Automated measurement of transplantable solid tumors using digital electronic calipers interfaced to a microcomputer

Worzalla, John F.; Bewley, Jesse R.; Grindey, Gerald B.

doi:10.1007/bf00171833

Cited by 14 publications

(4 citation statements)

References 6 publications

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“…with 1 mg/kg MT95‐4 or control human IgG (Sigma) twice per week. The length and width of the tumors were measured using calipers, and the tumor volume was calculated using the formula: width 2 × length × 0.5 …”

Section: Methodsmentioning

confidence: 99%

MT95‐4, a fully humanized antibody raised against aminopeptidase N, reduces tumor progression in a mouse model

et al. 2015

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Aminopeptidase N (APN/CD13) is involved in tumor cell invasion and tumor angiogenesis and is considered a promising therapeutic target in the treatment of cancer. To develop a novel monoclonal antibody-based cancer therapy targeting APN/CD13, we established a fully humanized anti-APN/CD13 monoclonal antibody, MT95-4. In vitro, MT95-4 inhibited APN/CD13 enzymatic activity on the tumor cell surface and blocked tumor cell invasion. B16 mouse melanoma cells stably expressing human APN/CD13 were also established and were inoculated s.c. or injected i.v. into nude mice. We found that expression of human APN/CD13 in murine melanoma cells increased the size of subcutaneous tumors, extent of lung metastasis and degree of angiogenesis in the subcutaneous tumors; these tumor-promoting and angiogenesis-promoting characteristics were reduced by the i.p. administration of MT95-4. To further verify the specificity of MT95-4 for neutralization of APN/CD13 activity, MT95-4 was administered into NOD/SCID mice inoculated s.c. with H1299 or PC14 cells, which exhibit high expression of APN/CD13, or with A549 cells, which exhibit weak expression of APN/CD13. MT95-4 reduced tumor growth and angiogenesis in mice bearing H1299-derived and PC14-derived tumors, but not in mice bearing A549-derived tumors. These results suggested that the antitumor and anti-angiogenic effects of MT95-4 were dependent on APN/CD13 expression in tumor cells. Given that MT95-4 is the first fully humanized monoclonal antibody against APN/CD13, MT95-4 should be recognized as a promising candidate for monoclonal antibody therapy against tumors expressing APN/CD13.

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Section: Methodsmentioning

confidence: 99%

MT95‐4, a fully humanized antibody raised against aminopeptidase N, reduces tumor progression in a mouse model

et al. 2015

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“…For SK-216 experiments, the mice were given drinking water containing or lacking SK-216 (100 or 500 ppm). Until 14 days after the inoculation, the length and width of the tumors were measured using a caliper twice a week and tumor volume was calculated using the formula: width 2 Â length Â 0.5 (25).…”

Section: Subcutaneous Tumor Modelmentioning

confidence: 99%

SK-216, an Inhibitor of Plasminogen Activator Inhibitor-1, Limits Tumor Progression and Angiogenesis

Masuda

Hattori

Senoo

et al. 2013

Molecular Cancer Therapeutics

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Plasminogen activator inhibitor-1 (PAI-1), which can be produced by host and tumor cells in the tumor microenvironment, is intimately involved in tumor progression. In the present study, to pursue the possibility that PAI-1 could be a therapeutic target in the management of malignancy, SK-216, a specific PAI-1 inhibitor, was orally administered to wild-type mice that were subcutaneously implanted or intravenously injected with either PAI-1-secreting Lewis lung carcinoma (LLC) or PAI-1-nonsecreting B16 melanoma cells. The systemic administration of SK-216 was found to reduce the size of subcutaneous tumors and the extent of metastases, regardless of PAI-1 secretion levels from the tumor cells. SK-216 also reduced the extent of angiogenesis in the tumors and inhibited VEGF-induced migration and tube formation by human umbilical vein endothelial cells in vitro. Then, to determine whether host or tumor PAI-1 was more crucial in tumor progression and angiogenesis, PAI-1-deficient or wild-type mice were subcutaneously implanted or intravenously injected with LLC or PAI-1 knockdown LLC cells. Tumor progression was shown to be controlled by the presence of host PAI-1 and not affected by the PAI-1 levels in the tumors. Similarly, host PAI-1 played a more crucial role in tumor angiogenesis than did tumor PAI-1. These observations suggest that regardless of the PAI-1 levels in the tumor, the systemic administration of SK-216 exerts an antitumor effect through its interaction with host PAI-1. This antitumor effect might be mediated by the antiangiogenic properties of SK-216. Mol Cancer Ther; 12(11); 2378-88. Ó2013 AACR.

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“…Each week following tumor implantation (each group contained seven mice), two-dimensional measurements (width and length in mm) of all tumors were taken using digital electronic calipers interfaced to a microcomputer and converted into tumor weight (Worzalla et al, 1990).…”

Section: Assay For Growth In Soft Agarosementioning

confidence: 99%

Conditional transformation of rat embryo fibroblast cells by a cyclin D1-cdk4 fusion gene

et al. 1999

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Cyclin D1 gene overexpression is a frequent event in a number of human cancers. These observations have led to the suggestion that cyclin D1 alterations might play a role in the etiology of cancer. This possibility is supported by the ®nding that transfection of mammalian cells with cyclin D1 can accelerate progression through the G1 phase of the cell cycle. Moreover, cyclin D1 can function as an oncogene by cooperating with activated Ha-ras to transform primary rat embryo ®broblasts (REFs). In addition, cyclin D1 transgenics develop hyperplasia and neoplasia of the thymus and mammary gland. We have constructed a novel fusion gene consisting of full-length human cyclin D1 and cdk4 genes. This fusion gene was expressed in insect cells and the fusion protein was shown to be enzymatically active. The fusion gene was expressed in mammalian cells under the control of tet-repressor. This fusion gene immortalized primary REFs, and cooperated with activated Haras to transform primary REFs, in terms of anchorageindependent growth in vitro and formation of tumors in vivo. Utilizing a tet-regulated gene expression system, we have shown that proliferation of stably transfected primary REFs in vitro and in vivo is dependent on the continued expression of the cyclin D1-cdk4 fusion gene. These cell lines could be useful in the discovery of novel cancer therapeutics to modulate cyclin D1.cdk4 activity.

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Automated measurement of transplantable solid tumors using digital electronic calipers interfaced to a microcomputer

Cited by 14 publications

References 6 publications

MT95‐4, a fully humanized antibody raised against aminopeptidase N, reduces tumor progression in a mouse model

MT95‐4, a fully humanized antibody raised against aminopeptidase N, reduces tumor progression in a mouse model

SK-216, an Inhibitor of Plasminogen Activator Inhibitor-1, Limits Tumor Progression and Angiogenesis

Conditional transformation of rat embryo fibroblast cells by a cyclin D1-cdk4 fusion gene

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