Comparison of bleomycin and peplomycin toxicity on clonogenic tumor cells from various human tumors

1986 ◽  
Vol 112 (2) ◽  
pp. 165-169 ◽  
Author(s):  
H. A. Neumann ◽  
H. M. Runge ◽  
H. H. Fiebig ◽  
R. Engelhardt ◽  
G. W. L�hr
Keyword(s):  
Tumor Cells ◽  
Human Tumors ◽  
Clonogenic Tumor Cells

scholarly journals Focal Adhesion Kinase Suppresses Apoptosis by Binding to the Death Domain of Receptor-Interacting Protein

2004 ◽  
Vol 24 (10) ◽  
pp. 4361-4371 ◽  
Author(s):  
Elena Kurenova ◽  
Li-Hui Xu ◽  
Xihui Yang ◽  
Albert S. Baldwin ◽  
Rolf J. Craven ◽  
...  
Keyword(s):  
Focal Adhesion Kinase ◽  
Tumor Cells ◽  
Focal Adhesion ◽  
Death Receptor ◽  
Human Tumors ◽  
Receptor Complex ◽  
Death Domain ◽  
Functional Link ◽  
Interacting Protein ◽  
Survival Signals

ABSTRACT Tumor cells resist the apoptotic stimuli associated with invasion and metastasis by activating survival signals that suppress apoptosis. Focal adhesion kinase (FAK), a tyrosine kinase that is overexpressed in a variety of human tumors, mediates one of these survival signals. Attenuation of FAK expression in tumor cells results in apoptosis that is mediated by caspase 8- and FADD-dependent pathways, suggesting that death receptor pathways are involved in the process. Here, we report a functional link between FAK and death receptors. We have demonstrated that FAK binds to the death domain kinase receptor-interacting protein (RIP). RIP is a major component of the death receptor complex and has been shown to interact with Fas and tumor necrosis factor receptor 1 through its binding to adapter proteins. We have shown that RIP provides proapoptotic signals that are suppressed by its binding to FAK. We thus propose that FAK overexpression in human tumors provides a survival signal function by binding to RIP and inhibiting its interaction with the death receptor complex.

Platelet Interaction with Tumor Cells

1975 ◽  
Author(s):  
G. Gasic ◽  
T. Gasic ◽  
B. Hsu ◽  
P. Koch ◽  
S. Niewiarowski
Keyword(s):  
Tumor Cells ◽  
Gamma Globulin ◽  
Wilms Tumor ◽  
Preliminary Evidence ◽  
Human Tumors ◽  
Research Support ◽  
Mouse Tumors ◽  
Adp Release ◽  
Colonic Adenocarcinomas ◽  
Mammary Adenocarcinomas

Previous investigations demonstrated that mouse tumors cause platelet aggregation (PA) and increase platelet turnover. Depletion of platelets by neuraminidase and inhibition of PA by aspirin reduced the munber of metastases (Gasic et al., Int. J. Cancer 11, 704, 1973). The purpose of this investigation was to study further interaction of cells from various mouse and human tumors with platelets. Cells of 7 mouse tumors (1 mammary adenocarcinomas, 5 sarcomas, I melanoma) and 14 human tumors (8 breast, 3 colonic adenocarcinomas, 1 cancer of the ureter, 1 Wilms tumor, and 1 neuroblastoma) aggregated homologous platelets suspended in heparinized plasma. Three mouse tumors (2 mammary and 1 sarcoma) and 5 human tumors (2 breast, 1 sarcoma, 1 Wilms, and 1 neuroblastoma) did not. PA was accompanied by the release of radio-activity from 14C-serotonin labeled platelets (range 15–90%). PA activity was not correlated with fibrinolytic or procoagulant activity. The contribution of plasminogen activators, thrombin, and tumor immune complexes has been excluded. However, gamma globulin of tumor bearing mice contained a “blocking factor” which delayed PA. Since enzymatic removal of ADP reduced PA it is possible that the ADP release either by tumors or by platelets played a contributory role. The pattern of PA by tumor cells rossembled that induced by collagen. Indeed preliminary evidence suggests that collagen-like material associated with tumor cells might be involved in platelet adherence to these cells and subsequent aggregation.(Supported by NIH Grants CA-15728, HL 14217. HL 15226, and by a Univ. of Penna.’s General Research Support Grant.)

