Analysis Tools
neoplasm
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• skin papillomas (intitiated by 200 nmol DMBA; 7,12-dimethylbenzanthracene and promoted with 4 ug TPA; 12-O-tetradecanolyphorbol-13-acetate/application) do not occur in Cd34-null mice whereas wild-type mice do develop papillomas; males develop more tumors than females
• by 11-12 weeks, significantly more wild-type male mice have skin tumors than mutant mice, and after 20 weeks, tumor incidence and multiplicity is much greater
• using a more stringent tumor initiation paradigm (400 nmol DMBA, 5 ug TPA), male null mice develop skin papillomas starting at week 15, compared to wild-type which develop tumors at 8 weeks; overall tumor numbers (0.4 tumors/mouse) are lower than in wild type (4.6/mouse) by week 20
• female mutants also develop a low incidence of tumors
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immune system
| N |
• mutants and wild-type controls have similar lymphocyte adhesion to high endothelial venules (HEV), leukocyte rolling, neutrophil migration and delayed-type hypersensitivity response (DTH)
• numbers of CD4-positive and CD8-positive cells in lung sections after OVA inhalation appear reduced, but significance was not reached
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• 3 hours after OVA inhalation, mutant lungs show 3-fold lower accumulation of eosinophils in perivascular areas as measured in bronchoalveolar lavage than wild-type
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homeostasis/metabolism
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• primary carcinogenic DMBA adduct levels are slightly lower in mutants than wild-type 24 hours after 400 nmol DMBA dose, but DMBA is metabolically activated by keratinocytes in both mutants and wild-type
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• skin papillomas (intitiated by 200 nmol DMBA; 7,12-dimethylbenzanthracene and promoted with 4 ug TPA; 12-O-tetradecanolyphorbol-13-acetate/application) do not occur in Cd34-null mice whereas wild-type mice do develop papillomas; males develop more tumors than females
• by 11-12 weeks, significantly more wild-type male mice have skin tumors than mutant mice, and after 20 weeks, tumor incidence and multiplicity is much greater
• using a more stringent tumor initiation paradigm (400 nmol DMBA, 5 ug TPA), male null mice develop skin papillomas starting at week 15, compared to wild-type which develop tumors at 8 weeks; overall tumor numbers (0.4 tumors/mouse) are lower than in wild type (4.6/mouse) by week 20
• female mutants also develop a low incidence of tumors
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cellular
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• BrdU-labeled follicle bulge cells do not show as great a proliferative response (dilution of label) as wild-type cells after TPA treatment
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hematopoietic system
| N |
• platelet, red and white blood cell, and hematopoietic stem cell (HSC) counts are normal in mutants
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• 3 hours after OVA inhalation, mutant lungs show 3-fold lower accumulation of eosinophils in perivascular areas as measured in bronchoalveolar lavage than wild-type
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integument
| N |
• untreated 7-week old mice have normal hair follicle morphology as well as normal marker gene expression
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• after TPA treatment, hair follicles in mutant skin remain in telogen or early anagen, in contrast to wild-type follicles which are in anagen and have large, heavily pigmented, and basophilic hair bulbs extending deep in to the dermis
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• after treatment, epidermis of B6;129 control mice is thicker than that of mutants at 1 and 48 hours, but epidermis of C57BL/6 controls and mutant mice show similar thickness at both time points after treatment
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• after TPA treatment, basal layer cell number is increased in wild-type and cells have elongated rectangular shapes, compared to small, uniformly cuboidal cells in basal layer in treated mutant mice
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