Incidence of spontaneous neoplasms in breeding and retired breeder BALB/cCr mice throughout the natural life span

Peters, Robert L.; Rabstein, Louise S.; Spahn, Gerard J.; Madison, Russell M.; Huebner, Robert J.

doi:10.1002/ijc.2910100207

Cited by 47 publications

(15 citation statements)

References 11 publications

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“…Generally, benign tumors of vascular origin ± hemangiomas, are extremely rare in the populations of laboratory mice. The incidence of spontaneous hemangiomas in mice of dierent strains throughout their natural life ranges from 0.16% to 0.6% (Frith and Wiley, 1982;Peters et al, 1972;Booth and Sundberg, 1995).…”

Section: Analysis Of Hemangiomas In the Hmgcr/mts1 Transgenic Micementioning

confidence: 99%

The metastasis-associated Mts1(S100A4) protein could act as an angiogenic factor

et al. 2001

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The involvement of Mts1(S100A4), a small Ca 2+ -binding protein in tumor progression and metastasis had been demonstrated. However, the mechanism by which mts1(S100A4) promoted metastasis had not been identi®ed. Here we demonstrated that Mts1(S100A4) had signi®cant stimulatory eect on the angiogenesis. We detected high incidence of hemangiomas ± benign tumors of vascular origin in aged transgenic mice ubiquitously expressing the mts1(S100A4) gene. Furthermore, the serum level of the Mts1(S100A4) protein increased with ageing. Tumors developed in Mts1-transgenic mice revealed an enhanced vascular density. We showed that an oligomeric, but not a dimeric form of the Mts1(S100A4) protein was capable of enhancing the endothelial cell motility in vitro and stimulate the corneal neovascularization in vivo. An oligomeric fraction of the protein was detected in the conditioned media as well as in human serum. The data obtained allowed us to conclude that mts1(S100A4) might induce tumor progression via stimulation of angiogenesis. Oncogene (2001) 20, 4685 ± 4695.

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Section: Analysis Of Hemangiomas In the Hmgcr/mts1 Transgenic Micementioning

confidence: 99%

The metastasis-associated Mts1(S100A4) protein could act as an angiogenic factor

et al. 2001

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“…by brother x sister matings with I to 2 generations of random breeding in the production colonies. In order to observe mice at old ages, retired breeders (predominantly females) were entered into a holding colony at 7 to 10 months of age and held for their natural life span (pee accompanying report for complete description -Peters et al, 1972).…”

Section: Micementioning

confidence: 99%

Prevalence of the group‐specific (gs) antigen and infectious virus expressions of the murine C‐type RNA viruses during the life span of BALB/cCr mice

Peters

Hartley

Spahn

et al. 1972

Intl Journal of Cancer

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“…Most spontaneous human and animal tumors develop in older individuals (6-9). As people age, they are predisposed to developing cancer likely due to increasingly more mutations in their somatic cells as well as a decrease in their ability to mount effective immune responses against these malignant cells.…”

Section: Introductionmentioning

confidence: 99%

Spleen Cells from Young but Not Old Immunized Mice Eradicate Large Established Cancers

Schreiber

Arina

Engels

et al. 2012

Clinical Cancer Research

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PurposeSolid tumors that have grown two weeks or longer in mice and have diameters larger than 1 cm are histologically indistinguishable from autochthonous human cancers. When experimental tumors reach this clinically relevant size, they are usually refractory to most immunotherapies but may be destroyed by adoptive T cell transfer. However, TCR-transgenic T cells and/or tumor cells overexpressing antigens are frequently used in these experiments. Here we studied the requirements for destroying clinical size, unmanipulated 8101 tumors by adoptive cell therapy.Experimental Design8101 arose in an old mouse after chronic exposure to UV light. A cancer line was established, which was never serially transplanted. The immunodominant CD8+ T cell-recognized antigen of this tumor is caused by a somatic tumor-specific mutation in the RNA helicase p68. 8101 tumors were treated with spleen cells from young naïve, or young and old immunized mice to ascertain the characteristics of immune cells that lead to rejection.ResultsHere we show that the mutant p68 peptide has an exceptionally high affinity to the presenting MHC class I molecule Kb and that spleen cells from immunized young syngeneic mice adoptively transferred to Rag-/- or cancer-suppressed euthymic mice eradicate 8101 tumors larger than 1 cm in average diameter and established for several weeks. Spleen cells from naïve young mice or from old and boosted (re-immunized) mice were ineffective.ConclusionsRelapse-free destruction of large and long-established tumors expressing a genuine very high-affinity tumor-specific antigen can be achieved by using adoptive transfer of lymphocytes from immunized young individuals.

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Incidence of spontaneous neoplasms in breeding and retired breeder BALB/cCr mice throughout the natural life span

Cited by 47 publications

References 11 publications

The metastasis-associated Mts1(S100A4) protein could act as an angiogenic factor

The metastasis-associated Mts1(S100A4) protein could act as an angiogenic factor

Prevalence of the group‐specific (gs) antigen and infectious virus expressions of the murine C‐type RNA viruses during the life span of BALB/cCr mice

Spleen Cells from Young but Not Old Immunized Mice Eradicate Large Established Cancers

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