The Experts below are selected from a list of 252 Experts worldwide ranked by ideXlab platform
Takeshi Ogura - One of the best experts on this subject based on the ideXlab platform.
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Inhibition by Fibrin Coagulation of Lung Cancer Cell Destruction by Human Interleukin‐2‐activated Killer Cells
Japanese journal of cancer research : Gann, 1992Co-Authors: Shinji Atagi, Saburo Sone, Katsuyuki Fukuta, Takeshi OguraAbstract:We examined the effect of fibrin coagulation on tumor cytotoxicity mediated by human lymphokine (IL-2)-activated killer (LAK) cells. LAK cells were induced from peripheral blood mononuclear cells (MNC) by culture with recombinant IL-2 for 4 or 5 days, and LAK cell-mediated cytotoxicity against tumor cells was assessed by 51Cr release assay in the presence or absence of plasma from normal subjects and lung cancer patients. Plasma did not affect the phase of induction of LAK activity by IL-2, but dose-dependently inhibited the effector phase of LAK cell-mediated cytotoxicity against Daudi cells. Similar inhibition of LAK cell-mediated cytotoxicity was observed on pretreatment of Daudi cells and human lung cancer cell lines with human Fibrinogen Plus Thrombin. A parallel relationship was found between the amount of Fibrinogen in plasma of lung cancer patients and inhibition of LAK cytotoxicity. This inhibition was reduced by addition of anticoagulants (heparin or argatroban). These findings suggest that fibrin coagulation on tumor cells protects them from LAK cell-mediated tumor cytotoxicity in malignant lesions and that a combination of an anticoagulant drug and IL-2/LAK therapy may be effective for treatment of lung cancer patients.
Shinji Atagi - One of the best experts on this subject based on the ideXlab platform.
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Inhibition by Fibrin Coagulation of Lung Cancer Cell Destruction by Human Interleukin‐2‐activated Killer Cells
Japanese journal of cancer research : Gann, 1992Co-Authors: Shinji Atagi, Saburo Sone, Katsuyuki Fukuta, Takeshi OguraAbstract:We examined the effect of fibrin coagulation on tumor cytotoxicity mediated by human lymphokine (IL-2)-activated killer (LAK) cells. LAK cells were induced from peripheral blood mononuclear cells (MNC) by culture with recombinant IL-2 for 4 or 5 days, and LAK cell-mediated cytotoxicity against tumor cells was assessed by 51Cr release assay in the presence or absence of plasma from normal subjects and lung cancer patients. Plasma did not affect the phase of induction of LAK activity by IL-2, but dose-dependently inhibited the effector phase of LAK cell-mediated cytotoxicity against Daudi cells. Similar inhibition of LAK cell-mediated cytotoxicity was observed on pretreatment of Daudi cells and human lung cancer cell lines with human Fibrinogen Plus Thrombin. A parallel relationship was found between the amount of Fibrinogen in plasma of lung cancer patients and inhibition of LAK cytotoxicity. This inhibition was reduced by addition of anticoagulants (heparin or argatroban). These findings suggest that fibrin coagulation on tumor cells protects them from LAK cell-mediated tumor cytotoxicity in malignant lesions and that a combination of an anticoagulant drug and IL-2/LAK therapy may be effective for treatment of lung cancer patients.
Saburo Sone - One of the best experts on this subject based on the ideXlab platform.
