Variant (6;15) translocations in murine plasmacytomas involve a chromosome 15 locus at least 72 kb from the c-myc oncogene.

Cory, Suzanne; Graham, Michael W.; Webb, Elizabeth; Corcoran, Lynn M.; Adams, Jerry M.

doi:10.1002/j.1460-2075.1985.tb03682.x

Cited by 173 publications

(87 citation statements)

References 50 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…1), which is free of highly repetitive sequences. Hybridization of DNAs from human-hamster hybrid cell lines, which retain in common only the human chromosome 8 intron sequence (15), 205 bp downstream of J5 ( Fig. 2A).…”

Section: Resultsmentioning

confidence: 99%

“…With probe 8q305, we screened a genomic library, prepared from placental DNA in phage XEMBL3, and isolated a set of overlapping clones spanning a total of 30 kbp. Figure 3A shows a restriction map of the cloned chromosome 8 Cell line BL21 (27) harbors a complex translocation, t(2;8;9), in which, as judged by the banding pattern, a segment of chromosome 9 is inserted between the long arm of chromosome 8 and the translocated short arm of chromosome 2 on the 8q+ marker chromosome. To cloned size-fractionated HindIII fragments of BL21 DNA in phage XL47 and isolated clone 21.1 ( Fig.…”

Section: Resultsmentioning

confidence: 99%

“…The situation is similar in mouse plasmacytoma, a tumor with analogous chromosomal translocations involving c-myc and the immunoglobulin heavy-chain [t (12;15)] and light-chain [t(6;15)] loci, respectively. In mouse plasmacytoma cells with the t(6;15) translocation, the breakpoints of chromosome 6 fall within a narrow range that is adjacent to the CK IOCUS; the breakpoints of chromosome 15 are found to occur more than 85 kbp distal of c-myc, within a cluster called pvt-J (8). This locus was shown to be homologous to (12) and colinear with (24) cell line JBL2 had occurred.…”

mentioning

confidence: 97%

See 2 more Smart Citations

Three breakpoints of variant t(2;8) translocations in Burkitt's lymphoma cells fall within a region 140 kilobases distal from c-myc.

Henglein¹,

Synovzik²,

Groitl³

et al. 1989

Mol. Cell. Biol.

View full text Add to dashboard Cite

The variant translocations t(2;8) in Burkitt's lymphoma cells join band q24 of chromosome 8, distal from c-myc, to the Igkappa locus, with considerable variation in the location of the breakpoints on chromosome 8. We report the cloning and molecular characterization of a chromosome 8 region, distal from the c-myc locus, which encompasses the breakpoints of the Burkitt's lymphoma cell lines BL64, BL21, and LY91 within 11 kilobase pairs, termed provisionally bvr-1 (Burkitt's variants' rearranging region 1). Using probes from the c-myc, the bvr-1, and the human pvt-1 loci obtained by chromosome walking coupled with pulsed-field gel electrophoresis, we have constructed a physical map of the region 3' of c-myc. We map bvr-1 and pvt-1 about 140 and 260 kilobase pairs, respectively, distal from c-myc.

show abstract

Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

mentioning

confidence: 97%

See 1 more Smart Citation

Three breakpoints of variant t(2;8) translocations in Burkitt's lymphoma cells fall within a region 140 kilobases distal from c-myc.

Henglein¹,

Synovzik²,

Groitl³

et al. 1989

Mol. Cell. Biol.

