneumonitis, we investigated the plasma levels of von Willebrand Factor (Factor VIII Related Antigen, FVIII:RAg) in 14 patients undergoing pulmonary irradiation. This study was based on observations indicating that damage to the endothelium-rich pulmonary parenchyma may produce alterations in the synthesis, storage or release of FVIII:RAg, detectable in plasma. There was no correlation between FVIII:RAg levels and radiation pneumonitis, radiation dose, volume of irradiated lung, tumor burden, or time-interval between exposure and sampling. The heterogeneity of the neoplasms and the inconstant effects of radiation in the tumor vasculature are among several variables that may explain this lack of correlation. The plasma levels of FVIII:RAg cannot be used to diagnose or predict radiation pneumonitis.
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PMID:Von Willebrand factor levels do not predict or diagnose radiation pneumonitis. 348 36

The distribution of type VI collagen was examined immunohistochemically in normal tissues and in 24 human gliomas and six medulloblastomas. Its localization in the neoplasms was compared with that of fibronectin and glioma-mesenchymal extracellular matrix (GMEM) glycoprotein. In normal non-neural tissues type VI collagen was demonstrated in the interstitial connective tissue and in some basement membranes. In normal brain it was localized to the vasculature, leptomeninges, and pial-glial membrane. In neoplasms type VI collagen and fibronectin codistributed in the vasculature and stromal connective tissue. The GMEM glycoprotein, as identified by monoclonal antibody (MAb) 81C6, and a related glioma-mesenchymal matrix antigen identified by MAb 2A6, were expressed not only in the tumor vasculature and connective tissue, but also within the tumor parenchyma in association with glioma cells. The staining intensity was variable in 20 malignant gliomas and weak to absent in two pilocytic astrocytomas and six medulloblastomas. An oligodendroglioma and ependymoma both expressed the 2A6 epitope, but staining with MAb 81C6 was weak to absent. The antigens identified by MAb 81C6 and MAb 2A6 represent the only recognized extracellular matrix components, other than proteoglycans, that are associated with glioma cells in vivo. As prominent constituents of the pericellular matrix, they may be involved in recognized matrix functions such as the modulation of cell adhesion and migration.
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PMID:Distribution of type VI collagen in human gliomas: comparison with fibronectin and glioma-mesenchymal matrix glycoprotein. 365 35

The extracellular matrix is involved in many aspects of tumor cell biology, including tumor invasion and metastasis. 2A6 and 81C6 are murine monoclonal antibodies that identify glioma-mesenchymal extracellular matrix antigens. The 81C6 antigen is a high molecular weight glycoprotein composed of Mr 230,000 subunits. The expression of 2A6 antigen, 81C6 glycoprotein, fibronectin (FN), and laminin (LN) was examined immunohistochemically in ten malignant gliomas (MG) and four medulloblastomas (MBT). 2A6 and 81C6 were expressed in similar patterns by the neoplastic neuroepithelial cells in 9/10 MG and 1/4 MBT. The staining was typically diffuse and amorphous, without visualization of distinct cell bodies or processes. Less frequently, antigen was detected within tumor cell cytoplasm. In most tumors the staining was greatest in the perivascular regions. In two MG, 2A6 and 81C6 were expressed only by a subpopulation of neoplastic cells. Although intense staining was also associated with hyperplastic vascular and mesenchymal cells, many small and medium size blood vessels stained weakly or not at all. In contrast, FN and LN were expressed uniformly and intensely in the tumor vasculature, but were not expressed by neoplastic neuroepithelial cells. The 2A6 antigen and 81C6 glycoprotein are immunohistochemically distinct from FN and LN. These monoclonal antibody-defined antigens are heterogeneously expressed by neoplastic neuroepithelial cells and hyperplastic vascular-mesenchymal elements in MG and MBT. The 2A6 and 81C6 monoclonal antibodies will be useful reagents in the investigation of the extracellular matrix of malignant neuroepithelial neoplasms.
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PMID:Immunolocalization of monoclonal antibody-defined extracellular matrix antigens in human brain tumors. 403 75

This study was undertaken to determine the fluorescein angiographic characteristics of retinoblastomas, to determine the effect of various methods of treatment of these fluorescein patterns, and to determine whether fluorescein angiography can be of value in determining the response to treatment. We performed fluorescein angiography one or more times on 31 patients with retinoblastoma. Small tumors confined to the retina characteristically showed a well-defined pattern of retinal capillaries that filled during the arterial phase and became diffusely hyperfluorescent in the later phases. The fluorescein pattern varied with endophytic or exophytic tumors, depending upon the size of the tumor and the extent of vitreous or subretinal seeding. Following successful photocoagulation of a retinoblastoma, the tumor vascularity is markedly decreased and the tumor is replaced by fibrovascular tissue. Following successful radiotherapy, the tumor vasculature is altered but not typically obliterated. Three cases of presumed spontaneously regressed or arrested retinoblastomas showed much less vascularity than the active viable tumors. It is concluded that fluorescein angiography can be useful in the diagnosis and management of children with retinoblastoma.
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PMID:Fluorescein angiography of retinoblastoma. 610 Nov 27

