Genes (42)
Species: human : 20 mouse : 22 | |
Mouse | BCL11B | 64919 | B-cell CLL/lymphoma 11B (zinc finger protein) | Mouse thymic lymphomas induced by gamma-irradiation exhibited homozygous deletions of the Rit1/Bcl11b tumor suppressor gene on chromosome 12 at high frequencies. Homozygous deletions and point mutations of the Rit1/Bcl11b gene in gamma-ray induced mouse thymic lymphomas. Involvement of V(D)J recombinase in the generation of intragenic deletions in the Rit1/Bcl11b tumor suppressor gene in gamma-ray-induced thymic lymphomas and in normal thymus of the mouse. | Mouse | FADD | 8772 | Fas (TNFRSF6)-associated via death domain | Later in life all FADD-DN rag-1(-/-) mice developed thymic lymphoma, indicating that FADD/MORT1 can act as a tumour suppressor. | Mouse | EED | 8726 | embryonic ectoderm development | The present report demonstrates two novel functional activities of eed: alteration of thymocyte maturation and suppression of thymic lymphoma development. Furthermore, mice that are homozygous or heterozygous for the hypomorphic eed allele have an increased incidence and decreased latency of N-methyl-N-nitrosourea-induced thymic lymphoma compared to wild-type littermates. | Mouse | TRB@ | 6957 | | The first constant region of the Tcrb gene was completely deleted from the DNA of 8/10 mouse cell lines established from 3-methylcholanthrene-induced RF/J thymic lymphomas, but 6/7 primary lymphomas contained the first constant region sequences. | Mouse | TCF3 | 6929 | transcription factor 3 | Mice with null mutations in the E2A gene are highly susceptible to the spontaneous development of thymic lymphomas. In addition, mice deficient for E2A are highly susceptible to thymic lymphoma. | Mouse | TAL1 | 6886 | T-cell acute lymphocytic leukemia 1 | In fact, expression of scl in both genetic backgrounds paradoxically reduced the frequency of thymic lymphomas and, at least in the p53 nullizygous mice, shifted the pattern of organ involvement to the peripheral lymphoid organs. | Mouse | STAT4 | 6775 | signal transducer and activator of transcription 4 | At the time of termination of the experiment 16 weeks after injection, 78% of homozygous Stat4-deficient mice had developed thymic lymphomas. Dysfunction of Stat4 leads to accelerated incidence of chemical-induced thymic lymphomas in mice. | Mouse | RAG2 | 5897 | recombination activating gene 2 | In contrast to expectation, the data presented here indicate that development of malignant thymic lymphoma in Atm(-/-) mice is not prevented by loss of RAG-2 and thus is not dependent on V(D)J recombination. | Mouse | RAG1 | 5896 | recombination activating gene 1 | A cell line derived from a RAG-1 x p53 double mutant thymic lymphoma expressed low levels of CD3-epsilon, -gamma, and -delta on the surface. | Mouse | PVT1 | 5820 | Pvt1 oncogene (non-protein coding) | It is interesting however that two of them (Mlvi-1 and Mlvi-2), as well as pvt-1/mis-1, map to mouse chromosome 15 which is known to become trisomic in murine thymic lymphomas. Dot blot analysis of RNA from radiation-induced thymic lymphomas and normal thymuses demonstrated that there was no substantial difference between them in the expression of retroviral sequences, pim-1, pvt-1, int-1, or int-2, although transcripts that could be hybridized to the retroviral sequences were slightly elevated in some radiation-induced thymic lymphomas. | Mouse | PMS2 | 5395 | PMS2 postmeiotic segregation increased 2 (S. cerevisiae) | Mice deficient in the DNA mismatch repair (MMR) gene, PMS2, develop spontaneous thymic lymphomas and sarcomas. A significantly higher incidence of thymic lymphomas was observed in MNU-treated PMS2-/- mice, compared to wildtype PMS2+/+ mice (100 vs 52%; P _lt_ 0.001). They demonstrated a similar incidence of thymic lymphomas, suggesting that expression of the single normal PMS2 allele is sufficient to protect the thymus and implying that a single dose of MNU may not efficiently knock out the remaining PMS2 