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At least 199 records · Page 11Linked to original sources
PubMed1992

Increased numbers of pulmonary megakaryocytes in patients with arterial pulmonary tumour embolism and with lung metastases seen at necropsy.

AIMS: To compare the number of pulmonary megakaryocytes in patients with local malignant disease without metastases with the numbers in patients with pulmonary tumour emboli without lung metastases and with those with pulmonary metastases. METHODS: The prevalence of pulmonary megakaryocytes was studied in 40 necropsies divided into four groups of 10 cases each: normal lungs (I); localised malignancies (II); pulmonary tumour embolism without lung metastases (III); pulmonary tumour embolism and lung metastases (IV). Five fragments (one of each pulmonary lobe) of tissue lung were collected, embedded in paraffin wax, sectioned, and stained by an immunohistochemical method to detect factor VIII related antigen. The number of megakaryocytes was evaluated in 500 high power fields/case. RESULTS: No differences were observed between groups I and II or between groups III and IV, but there was a 3.5-fold increase in the number of megakaryocytes in the groups with pulmonary tumour embolism or lung metastases compared with those with local neoplasms or normal lungs. CONCLUSIONS: An increased number of pulmonary megakaryocytes correlated with the presence of tumour cells in the microcirculation of the lungs or parenchymal metastases, but not with local malignancies without lung disease. The permanent siting of tumour emboli may stimulate megakaryocytes to migrate to the lungs, and may increase the release of platelets into the pulmonary circulation.

Cell Count↗
PubMed1979

Quantitative study on the liberation of tumor cells into the circulating blood.

A study was undertaken to investigate the mechanism of liberation of tumor cells into the blood stream in connection with the process of tumor growth, using three strains of ascites tumor such as Yoshida sarcoma (YS) with infiltrative growth pattern, AH100B with expansive one, and AH109A with intermediate one. For this experiment, a new method for the quantitation of the number of circulating tumor cells was devised. From its results, it was concluded as follows: (1) Tumor cells appear first in the circulating blood at the transitional phase from logarithmic growth to declining growth. (2) Tumor size is a macroscopical index of the risk of the liberation of tumor cells into the blood stream. (3) Tumor necrosis is a histological sign suggesting that the tumor growth phase is declining, namely, that hematogenous dissemination of tumor cells has begun already. (4) There is a striking difference in the frequency and number of tumor cells in the venous blood among these three tumor strains. The tumour strains in order of the number of the circulating tumor cells are YS, AH109A, and AH100B. (5) In YS and AH109A, the transition of the number of tumor cells liberated into the blood stream is closely related to the growth process of tumor tissue. (6) Liberated cells of AH109A and AH100B disappear promptly from the blood stream.

Animals↗
PubMed1988

Circulating malignant cells in non-Hodgkin's lymphoma: correlation with binding by peanut agglutinin.

A significant number of patients with non-Hodgkin's lymphoma have peripheral blood involvement during the course of their disease. Because the expression of receptor for the lectin peanut agglutinin PNA by normal lymphocytes is associated with noncirculating (stationary phase) cells, we studied the relationship between PNA binding by lymphoma cells and the presence of clonal B cells in the blood of 38 patients with B-cell lymphoma. The binding of PNA by cells in tissues was determined by the immunoperoxidase method and by two-color flow cytometry. Circulating lymphoma cells (clonal B cells) were identified by a sensitive flow-cytometric technique (kappa-lambda analysis) and were also studied for PNA binding in some cases. In all, 16 of 38 (42%) of lymphomas were PNA+, including a spectrum of histologic types. Circulating lymphoma cells were demonstrated in 17 of 22 PNA-lymphomas, whereas only 3 of 16 of PNA+ lymphomas had such circulating cells. Thus, there is a significant association between PNA binding and peripheral blood involvement by lymphoma (P less than .005 by chi-square analysis). In 12 cases, the circulating and tissue lymphoma cells had similar expression of PNA receptor (2 PNA+ and 10 PNA- cases), indicating that modulation of the PNA binding sites did not occur. In three patients who presented with lymphosarcoma cell leukemia, the circulating malignant cells were PNA-. These findings suggest that for both normal and malignant lymphocytes the absence of binding sites for PNA is associated with the capacity of these cells to circulate freely.

