Indirect induction of radiation lymphomas in mice. Evidence for a novel, transmissible leukemogen.

Lieberman, Miriam; Hansteen, Gun; McCune, JM; Scott, Martin; White, J. C.

doi:10.1084/jem.166.6.1883

Cited by 18 publications

(9 citation statements)

References 16 publications

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“…A more generalized role for BAD in suppressing oncogenesis was provided by the emergence of earlier stage pre-T and pro-͞pre-B cell lymphoblastic leukemia͞lymphoma after ␥-irradiation. Irradiation induces genomic instability and, secondarily, can activate B cell ecotropic retroviruses as a consequence of genetic recombination between endogenous eco-and xenotropic retroviruses in the genesis of lymphoma (32). Mice defective in p53, which induces an apoptotic response to double-stranded DNA breaks, demonstrate enhanced susceptibility to irradiation-induced tumors.…”

Section: Discussionmentioning

confidence: 99%

Bad -deficient mice develop diffuse large B cell lymphoma

Ranger

Zha

Harada

et al. 2003

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

255

222

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The proapoptotic activity of the ''BH3-only'' molecule BAD can be differentially regulated by survival factor signaling. Bad-deficient mice lacking both BAD long and BAD short proteins proved viable, and most cell types appeared to develop normally. BAD did not exclusively account for cell death after withdrawal of survival factors, but it was an intermediate for epidermal growth factor-or insulin-like growth factor I-countered apoptosis, consistent with a ''sensitizing'' BH3-only molecule. Lymphocytes developed normally with no premalignant hyperplasia, but they displayed subtle abnormalities in proliferation and IgG production. Despite the minimal phenotype, Bad-deficient mice progressed, with aging, to diffuse large B cell lymphoma of germinal center origin. Exposure of Bad-null mice to sublethal ␥-irradiation resulted in an increased incidence of pre-T cell and pro-͞pre-B cell lymphoblastic leukemia͞ lymphoma. Thus, proapoptotic BAD suppresses tumorigenesis in the lymphocyte lineage.

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Section: Discussionmentioning

confidence: 99%

Bad -deficient mice develop diffuse large B cell lymphoma

Ranger

Zha

Harada

et al. 2003

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

255

222

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“…At necropsy, we noted that 5 of the 11 moribund or dead mice from the group receiving only the conditioning regimen had developed thymic lymphomas. 48,49 The mice analyzed had lymphomas of T-cell origin. We did not observe any thymic lymphomas in the mice that received allotransplants.…”

Section: Attenuation Of Autoimmune Disease By Transplantation Of Allomentioning

confidence: 99%

Reversal of autoimmune disease in lupus-prone New Zealand black/New Zealand white mice by nonmyeloablative transplantation of purified allogeneic hematopoietic stem cells

Smith-Berdan

Gille

Weissman

et al. 2007

Blood

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Patients with severe systemic lupus erythematosus (SLE) refractory to conventional treatment are candidates for autologous hematopoietic stem cell (HSC) transplantation if the intent is to reset the immunologic clock. These patients might be candidates for allotransplantation with (SLE)-resistant major histocompatibility complex (MHC) haplotype-matched HSC if partial or complete replacement of an autoimmune-prone system is the intent. Using lupus-prone New Zealand black ؋ New Zealand white (NZBW) mice, we investigated the use of highly enriched, haplomismatched, allogeneic HSC to prevent development of or to treat established autoimmune pathology. Young NZBW mice receiving purified allogeneic HSC transplants had improved survival, decreased proteinuria, circulating immune complexes, and autoantibodies to nuclear antigens than did untreated mice or mice given NZBW HSCs. NZBW mice with established lupus-like disease that received nonmyeloablative conditioning and transplants of (MHC) haplomismatched allogeneic HSCs also had greatly increased overall survival. Mice that received transplants exhibited stabilization or reversal of their lupus symptoms; stabilized or decreased proteinuria, and a lower frequency of elevated circulating immune complexes or autoantibodies than did control mice. Induction of durable mixed chimerism by transplantation of purified allogeneic HSCs after nonmyeloablative conditioning has the potential to reverse symptoms of established NZBW lupus. (Blood.

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“…The recent study by Lie-berman et al . (46) has confirmed the indirect mechanism of radiation-induced lymphomagenesis but has demonstrated that such lymphomagenesis is mediated by the transmissible agent that is not identical to RadLV. Recently it has also been reported that irradiation of hematopoietic stroma cells induces the production of certain growth factor(s) that support the development of myelogenous leukemia (47).…”

Section: Discussionmentioning

confidence: 91%

Strain dependency of B and T lymphoma development in immunoglobulin heavy chain enhancer (E mu)-myc transgenic mice.

Yukawa

Kikutani

Inomoto

et al. 1989

The Journal of Experimental Medicine

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The involvement of dysregulated c-myc expression has been well established in certain virus-or chemical-induced and naturally developing tumors (1-5). Most of murine plasmacytomas and human Burkitt's lymphomas have been shown to carry a chromosomal translocation involving c-myc and Ig genes (2-5). In such tumor cells, only the c-myc transcripts from the translocated allele are constitutively expressed, while the normal allele is completely suppressed, suggesting that the translocation affects the expression of the c-myc gene of the normal allele as well as that of the translocated one (6, 7). Recently it has been shown that Ig heavy chain enhancer (Ew) t-driven c-myc can induce immature B cell tumors in the transgenic mice (8), which is a direct demonstration of the involvement of the translocated c-myc gene in B lymphomagenesis . Moreover, tumors developed in such transgenic mice have been demonstrated to be monoclonal or oligoclonal, suggesting that the malignant transformation requires secondary events following an abnormal expression of c-myc gene. It is likely that such events might be determined or influenced by factors intrinsic to certain cells, or by environmental and genetic factors. Thus, the transgenic mice carrying activated oncogenes such as c-myc can also be a useful system to study such factors influencing tumorigenesis.To study the genetic or environmental factors that affect the myc-induced lymphomagenesis, we introduced the translocated human c-myc gene into two inbred strains ofmice, C57BL/6 and C3H/HeJ, which have different genetic backgrounds. We have observed the preferential development ofT lymphomas in C3H/HeJ transgenic mice, whereas B6 transgenic mice mostly developed B lymphomas. Furthermore, the bone marrow transfer experiments using prelymphomatous transgenic mice suggest that environmental factors might influence the development ofT lymphoma in C3H/HeJ mouse.

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Indirect induction of radiation lymphomas in mice. Evidence for a novel, transmissible leukemogen.

Cited by 18 publications

References 16 publications

Bad -deficient mice develop diffuse large B cell lymphoma

Bad -deficient mice develop diffuse large B cell lymphoma

Reversal of autoimmune disease in lupus-prone New Zealand black/New Zealand white mice by nonmyeloablative transplantation of purified allogeneic hematopoietic stem cells

Strain dependency of B and T lymphoma development in immunoglobulin heavy chain enhancer (E mu)-myc transgenic mice.

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