Inhibition by Hydrazine Sulfate and Various Hydrazides, of in vivo Growth of Walker 256 Intramuscular Carcinoma, B-16 Melanoma, Murphy-Sturm Lymphosarcoma and L-1210 Solid Leukemia

Oncology ◽  
1973 ◽  
Vol 27 (1) ◽  
pp. 69-80 ◽  
Author(s):  
J. Gold
Keyword(s):  
Hydrazine Sulfate ◽  
Walker 256

THE INFLUENCE OF TUMOR GROWTH ON THE SYNTHESIS OF α2-AP (ACUTE PHASE) GLOBULIN OF RAT SERUM

1967 ◽  
Vol 45 (12) ◽  
pp. 1937-1941 ◽  
Author(s):  
Henry E. Weimer ◽  
Constance Humelbaugh ◽  
Dorothy M. Roberts
Keyword(s):  
Tumor Growth ◽  
Acute Phase ◽  
Tissue Injury ◽  
Sprague Dawley ◽  
Rat Serum ◽  
Serum Haptoglobin ◽  
Sprague Dawley Rats ◽  
Walker 256 ◽  
Implantation Procedure

The effects of growth of the Walker 256 carcinosarcoma on the α2-AP (acute phase) globulin, fibrinogen, seromucoid, and haptoglobin fractions of plasma were investigated in adult, male Sprague–Dawley rats in a longitudinal study. Early increases in α2-AP globulin and seromucoid levels were found to be related to the tissue injury associated with the implantation procedure. Significant elevations in the α2-AP globulin, fibrinogen, and seromucoid fractions coincided with the onset of progressive tumor growth. Serum haptoglobin concentrations exhibited a delayed rise. This was attributed to the in vivo formation of haptoglobin–hemoglobin complexes. It was suggested that the increases in all fractions reflected the release of humoral mediators from injured or necrotic cells wrhich stimulated increased synthesis of the fractions by the liver.

Evidence for in vivo non-mutagenicity of the carcinogen hydrazine sulfate in target tissues of lacZ transgenic mice

1995 ◽  
Vol 16 (4) ◽  
pp. 801-804 ◽  
Author(s):  
George R. Douglas ◽  
John D. Gingerich ◽  
Lynda M. Soper
Keyword(s):  
Transgenic Mice ◽  
Hydrazine Sulfate

Synthese, in vivo- und in vitro-Untersuchungen zur tumorhemmenden Wirkung von cis-Dichloro-dipeptidester-platin(II)-Komplexen / Synthesis, in vivo and in vitro Studies on the Antineoplastic Effect of cis-Dichloro-dipeptide Ester Platinum(II) Complexes

1976 ◽  
Vol 31 (6) ◽  
pp. 832-845 ◽  
Author(s):  
Wolfgang Beck ◽  
Bernhard Purucker ◽  
Michael Girnth ◽  
Helmut Schönenberger ◽  
Horst Seidenberger ◽  
...  
Keyword(s):  
Protein Biosynthesis ◽  
Sarcoma 180 ◽  
Protecting Group ◽  
Yoshida Sarcoma ◽  
Walker 256 Carcinosarcoma ◽  
E Coli ◽  
Antineoplastic Effect ◽  
Walker 256

cis-Dichlorodipeptide esterplatinum complexesCl2Pt(MetGlyOEt),Cl2Pt(EthionylGlyOEt), Cl2Pt(GlyGlyOEt)2 and Cl2Pt(GlySerOEt)2 are prepared from the α-amino acid complexes by peptide synthesis using platinum as an amino protecting group. cis-Cl2Pt(GlyGlyOEt)2 and cis-Cl2Pt(GlySerOEt)2 have been prepared also directly from K2PtCl4 and the dipeptidesters. cis-Cl2Pt(GlyGlyOEt)2 (2 a) and cis-Cl2Pt(NH3)2 (5) lead to a prefered inhibition of the DNA-synthesis of sarcoma 180, Yoshida-sarcoma and Walker-256-carcinosarcoma in vitro; RNA- and protein biosynthesis are influenced to a much lower degree. 2a and 5 cause filamentous growth in Escherichia coli B. The DNA polymerase deficient strain of E. coli, p 3478 pol A-, is more inhibited by 2 a and 5 than the non deficient strain W 3110 pol A+. Tumor growth of di-2-chloro-ethylmethylamine (HN2) resistant sarcoma 180 and of Yoshida sarcoma is weakly inhibited, whereas Walker-256-carcinosarcoma is markedly inhibited; however 2a and 5 show similar inhibition of the same tumor.

