Origin and Significance of Transplantation Antigens Induced on Cells Transformed by UV Radiation

Hostetler, Lisa W.; Kripke, Margaret L.

doi:10.1007/978-1-4613-1925-2_20

Cited by 7 publications

(4 citation statements)

References 80 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…If the lymphoid tumors that arise in the p53 ϩ/Ϫ mice expressed the UV-associated common antigen found on UV-induced skin cancers, they would be able to survive and grow only in UVirradiated mice, which are unable to reject tumor cells bearing this antigen. This raises the interesting and testable hypothesis that perhaps p53 plays a critical role in expression of the elusive UV-associated common antigen recognized by UV-induced suppressor T cells (40).…”

Section: Discussionmentioning

confidence: 99%

UV irradiation augments lymphoid malignancies in mice with one functional copy of wild-type p53

Jiang

Ananthaswamy

Muller

et al. 2001

Proc. Natl. Acad. Sci. U.S.A.

Self Cite

View full text Add to dashboard Cite

Epidemiological studies have suggested an association between exposure to solar UV radiation and the incidence of lymphoid malignancies, which has increased substantially worldwide during the last two decades. Findings from animal studies have raised the question of whether UV radiation might influence the development of lymphoid malignancies by means of its immunosuppressive effect. In this study, we examined the effect of UV irradiation on the development of lymphoid malignancies in mice with no or only one functional copy of p53. Mice that lack both copies of p53 spontaneously develop high frequency of lymphoid malignancies in the thymus and spleen. p53 heterozygous mice with only one copy of the wild-type allele also develop lymphoid malignancies, but with a much lower frequency and a long latent period. In our study using mice of the C57BL͞6 background, only one of the unirradiated mice lacking one copy of p53 (p53 ؉/؊ ) spontaneously developed a lymphoid tumor (6%), whereas 88% of UV-irradiated p53 ؉/؊ mice developed lymphoid tumors in the spleen or liver. None of the control or UV-irradiated p53 wild-type mice developed lymphoid tumors during the 60-week observation period. Both UV-irradiated and unirradiated mice lacking both copies of p53 (p53 ؊/؊ ) rapidly developed thymic lymphomas and͞or lymphoid tumors in spleen or liver. All of the lymphoid tumors tested were of T cell type. The immune responses of the mice to contact sensitization were identical and were suppressed to the same extent by UV irradiation regardless of the genotype. These results indicate that differences in immune reactivity do not account for the different effects of UV radiation on lymphoid malignancies and, in addition, that p53 is not required for generation of T cell-mediated immunity. Interestingly, whereas p53 mutations or loss of heterozygosity did not account for the accelerated development of lymphoid tumors in UV-irradiated p53 ؉/؊ mice, deletions in the p16 INK4a gene were quite common. These data provide the experimental evidence that UV irradiation induces lymphoid neoplasms in genetically susceptible mice and support the hypothesis that extensive sunlight exposure contributes to the induction of lymphoma in humans.tumor suppressor gene ͉ immune suppression T he incidence of non-Hodgkin's lymphoma (NHL) worldwide has increased substantially during the last two decades (1-3). This surge cannot be totally explained by the improvement in diagnosis and recording. Recently, epidemiological studies have suggested an association between the UV radiation in sunlight and the incidence of NHL (3-7). The rise in the incidence of NHL parallels the global increase in melanoma incidence, and patients with NHL are at higher risk of developing melanomas (4, 5). Studies from several groups have demonstrated an increased incidence of nonmelanoma skin cancers in persons with a history of NHL or chronic lymphocytic leukemia, and of NHL or chronic lymphocytic leukemia in persons with a history of skin cancers (5-7). UV radiation, especially...

show abstract

Section: Discussionmentioning

confidence: 99%

UV irradiation augments lymphoid malignancies in mice with one functional copy of wild-type p53

Jiang

Ananthaswamy

Muller

et al. 2001

Proc. Natl. Acad. Sci. U.S.A.

Self Cite

View full text Add to dashboard Cite

show abstract

“…In animal systems, the immunogenicity of such antigens can be monitored in vivo by tumor transplantation assays, and progress has been made in defining antigens that elicit transplantation immunity in several mouse and rat tumors (1)(2)(3). In contrast, immunological analysis of human cancer is limited in the main to the study of humoral and cellular antitumor responses that can be demonstrated in vitro.…”

mentioning

confidence: 99%

Human homologue of murine tumor rejection antigen gp96: 5'-regulatory and coding regions and relationship to stress-induced proteins.

Maki

Old

Srivastava

1990

Proc. Natl. Acad. Sci. U.S.A.

130

View full text Add to dashboard Cite

show abstract

“…The first indication of an association between UV radiation and immune suppression came from studies on UVR-induced skin cancers of mice (reviewed in Kripke, 1981, andHostetler andKripke, 1987). These cancers are highly antigenic and are often immunologically rejected upon transplantation into mice genetically identical to the donor.…”

Section: The Uv Tumor Systemmentioning

confidence: 99%

Photobiology School

Kripke

1990

Photochem & Photobiology

Self Cite

View full text Add to dashboard Cite

Origin and Significance of Transplantation Antigens Induced on Cells Transformed by UV Radiation

Cited by 7 publications

References 80 publications

UV irradiation augments lymphoid malignancies in mice with one functional copy of wild-type p53

UV irradiation augments lymphoid malignancies in mice with one functional copy of wild-type p53

Human homologue of murine tumor rejection antigen gp96: 5'-regulatory and coding regions and relationship to stress-induced proteins.

Photobiology School

Contact Info

Product

Resources

About