An E mu-v-abl transgene elicits plasmacytomas in concert with an activated myc gene.

Rosenbaum, H.; Harris, Alan W.; Bath, Mary L.; McNeall, J.; Webb, Elizabeth; Adams, Jerry M.; Cory, Suzanne

doi:10.1002/j.1460-2075.1990.tb08187.x

Cited by 81 publications

(64 citation statements)

References 50 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…While some of the spontaneous tumors that were analysed showed an elevated Pim1 expression (6/16), all tumors expressed the c-Myc gene at high levels (16/16) (data not shown). Southern blot analysis indicated that the c-Myc activation in these tumors was not the result of translocation, as observed in most plasmacytomas of the Em-v-Abl mice (Rosenbaum et al, 1990). Injection of tumor cells of three dierent lymphomas into syngeneic hosts caused secondary tumors after a latency of 2 ± 4 weeks.…”

Section: Embmi1 Transgenic Mice Are Predisposed To B and T Cell Lymphmentioning

confidence: 80%

Perturbation of B and T cell development and predisposition to lymphomagenesis in EμBmi1 transgenic mice require the Bmi1 RING finger

et al. 1997

View full text Add to dashboard Cite

Proviral activation of the Bmi1 gene has implicated Bmi1 as a collaborator of c-Myc in lymphomagenesis. To determine the eect of Bmi1 overexpression on hematopoiesis and lymphomagenesis transgenic mice were generated that overexpress dierent forms of the Bmi1 protein in their lymphoid compartment. EmBmi1 transgenic mice, overexpressing the wild type Bmi1 protein showed a perturbed lymphoid development and were highly susceptible to B and T cell lymphomagenesis. Mutational analysis of the Bmi1 protein demonstrated that the conserved N-terminal RING ®nger and central part of Bmi1 are essential for its oncogenic potential whereas the C-terminal Pro-Ser rich region is not required. We have used provirus tagging in the EmBmi1 mice to identify genes that cooperate with Bmi1 in lymphomagenesis. MoMLV infection in EmBmi1 transgenic mice accelerated lymphoma development. Proviral activation of the Pim and Myc genes but not the G®1 gene were frequently observed in these tumors. These results demonstrate that Bmi1 is a potent oncogene and suggest that it plays an important role in early lymphoid development.

show abstract

Section: Embmi1 Transgenic Mice Are Predisposed To B and T Cell Lymphmentioning

confidence: 80%

Perturbation of B and T cell development and predisposition to lymphomagenesis in EμBmi1 transgenic mice require the Bmi1 RING finger

et al. 1997

View full text Add to dashboard Cite

show abstract

“…For this purpose, we generated transgenic mice for Zfp521 and crossed them with EHKI DNeo mice. To express Zfp521 in lymphoid cells, Zfp521 complementary DNA with an HA tag (Zfp521HA) was subcloned into EmSV vector, which has been successfully used to express target genes in the lymphoid lineage (Rosenbaum et al, 1990) (Figure 5a). Among several transgenic lines established (EmSV/ Zfp521), mice of a line that expresses Zfp521HA at a high level in lymphoid cells (data not shown) were chosen and crossed with EHKI DNeo mice.…”

Section: Resultsmentioning

confidence: 99%

Identification of Zfp521/ZNF521 as a cooperative gene for E2A-HLF to develop acute B-lineage leukemia

et al. 2010

View full text Add to dashboard Cite

E2A-hepatic leukemia factor (HLF) is a chimeric protein found in B-lineage acute lymphoblastic leukemia (ALL) with t(17;19). To analyze the leukemogenic process and to create model mice for t(17;19)-positive leukemia, we generated inducible knock-in (iKI) mice for E2A-HLF. Despite the induced expression of E2A-HLF in the hematopoietic tissues, no disease was developed during the long observation period, indicating that additional gene alterations are required to develop leukemia. To elucidate this process, E2A-HLF iKI and control littermates were subjected to retroviral insertional mutagenesis. Virus infection induced acute leukemias in E2A-HLF iKI mice with higher morbidity and mortality than in control mice. Inverse PCR detected three common integration sites specific for E2A-HLF iKI leukemic mice, which induced overexpression of zinc-finger transcription factors: growth factor independent 1 (Gfi1), zinc-finger protein subfamily 1A1 isoform a (Zfp1a1, also known as Ikaros) and zinc-finger protein 521 (Zfp521). Interestingly, tumors with Zfp521 integration exclusively showed B-lineage ALL, which corresponds to the phenotype of human t(17;19)-positive leukemia. In addition, ZNF521 (human counterpart of Zfp521) was found to be overexpressed in human leukemic cell lines harboring t(17;19). Moreover, both iKI for E2A-HLF and transgenic for Zfp521 mice frequently developed B-lineage ALL. These results indicate that a set of transcription factors promote leukemic transformation of E2A-HLF-expressing hematopoietic progenitors and suggest that aberrant expression of Zfp521/ZNF521 may be clinically relevant to t(17;19)-positive B-lineage ALL.

show abstract

“…Human myelomas overexpress the tyrosine kinase protein, Abl (23), and a proportion of transgenic mice expressing v-Abl, the oncogene product of the Abelson murine leukemia virus under the control of the Ig heavy chain (E ) enhancer and the SV40 Tag promoter, develop plasmacytomas with age (24,25). C57BL/6 mice are normally relatively resistant to plasmacytoma formation, both in transgenic models and in peritoneal irritant-induced tumor models (26)(27)(28).…”

Section: Mlh Loss Accelerates B-cell Lymphomagenesis In Pfp-deficientmentioning

confidence: 99%

Perforin-mediated suppression of B-cell lymphoma

Bolitho

Street

Westwood

et al. 2009

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

View full text Add to dashboard Cite

An E mu-v-abl transgene elicits plasmacytomas in concert with an activated myc gene.

Cited by 81 publications

References 50 publications

Perturbation of B and T cell development and predisposition to lymphomagenesis in EμBmi1 transgenic mice require the Bmi1 RING finger

Perturbation of B and T cell development and predisposition to lymphomagenesis in EμBmi1 transgenic mice require the Bmi1 RING finger

Identification of Zfp521/ZNF521 as a cooperative gene for E2A-HLF to develop acute B-lineage leukemia

Perforin-mediated suppression of B-cell lymphoma

Contact Info

Product

Resources

About