A digital video fluorescence microscopy technique was used to evaluate the distribution of hematoporphyrin derivative (HPD) in the rat intracerebral 9L gliosarcoma brain-tumor model at 4, 24, 48, and 72 hours after intravenous administration of 10 mg/kg of the drug. Compared to surrounding normal brain, there was significant preferential uptake of HPD into the tumor. In sections surveyed, fluorescence reached a maximum value by 24 hours; however, only 33% to 44% of the tumor was fluorescent. In contrast, fluorescence within the surrounding normal brain was maximum at 4 hours, but was present in less than 1% of the brain tissue evaluated. The effect of HPD sensitization to a laser light dose (633 nm) of 30 joules/sq cm delivered through the intact skull was evaluated histologically in 10 rats. A patchy coagulation necrosis, possibly corresponding to the distribution of HPD fluorescence seen within the tumor, was observed. There was evidence that photoradiation therapy (PRT) affects defective tumor vasculature and that a direct tumor cell toxicity spared normal brain tissue. Despite these findings, limited uptake of HPD in tumor and the brain adjacent to tumor may decrease the effectiveness of PRT in the 9L gliosarcoma brain-tumor model. Because of the similarity between the capillary system of the 9L tumor and human brain tumors, PRT may have a limited therapeutic effect in patients with malignant brain tumors.
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PMID:Distribution of hematoporphyrin derivative in the rat 9l gliosarcoma brain tumor analyzed by digital video fluorescence microscopy. 623 14

Polyclonal 131I rabbit anti-rat ferritin localizes in the H-4-II-E hepatoma model. The effect of tumor size, vascularity, and ferritin content on tumor localization was examined. The extravascular and intravascular quantity and location of 131I non-specific IgG and 131I-antiferritin IgG in tumors were determined by gamma counter analysis of tissue samples and autoradiography. Separate groups of 8-10 tumor bearing rats with 0.6-1 g, 1-3 g, 4-8 g, 8-14 g, and greater than 14 g tumors were injected with 500 microCi (200 micrograms) of 131I non-specific IgG or 131I-antiferritin. Tumor targeting with antiferritin occurred maximally in primary or metastatic lesions less than 1 g in size. Decreased localization occurred with increasing tumor size and no localization took place in tumors greater than 8 g in size. This finding is independent of administered dose because increasing the amount of injected antiferritin from 2- to 10-fold did not increase the antiferritin/normal IgG targeting ratio in any group of tumors greater than 4 g. The quantity and physical characteristics of the tumor vasculature may in part explain selective tumor localization. Tumor vascularity per gram as measured by 51Cr labeled erythrocytes decreased as tumor size increased. Decreased localization was evident in the necrotic portions of large tumors. Autoradiography of tumor sections revealed that most of the 125I-IgG activity is deposited perivascularly with decreased deposition of antibody in necrotic areas of tumors and at increasing distance from the lumen of vessels. These findings have clinical importance since this non-homogeneous distribution of antibody could result in the delivery of low doses of radiation to large necrotic areas of tumors. These results help to demonstrate some of the complex physiologic factors that affect tumor localization and antibody distribution.
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PMID:Distribution of and physiologic factors that affect 131I-antiferritin tumor localization in experimental hepatoma. 674 54

Hyperthermia alone and hyperthermia with lidocaine cause changes in the fine structure of the CA755 tumor cell as well as the breakdown of the tumor vasculature. The first structural change, observed immediately after termination of hyperthermia of 43.5 degrees for 1 hr, is the vesiculation of the Golgi apparatus. Other structural changes occur later but with variable times of onset. The changes appear to be unrelated to the presence of lidocaine. Vascular breakdown results in hemorrhaging within the tumor, and its onset and intensity appear to vary directly with the size of the tumor. Breakdown of the tumor cell plasmalemma and degenerative changes of the cytoplasm and nucleoplasm are seen more frequently in large tumors and in the interior of small tumors at any given time after the end of hyperthermia. The vesiculation of the Golgi persists in treated cells for as long as 30 hr. This modification may represent an intensification in the function of the Golgi apparatus; however, it closely corresponds to that found in a variety of other cells treated with a class of compounds, including lidocaine, that specifically inhibits the function of the Golgi apparatus. The effect of these compounds is rapidly reversible, unlike hyperthermia. Since the Golgi apparatus probably is crucial in repairing any deleterious effects of hyperthermia, any impairment of its normal function would place most treated tumor cells in a difficult position. The rate of tumor destruction may ultimately depend on the breakdown of the tumor vasculature following hyperthermia and lidocaine.
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PMID:Structural changes in murine cancer associated with hyperthermia and lidocaine. 683 16

In this review, some of the current literature on the regulation of proteolysis and angiogenesis during tumor invasion is discussed. Due to the critical location of brain tumors, an understanding of tumor cell interactions with the local environment is particularly relevant. Tissue breakdown during tumor invasion is associated with proteolytic activity, mediated by tumor cells, and surrounding host cells. This review covers two classes of proteinases and inhibitors that have commonly been associated with tumor invasion i.e., plasminogen activator (PA)/plasmin and matrix metalloproteinases (MMP) with special emphasis on the MMP inhibitors, TIMP-1 and TIMP-2. At different steps of the metastatic process, tumor cells interact with endothelial cells. Tumor cells also stimulate the formation of new vessels through the expression of specific angiogenic molecules. At least eight angiogenic molecules have been purified, sequenced and cloned, four of which are discussed here. Regulation of angiogenic activity has been the focus of intense studies recently, and a wide range of synthetic and natural angiogenesis inhibitors have been discovered. Targeting of angiogenic molecules and tumor vasculature may prove useful in future cancer therapeutic strategies.
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PMID:Tumor invasion, proteolysis, and angiogenesis. 752 88


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