Binding Sites↗
PubMed1998

Reliability of reverse transcription-polymerase chain reaction (RT-PCR)-based assays for the detection of circulating tumour cells: a quality-assurance initiative of the EORTC Melanoma Cooperative Group.

Reverse transcription-polymerase chain reaction (RT-PCR)-based assays detecting occult neoplastic cells are increasingly being used for the study of tumour dissemination and minimal residual disease. However, different methods are employed by various research groups and the results are heterogenous. We prospectively assessed the results from nine laboratories performing tyrosinase RT-PCR assays for the detection of melanoma cells on a series of blind samples. After complete analysis, the results were compared for sensitivity and specificity. All laboratories reported correct results for cDNA standards. Five laboratories attained acceptable specificity and a sensitivity detecting 10 cells in 10 ml of whole blood. Four laboratories had unacceptable specificity and/or sensitivity. This blind study highlights the difficulty of RT-PCR data interpretation and the need for quality assurance between laboratories. Measures to increase the reliability of RT-PCR assays are proposed, which have to be prospectively evaluated in future studies.

DNA, Neoplasm↗
PubMed2004

Direct visualization of nitric oxide release by liver cells after the arrest of metastatic tumor cells in the hepatic microvasculature.

BACKGROUND: Our previous studies have shown that the injection of B16F1 melanoma cells into the mesenteric vein can induce the rapid local release of nitric oxide (NO) in the liver, causing apoptosis of the melanoma cells in the liver sinusoids and inhibiting the subsequent formation of hepatic metastases. In this study, we have investigated the distribution and cellular source of NO in this model. MATERIALS AND METHODS: In situ liver perfusion was established in both wild-type (wt) and endothelial nitric oxide synthase knockout (eNOS KO) C57BL/6 mice. A specific fluorescent NO probe, 4,5-diaminofluorescein diacetate (DAF-2 DA) (5 micromol/L), was perfused into the portal venous system to label the liver tissue. Then, a MitoTracker Orange labeled B16F1 melanoma cell suspension (2 x 10(6) cells/ml) was injected through a portal vein catheter by a peristaltic pump. Images of the liver tissue were taken by confocal microscopy from a selected area to determine the cellular source of NO. For quantification, the fluorescence intensity of this area was measured over time by Fluoview software. RESULTS: Diaminotriazolofluorescein (DAF-2T) fluorescence (indicating NO generation) was detected in hepatic parenchymal cells located in the periportal region in both wt C57BL/6 and eNOS KO C57BL/6 mice and was intensified by increased flow rate in the portal venous system. The B16F1 cells arrested in the periportal sinusoids, corresponding to zone 1 of the hepatic acinus. DAF-2T fluorescence was expressed by both sinusoidal lining cells and hepatocytes at the site of tumor cell arrest. The fluorescence intensity of these cells increased approximately 2-fold over a time of 500 s. In contrast, there was no increase in the fluorescence intensity of the sinusoidal lining cells and hepatocytes in mice perfused with buffer or in eNOS KO mice perfused with B16F1 cells. CONCLUSION: This study demonstrates that NO is produced by hepatic parenchymal cells mainly located in the periportal zones and that the arrest of the B16F1 melanoma cells causes an eNOS-dependent local burst of NO by the sinusoidal lining cells and hepatocytes in the periportal areas.

Animals↗
PubMed1994

[Tumor involvement of the vena cava in renal cell carcinoma. Surgical technique, results and prognosis].

In 45 patients with a vena cava tumor thrombus secondary to renal cell carcinoma we present the diagnostic and operative management and relevant data on the extent of the thrombus (classified into 4 stages), postoperative complications and patient survival. Extensive thrombi of the vena cava were removed surgically in hypothermia and with extracorporeal circulation. The importance of an interdisciplinary approach involving cardiac and urologic surgeons is therefore emphasized. With due consideration for relevant prognostic parameters such as tumor differentiation or spread, we estimated a 5-year survival of 29% for our Heidelberg patients. Neither the extent of the tumor thrombus nor tumor infiltration of the perirenal adipose tissue had any influence on patient survival.

Adult↗