Salmonella engineered to express CD20-targeting antibodies and a drug-converting enzyme can eradicate human lymphomas

Blood ◽  
2013 ◽  
Vol 122 (5) ◽  
pp. 705-714 ◽  
Author(s):  
Paul E. Massa ◽  
Aida Paniccia ◽  
Ana Monegal ◽  
Ario de Marco ◽  
Maria Rescigno
Keyword(s):  
Immune Response ◽  
Tumor Cells ◽  
Tumor Antigen ◽  
Adaptive Immune Response ◽  
Human Tumors ◽  
Converting Enzyme ◽  
Adaptive Immune ◽  
Key Points

Key PointsSalmonella is engineered to specifically infect tumor cells based on recognition of a tumor antigen by a bacterial-expressed antibody. Once inside, Salmonella can transfer cytotoxic cargos to destroy human tumors even in the absence of an adaptive immune response.

Autologous Activated and Expanded Natural Killer Cells Destroy Multiple Myeloma Clonogenic Tumor Cells through NKG2D and Its Ligands

2015 ◽  
Vol 15 ◽  
pp. e245-e246
Author(s):  
A. Leivas ◽  
R.M. Risueño ◽  
A. Pérez-Martínez ◽  
D. Campana ◽  
J.J. Lahuerta ◽  
...  
Keyword(s):  
Multiple Myeloma ◽  
Natural Killer Cells ◽  
Natural Killer ◽  
Tumor Cells ◽  
Killer Cells ◽  
Clonogenic Tumor Cells

scholarly journals Elimination of clonogenic Burkitt's lymphoma cells from human bone marrow using 4-hydroperoxycyclophosphamide in combination with monoclonal antibodies and complement

Blood ◽  
1985 ◽  
Vol 65 (5) ◽  
pp. 1064-1070 ◽  
Author(s):  
P De Fabritiis ◽  
M Bregni ◽  
J Lipton ◽  
J Greenberger ◽  
L Nadler ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Monoclonal Antibodies ◽  
Tumor Cells ◽  
Burkitt’S Lymphoma ◽  
Selective Removal ◽  
Human Bone ◽  
Human Bone Marrow ◽  
Malignant Cells ◽  
Lymphoma Cells ◽  
Clonogenic Tumor Cells

Abstract One requirement for autologous bone marrow transplantation is the selective removal of malignant cells from normal marrow precursors. Development of a clonogenic assay that detects elimination of up to 5 logs of Burkitt's lymphoma cells in the presence of a 20-fold excess of human bone marrow has permitted the evaluation of two different methods for the selective removal of malignant cells. Treatment with 4- hydroperoxycyclophosphamide (4-HC) (60 to 100 micrograms/mL) eliminated 2.0 to 3.5 logs of clonogenic cells. Antitumor activity depended upon the concentration of 4-HC and the length of incubation, but not upon the concentration of normal bone marrow cells. Comparable removal of clonogenic Burkitt's cells was achieved by treatment with rabbit complement (C') and a combination of J5 anti-common acute lymphoblastic leukemia antigen (J5 anti-CALLA), J2 anti-gp 26, and the B1 anti-B1 murine monoclonal antibodies. A combination of 4-HC and monoclonal antibodies proved slightly but significantly more effective than either single agent in eliminating clonogenic tumor cells. Although treatment with 4-HC markedly reduced granulocyte-macrophage colony-forming units- C (GM-CFU-C) content of human bone marrow, neither treatment with 4-HC nor treatment with monoclonal antibodies and C' eliminated precursor cells that could generate new GM-CFU-C after growth in continuous bone marrow cultures. Our data suggest that treatment with 4-HC in combination with multiple monoclonal antibody reagents could be a safe and effective method of eliminating clonogenic tumor cells from human bone marrow.

Sign in / Sign up

Export Citation Format

Share Document