allele in the thymus. Mice defective in the DNA mismatch gene PMS2 are hypersensitive to MNU induced thymic lymphoma and are partially protected by transgenic expression of human MGMT. Mice defective in the MMR gene PMS2 are susceptible to spontaneous thymic lymphoma and sarcomas. PMS2-deficient (PMS2(-/-)) mice are hypersensitive to N-methyl-N-nitrosourea (MNU)-induced thymic lymphomas based on the failure to initiate mismatch repair (MMR) at O(6)-methylguanine:T mismatches formed after MNU exposure. | Mouse | NOTCH2 | 4853 | notch 2 | In the present work we present evidence that gamma-radiation-induced thymic lymphomas in (C57BL/6 J x BALB/c) F1 hybrid mice often exhibit increased levels of Notch1 expression, but, contrary to what was expected, they also exhibit a clearly reduced Notch2 mRNA expression, suggesting a cooperative antagonism of these genes. | Mouse | NOTCH1 | 4851 | notch 1 | To elucidate the effect of Notch1 abnormalities in radiation-induced lymphomagenesis, we determined the structure of the Notch1 gene and examined the frequency and the sites of Notch1 rearrangements in radiation-induced mouse thymic lymphomas. More than 50% of radiation-induced thymic lymphomas exhibited Notch1 rearrangements, suggesting that Notch1 acts as a major oncogene in radiation-induced lymphomagenesis. In addition, we found activating Notch1 mutations in 31% of thymic lymphomas that occur in mice deficient for various combinations of the H2AX, Tp53, and Rag2 genes. Defective expression of Notch1 and Notch2 in connection to alterations of c-Myc and Ikaros in gamma-radiation-induced mouse thymic lymphomas. We describe three pathways for the formation of 5;-deletions of the Notch1 gene in thymic lymphomas of wild-type or V(D)J recombination-defective severe combined immune deficiency (scid) mice. In the present work we present evidence that gamma-radiation-induced thymic lymphomas in (C57BL/6 J x BALB/c) F1 hybrid mice often exhibit increased levels of Notch1 expression, but, contrary to what was expected, they also exhibit a clearly reduced Notch2 mRNA expression, suggesting a cooperative antagonism of these genes. Radiation-induced deletions in the 5; end region of Notch1 lead to the formation of truncated proteins and are involved in the development of mouse thymic lymphomas. Involvement of illegitimate v(d)j recombination or microhomology-mediated nonhomologous end-joining in the formation of intragenic deletions of the notch1 gene in mouse thymic lymphomas. | Mouse | MTF1 | 4520 | metal-regulatory transcription factor 1 | Predisposition to mouse thymic lymphomas in response to ionizing radiation depends on variant alleles encoding metal-responsive transcription factor-1 (Mtf-1). Using a mouse model of gamma-ray-induced thymic lymphomas, we performed linkage analysis and haplotype mapping that suggested Mtf-1, metal-responsive transcription factor-1 (Mtf-1), as a candidate lymphoma susceptibility gene. | Mouse | MLVI2 | 4309 | Moloney murine leukemia virus (MoMuLV) integration site 2 homolog | Cellular DNA region involved in induction of thymic lymphomas (Mlvi-2) maps to mouse chromosome 15. It is interesting however that two of them (Mlvi-1 and Mlvi-2), as well as pvt-1/mis-1, map to mouse chromosome 15 which is known to become trisomic in murine thymic lymphomas. | Mouse | IL9 | 3578 | interleukin 9 | We have recently shown that interleukin-9 (IL-9) strongly stimulates the proliferation of mouse thymic lymphomas in vitro. Thymic lymphomas in interleukin 9 transgenic mice. Indeed, IL-9 overexpression induces thymic lymphomas in mice, and IL-9 production is associated with Hodgkin disease and HTLV-I transformed T cells in humans. Interleukin-9 stimulates in vitro growth of mouse thymic lymphomas. Analysis of eight other factor-independent thymic lymphoma lines showed significant protection in seven and six cell lines with IL-9 and IL-4, respectively, whereas only three were protected by IL-7 and only two by IL-2. We have previously