scholarly journals MORPHOLOGICAL FEATURES OF DOXORUBICIN-RESISTANT WALKER 256 CARCINOSARCOMA AND RESPONSE OF MAST CELLS

2018 ◽  
Vol 40 (1) ◽  
pp. 42-47
Author(s):  
N V Boroday ◽  
V F Chekhun
Keyword(s):  
Drug Resistance ◽  
Mast Cells ◽  
Staining Intensity ◽  
Morphological Features ◽  
Histamine Content ◽  
Original Strain ◽  
Walker 256 Carcinosarcoma ◽  
Development Of Resistance ◽  
Walker 256

Background: The mechanisms of drug resistance of cancer have not been yet elucidated in details. Recently, the role of mast cells (MCs) in the development of drug resistance has been brought in the limelight. The aim of the study was to examine the morphological features of doxorubicin (DOX)-resistant Walker 256 carcinosarcoma and to assess the response of MCs and histamine content in these cells in relation to the development of resistance to DOX as well as in DOX-resistant tumors. Materials and Methods: The DOX resistance was induced by serial passages of Walker 256 carcinosarcoma in rats in the setting of DOX treatment in vivo. MCs in tumors were detected in the sections by staining with Toluidine Blue O. Histamine content in MCs stained with solution of Water Blue-Orcein was assessed by Astaldi semiquantitative method taking into account different staining intensity. Results: Formation of DOX resistance in the course of serial passages of Walker 256 carcinosarcoma was accompanied by the increase in the number of MCs in tumors and histamine content. Nevertheless, in tumors with phenotype of complete DOX resistance the number of histamine-containing MCs decreased to the same level as in tumors of the original strain that are DOX-sensitive. Conclusion: MCs are involved in formation of DOX resistance in Walker 256 carcinosarcoma.

scholarly journals Corydalis Saxicola Bunting Total Alkaloids Attenuate Walker 256-Induced Bone Pain and Osteoclastogenesis by Suppressing RANKL-Induced NF-κB and c-Fos/NFATc1 Pathways in Rats

2021 ◽  
Vol 11 ◽  
Author(s):  
Linjie Ju ◽  
Peipei Hu ◽  
Ping Chen ◽  
Jiejie Wu ◽  
Zhuoqun Li ◽  
...  
Keyword(s):  
Bone Pain ◽  
Bone Structure ◽  
Osteolytic Lesion ◽  
Bone Cancer ◽  
Total Alkaloids ◽  
Candidate Drug ◽  
Metastatic Bone Pain ◽  
Walker 256

Metastatic bone pain is characterized by insufferable bone pain and abnormal bone structure. A major goal of bone cancer treatment is to ameliorate osteolytic lesion induced by tumor cells. Corydalis saxicola Bunting total alkaloids (CSBTA), the alkaloid compounds extracted from the root of C. saxicola Bunting, have been shown to possess anticancer and analgesic properties. In this study, we aimed to verify whether CSBTA could relieve cancer induced bone pain and inhibit osteoclastogenesis. The in vivo results showed that CSBTA ameliorated Walker 256 induced bone pain and osteoporosis in rats. Histopathological changes also supported that CSBTA inhibited Walker 256 cell-mediated osteolysis. Further in vitro analysis confirmed that CSBTA reduced the expression of RANKL and downregulate the level of RANKL/OPG ratio in breast cancer cells. Moreover, CSBTA could inhibit osteoclastogenesis by suppressing RANKL-induced NF-κB and c-Fos/NFATc1 pathways. Collectively, this study demonstrated that CSBTA could attenuate cancer induced bone pain via a novel mechanism. Therefore, CSBTA might be a promising candidate drug for metastatic bone pain patients.

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