Neoplasms and Amyloidosis in Strains of Mice Treated With 3-Methylcholanthrene23

Akamatsu, Yuzuru; Barton, Betty P.

doi:10.1093/jnci/52.2.377

Cited by 6 publications

(4 citation statements)

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“…In addition, the spontaneous neoplasms of ϩ/ϩ mice developed with a much lower frequency, and were more morphologically diverse than the gld tumors (65,66). Consistent with the strain-related differences in tumor incidence observed in the present study, the incidence of B cell tumors in the BALB ϩ/ϩ mice was significantly higher than in the C3H ϩ/ϩ mice (66). The persistence in strain differences in tumor susceptibility in the gld mice, suggests that the pro-oncogenic effects of the FasL defect may complement, but not override, preexisting tumor susceptibility factors.…”

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

“…Both BALB ϩ/ϩ and C3H ϩ/ϩ mice have been reported to develop B lineage tumors, but these generally were not detected until the mice were 2-3 yr of age (65,66). In addition, the spontaneous neoplasms of ϩ/ϩ mice developed with a much lower frequency, and were more morphologically diverse than the gld tumors (65,66). Consistent with the strain-related differences in tumor incidence observed in the present study, the incidence of B cell tumors in the BALB ϩ/ϩ mice was significantly higher than in the C3H ϩ/ϩ mice (66).…”

Section: Discussionmentioning

confidence: 99%

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Spontaneous Development of Plasmacytoid Tumors in Mice with Defective Fas–Fas Ligand Interactions

Davidson

Giese

Fredrickson

1998

The Journal of Experimental Medicine

165

112

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B cell malignancies arise with increased frequency in aging individuals and in patients with genetic or acquired immunodeficiency (e.g., AIDS) or autoimmune diseases. The mechanisms of lymphomagenesis in these individuals are poorly understood. In this report we investigated the possibility that mutations at the Fas (lpr) and Fasl (gld) loci, which prevent Fas-mediated apoptosis and cause an early onset benign lymphoid hyperplasia and autoimmunity, also predispose mice to malignant lymphomas later in life. Up to 6 mo of age, hyperplasia in lpr and gld mice results from the predominant accumulation of polyclonal T cell subsets and smaller numbers of polyclonal B cells and plasma cells. Here, we examined C3H-lpr, C3H-gld, and BALB-gld mice 6–15 mo of age for the emergence of clonal T and B cell populations and found that a significant proportion of aging mice exclusively developed B cell malignancies with many of the hallmarks of immunodeficiency-associated B lymphomas. By 1 yr of age, ∼60% of BALB-gld and 30% of C3H-gld mice had monoclonal B cell populations that grew and metastasized in scid recipients but in most cases were rejected by immunocompetent mice. The tumors developed in a milieu greatly enriched for plasma cells, CD23− B cells and immunodeficient memory T cells and variably depleted of B220+ DN T cells. Growth factor–independent cell lines were established from five of the tumors. The majority of the tumors were CD23− and IgH isotype switched and a high proportion was CD5+ and dull Mac-1+. Considering their Ig secretion and morphology in vivo, most tumors were classified as malignant plasmacytoid lymphomas. The delayed development of the gld tumors indicated that genetic defects in addition to the Fas/Fasl mutations were necessary for malignant transformation. Interestingly, none of the tumors showed changes in the genomic organization of c-Myc but many had one or more somatically-acquired MuLV proviral integrations that were transmitted in scid passages and cell lines. Therefore, insertional mutagenesis may be a mechanism for transformation in gld B cells. Our panel of in vivo passaged and in vitro adapted gld lymphomas will be a valuable tool for the future identification of genetic abnormalities associated with B cell transformation in aging and autoimmune mice.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Spontaneous Development of Plasmacytoid Tumors in Mice with Defective Fas–Fas Ligand Interactions

Davidson

Giese

Fredrickson

1998

The Journal of Experimental Medicine

165

112

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“…The spleen is the organ affected earliest and most severely; the liver is the next most commonly affected organ; renal glomeruli and blood vessels may contain heavy deposits [1,4].…”

Section: Amyloidosis In Micementioning

confidence: 99%

Spontaneous Amyloidosis in Outbred CD-1 Mice

Conner¹,

Conner²,

Fox³

et al. 1983

Pathol Immunopathol Res

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No Evidence for Tumorigenesis of AAV Vectors in a Large-Scale Study in Mice

et al. 2005

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Six hundred ninety-five mice received adeno-associated virus (AAV) vectors, mostly via portal vein injection. At necropsy, the livers were inspected for tumors, and tissue sections were prepared for histology. We observed only one tumor, a lipoma, resulting in a tumor frequency of 0.14%. This tumor contained fewer vector genomes per total DNA than the surrounding liver tissue, as shown by quantitative PCR. In another mouse we found a macroscopically visible nodule containing lymphocytes. Immunohistochemistry revealed cells not of monoclonal origin, and they contained fewer AAV genomes than the surrounding hepatocytes. There were no macroscopic tumors in 226 control mice. Upon microscopic examination, lymphocytic infiltrates were found in 5% of livers of both control and vector-treated mice; no transgene expression was seen in those infiltrates in AAV-injected animals. Compared to an average frequency of spontaneous liver tumors in C57BL/6 mice (0-10%), and given the absence of high levels of vector DNA in the observed tumor, we conclude that AAV vectors do not predispose these target animals to the formation of liver tumors.

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Neoplasms and Amyloidosis in Strains of Mice Treated With 3-Methylcholanthrene23

Cited by 6 publications

References 0 publications

Spontaneous Development of Plasmacytoid Tumors in Mice with Defective Fas–Fas Ligand Interactions

Spontaneous Development of Plasmacytoid Tumors in Mice with Defective Fas–Fas Ligand Interactions

Spontaneous Amyloidosis in Outbred CD-1 Mice

No Evidence for Tumorigenesis of AAV Vectors in a Large-Scale Study in Mice

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