reported that cytokines such as IL-9, IL-4, and IL-6 protect murine thymic lymphoma cell lines against dexamethasone-induced apoptosis. Although freshly isolated normal T cells do not respond to IL-9, this cytokine induces the proliferation of murine T cell lymphomas in vitro and in vivo overexpression of IL-9 results in the development of thymic lymphomas. While freshly isolated normal T cells do not respond to IL-9, this cytokine induces the proliferation of murine T cell lymphomas in vitro, and in vivo overexpression of IL-9 results in the development of thymic lymphomas. IL-9 transgenic mice were chosen as the animal model system, because dysregulated expression of the IL-9 gene in transgenic mice results in the sporadic development of spontaneous thymic lymphomas. Interleukin-9 is a major anti-apoptotic factor for thymic lymphomas. | Mouse | CDKN2C | 1031 | cyclin-dependent kinase inhibitor 2C (p18, inhibits CDK4) | Whereas thymic lymphomas or pituitary tumors predominate in mice lacking p53 or Ink4c, respectively, animals lacking both genes develop many vascular tumors and also present with medulloblastomas not observed in the parental strains. | Mouse | BUB1B | 701 | BUB1 mitotic checkpoint serine/threonine kinase B | This report demonstrates that Bub1 and BubR1 mutant proteins from Brca2-/- thymic lymphomas have defects in the phosphorylation and kinetochore localization after spindle damage. Thymic lymphomas from Brca2-mutant mice harbor mutations in p53, Bub1, and BubR1, which function as mitotic checkpoint proteins. Impaired phosphorylation and mis-localization of Bub1 and BubR1 are responsible for the defective mitotic checkpoint function in Brca2-mutant thymic lymphomas. | Mouse | BUB1 | 699 | BUB1 mitotic checkpoint serine/threonine kinase | Impaired phosphorylation and mis-localization of Bub1 and BubR1 are responsible for the defective mitotic checkpoint function in Brca2-mutant thymic lymphomas. This report demonstrates that Bub1 and BubR1 mutant proteins from Brca2-/- thymic lymphomas have defects in the phosphorylation and kinetochore localization after spindle damage. Thymic lymphomas from Brca2-mutant mice harbor mutations in p53, Bub1, and BubR1, which function as mitotic checkpoint proteins. | Mouse | BRCA2 | 675 | breast cancer 2, early onset | Thymic lymphomas in mice with a truncating mutation in Brca2. | Mouse | BLK | 640 | B lymphoid tyrosine kinase | Expression of constitutively active Blk in the T lineage resulted in the appearance of clonal, thymic lymphomas composed of intermediate single positive cells. | Mouse | AKT1 | 207 | v-akt murine thymoma viral oncogene homolog 1 | These lymphomas had high levels of activated Akt/PKB, the protein product of a murine proto-oncogene with anti-apoptotic function, associated with thymic lymphomas. | Human | MLVI4 | 66001 | Moloney leukemia virus integration site 4, mouse, homolog of | To determine whether Myc expression was also affected by these provirus insertions, we constructed T-cell hybrids between two rat thymic lymphomas containing a provirus in Mlvi-4 or Mlvi-1 and the murine T-cell lymphoma line BW5147. | Human | BCL11B | 64919 | B-cell CLL/lymphoma 11B (zinc finger protein) | Homozygous deletions and point mutations of the Rit1/Bcl11b gene in gamma-ray induced mouse thymic lymphomas. Allelic loss (LOH) mapping and sequence analysis were conducted for gamma-ray induced mouse thymic lymphomas and a novel tumor suppressor gene, Rit1/Bcl11b, on chromosome 12 was isolated. Involvement of V(D)J recombinase in the generation of intragenic deletions in the Rit1/Bcl11b tumor suppressor gene in gamma-ray-induced thymic lymphomas and in normal thymus of the mouse. | Human | IL22 | 50616 | interleukin 22 | This protein, designated IL-10-related T cell-derived inducible factor (IL-TIF), is induced by IL-9 in thymic lymphomas, T cells, and mast cells, and by lectins in freshly isolated splenocytes. |
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