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Inhibition by Fibrin Coagulation of Lung Cancer Cell Destruction by Human Interleukin‐2‐activated Killer Cells
Japanese journal of cancer research : Gann, 1992Co-Authors: Shinji Atagi, Saburo Sone, Katsuyuki Fukuta, Takeshi OguraAbstract:We examined the effect of fibrin coagulation on tumor cytotoxicity mediated by human lymphokine (IL-2)-activated killer (LAK) cells. LAK cells were induced from peripheral blood mononuclear cells (MNC) by culture with recombinant IL-2 for 4 or 5 days, and LAK cell-mediated cytotoxicity against tumor cells was assessed by 51Cr release assay in the presence or absence of plasma from normal subjects and lung cancer patients. Plasma did not affect the phase of induction of LAK activity by IL-2, but dose-dependently inhibited the effector phase of LAK cell-mediated cytotoxicity against Daudi cells. Similar inhibition of LAK cell-mediated cytotoxicity was observed on pretreatment of Daudi cells and human lung cancer cell lines with human Fibrinogen Plus Thrombin. A parallel relationship was found between the amount of Fibrinogen in plasma of lung cancer patients and inhibition of LAK cytotoxicity. This inhibition was reduced by addition of anticoagulants (heparin or argatroban). These findings suggest that fibrin coagulation on tumor cells protects them from LAK cell-mediated tumor cytotoxicity in malignant lesions and that a combination of an anticoagulant drug and IL-2/LAK therapy may be effective for treatment of lung cancer patients.
Katsuyuki Fukuta - One of the best experts on this subject based on the ideXlab platform.
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Inhibition by Fibrin Coagulation of Lung Cancer Cell Destruction by Human Interleukin‐2‐activated Killer Cells
Japanese journal of cancer research : Gann, 1992Co-Authors: Shinji Atagi, Saburo Sone, Katsuyuki Fukuta, Takeshi OguraAbstract:We examined the effect of fibrin coagulation on tumor cytotoxicity mediated by human lymphokine (IL-2)-activated killer (LAK) cells. LAK cells were induced from peripheral blood mononuclear cells (MNC) by culture with recombinant IL-2 for 4 or 5 days, and LAK cell-mediated cytotoxicity against tumor cells was assessed by 51Cr release assay in the presence or absence of plasma from normal subjects and lung cancer patients. Plasma did not affect the phase of induction of LAK activity by IL-2, but dose-dependently inhibited the effector phase of LAK cell-mediated cytotoxicity against Daudi cells. Similar inhibition of LAK cell-mediated cytotoxicity was observed on pretreatment of Daudi cells and human lung cancer cell lines with human Fibrinogen Plus Thrombin. A parallel relationship was found between the amount of Fibrinogen in plasma of lung cancer patients and inhibition of LAK cytotoxicity. This inhibition was reduced by addition of anticoagulants (heparin or argatroban). These findings suggest that fibrin coagulation on tumor cells protects them from LAK cell-mediated tumor cytotoxicity in malignant lesions and that a combination of an anticoagulant drug and IL-2/LAK therapy may be effective for treatment of lung cancer patients.
Stephen M. Schwartz - One of the best experts on this subject based on the ideXlab platform.
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Vitronectin decreases microvascular endothelial cell apoptosis.
Journal of cellular physiology, 1998Co-Authors: F. Frank Isik, Nicole S. Gibran, Young Chul Jang, Linda Sandell, Stephen M. SchwartzAbstract:Angiogenesis after tissue injury occurs in a matrix environment consisting of fibrin, fibronectin, and vitronectin as the major extracellular matrix (ECM) constituents. ECM-integrin interactions is critical for angiogenesis and failure to bind a ligand to certain integrin receptors (αvβ3 or αvβ5) inhibits angiogenesis. The ligand that binds to αvβ3 or αvβ5 integrin receptors during microvascular angiogenesis has not been identified. Our hypothesis is that provisional matrix molecules provide the environmental context cues to microvascular endothelial cells and promote angiogenesis by decreased programmed cell death. Using cultured human microvascular endothelial cells, we show that vitronectin, in comparison to growth on alternative provisional matrix molecules (fibronectin, Fibrinogen Plus Thrombin), collagen I, and basement membrane molecules (collagen IV), significantly reduces microvascular endothelial cell death in vitro. This reduction was observed using morphologic criteria, TdT-mediated dUTP nick end labeling (TUNEL) assay, histone release into the cytoplasm, and thymidine release into the supernatant. Though our data confirm that vitronectin may bind to more than one integrin receptor to reduce MEC apoptosis, binding to the αv component appears to be the critical integrin subcomponent for reducing apoptosis. J. Cell. Physiol. 175:149–155, 1998. © 1998 Wiley-Liss, Inc.