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R 2, H2aa3 F-box protein 32 histone cluster 1, H3d SRY (sex determining region Y)box 4 fem-1 homolog b (C. elegans) BCL2-like 11 (apoptosis facilitator) WD repeat and SOCS boxcontaining 1 chromosome 1 open reading frame 21 muscleblind-like (Drosophila) selenium binding protein 1 butyrophilin, subfamily 3, member A1 AF4/FMR2 family, member 4 transmembrane protein 47 superoxide dismutase 2, mitochon
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R 2, H2aa3 F-box protein 32 histone cluster 1, H3d SRY (sex determining region Y)box 4 fem-1 homolog b (C. elegans) BCL2-like 11 (apoptosis facilitator) WD repeat and SOCS boxcontaining 1 chromosome 1 open reading frame 21 muscleblind-like (Drosophila) selenium binding protein 1 butyrophilin, subfamily 3, member A1 AF4/FMR2 family, member 4 transmembrane protein 47 superoxide dismutase 2, mitochon
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Y is consistent with the haploinsufficient effect of the gene observed in our mouse KO model. Indeed, mice hetero- or homozygous on the Tusc2 deletion shared similar immunological and tumorigenic phenotypes at comparable frequencies. These data suggest that even partial loss of the TUSC2 dosage is sufficient to trigger pathological inflammation and increase susceptibility to cancer [15]. We consid
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R 2, H2aa3 F-box protein 32 histone cluster 1, H3d SRY (sex determining region Y)box 4 fem-1 homolog b (C. elegans) BCL2-like 11 (apoptosis facilitator) WD repeat and SOCS boxcontaining 1 chromosome 1 open reading frame 21 muscleblind-like (Drosophila) selenium binding protein 1 butyrophilin, subfamily 3, member A1 AF4/FMR2 family, member 4 transmembrane protein 47 superoxide dismutase 2, mitochon
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A recurrentPage 8 of(page number not for citation purposes)Molecular Cancer 2009, 8:http://www.molecular-cancer.com/content/8/1/Table 4: Differentially expressed genes common for TUSC2-expressing MPM cells and clinical tumor specimens.Fold change and direction in TUSC2transfected MPM cells versus control 1 2 3 4 5 6 7 8 9 -8.04 -4.51 -4.10 -3.90 -3.64 -3.14 -3.08 -2.92 -2.Fold change and direction
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Y is consistent with the haploinsufficient effect of the gene observed in our mouse KO model. Indeed, mice hetero- or homozygous on the Tusc2 deletion shared similar immunological and tumorigenic phenotypes at comparable frequencies. These data suggest that even partial loss of the TUSC2 dosage is sufficient to trigger pathological inflammation and increase susceptibility to cancer [15]. We consid
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A recurrentPage 8 of(page number not for citation purposes)Molecular Cancer 2009, 8:http://www.molecular-cancer.com/content/8/1/Table 4: Differentially expressed genes common for TUSC2-expressing MPM cells and clinical tumor specimens.Fold change and direction in TUSC2transfected MPM cells versus control 1 2 3 4 5 6 7 8 9 -8.04 -4.51 -4.10 -3.90 -3.64 -3.14 -3.08 -2.92 -2.Fold change and direction
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F29* CAST* CCDC88A* CCNG2 CD274* CXCL16 DENND1B* DOCK11* EGR1 ETS1* FOXN3 GADD45A GADD45B HCP5* HIST1H2AE HIST1H2BG* HIST1H3D* HPSE* ICAM1/CD54 IL15* JUN LTB*UP UP UP UP UP UP DOWN DOWN UP DOWN UP UP UP UP DOWN UP DOWN DOWN UP DOWN DOWN DOWN UP UP UP DOWN UPAs a result, we delineated several groups of genes under the TUSC2 control. Interestingly, genes involved in chromatin modulation, nucleosome
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Box N3 zinc finger E-box binding homeobox 1 protocadherinRPS11 HIST1H2AE RGS4 PTHLH HIST1H2BG CD24 PSMB4 LOX PPP1R15A HIST1H4H ATF3 SET HIST2H2BE LOC284801 TMEM158 HIST2H2AA3 FBXO32 HIST1H3D SOX4 FEM1B BCL2L11 WSB1 C1orf21 MBNL1 SELENBP1 BTN3A1 AFF4 TMEM47 SOD2 SIDT2 TMCC1 EGR1 ALDH6A1 CCNG2 CDC2L6 RNASE4 TNS1 MLL5 FOXN3 ZEB1 PCDHPage 9 of(page number not for citation purposes)Molecular Cancer 200
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Mon cancers helps tumor progression contributing to evasion from immune surveillance [39]. Our data suggest that TUSC2 is a potent suppressor of this key immunoreceptor (Table 3 and Fig. 3). Since blocking of CD274 is now actively pursued as a novel immunotherapy [40,41], we suggest that TUSC2 may also have important immunotherapeutic implications. Our study on the TUSC2 role in mesothelioma under