View full text Add to dashboard Cite

show abstract

“…Examples include observations that rearrangement of the region at 8q24 encoding MYC and PVT1 is frequently involved in human leukemias and lymphomas (4,5), the regions is frequently amplified in solid tumors (2), and a site of recurrent tumorigenic viral integration in mice (25). MYC is well established as an oncogene in this region.…”

Section: Discussionmentioning

confidence: 99%

Amplification of PVT1 Contributes to the Pathophysiology of Ovarian and Breast Cancer

Guan

Kuo

Stilwell

et al. 2007

Clinical Cancer Research

326

325

View full text Add to dashboard Cite

Purpose: This study was designed to elucidate the role of amplification at 8q24 in the pathophysiology of ovarian and breast cancer because increased copy number at this locus is one of the most frequent genomic abnormalities in these cancers. Experimental Design:To accomplish this, we assessed the association of amplification at 8q24 with outcome in ovarian cancers using fluorescence in situ hybridization to tissue microarrays and measured responses of ovarian and breast cancer cell lines to specific small interfering RNAs against the oncogene MYC and a putative noncoding RNA, PVT1, both of which map to 8q24. Results: Amplification of 8q24 was associated with significantly reduced survival duration. In addition, small interfering RNA^mediated reduction in either PVT1 or MYC expression inhibited proliferation in breast and ovarian cancer cell lines in which they were both amplified and overexpressed but not in lines in which they were not amplified/overexpressed. Inhibition of PVT1 expression also induced a strong apoptotic response in cell lines in which it was overexpressed but not in lines in which it was not amplified/overexpressed. Inhibition of MYC, on the other hand, did not induce an apoptotic response in cell lines in which MYC was amplified and overexpressed. Conclusions: These results suggest that MYC and PVT1 contribute independently to ovarian and breast pathogenesis when overexpressed because of genomic abnormalities. They also suggest that PVT1-mediated inhibition of apoptosis may explain why amplification of 8q24 is associated with reduced survival duration in patients treated with agents that act through apoptotic mechanisms.Amplification of a region on chromosome 8q24 is one of the most frequent events in carcinomas, including serous ovarian and breast cancers, and has been associated with reduced survival duration in some studies (1, 2). The well-established oncogene MYC maps to this locus and likely contributes to the pathophysiology of cancers in which it is amplified. However, the PVT1 transcript also maps to this region and has been implicated in cancer pathophysiology as well (3). In mouse, for example, the pvt-1 locus is a site of recurrent translocation in plasmacytomas (4, 5) and is a common site of tumorigenic retroviral insertion in lymphomas (6). In humans, the region homologous to pvt-1 is a site of recurrent translocation between chromosomes 2 and 8 (7, 8) and its first exon is coamplified with MYC in colon carcinoma cell lines (9). PVT1 has been suggested as a MYC activator (10); however, little evidence exists to support that role. Moreover, evidence is now emerging that PVT1 may act as a noncoding RNA 12 that is strongly conserved between mouse and human.We now present evidence that both PVT1 and MYC contribute to ovarian and breast cancer pathophysiology when 12 Huppi et al., personal communication.

show abstract

“…The Pvt1 locus is also frequently targeted by proviral integrations in murine leukemia virus-induced T-cell lymphomas in mice (23) and in rats (24). It is also the site for breakpoints in ∼20% of human Burkitt's lymphomas (25) and in murine plasmacytomas (26). In conclusion, CAT thymocytes are a useful model to gain insights into the contribution of β-catenin to genomic instability because they sustain frequent illegitimate RAG recombination events leading to recurrent oncogenic translocations.…”

Section: T-cell Lymphomas Induced By β-Catenin Activation Have Recurrentmentioning

confidence: 95%

β-Catenin induces T-cell transformation by promoting genomic instability

Dose

Emmanuel

Chaumeil

et al. 2013

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

View full text Add to dashboard Cite

Deregulated activation of β-catenin in cancer has been correlated with genomic instability. During thymocyte development, β-catenin activates transcription in partnership with T-cell-specific transcription factor 1 (Tcf-1). We previously reported that targeted activation of β-catenin in thymocytes (CAT mice) induces lymphomas that depend on recombination activating gene (RAG) and myelocytomatosis oncogene (Myc) activities. Here we show that these lymphomas have recurring Tcra/Myc translocations that resulted from illegitimate RAG recombination events and resembled oncogenic translocations previously described in human T-ALL. We therefore used the CAT animal model to obtain mechanistic insights into the transformation process. ChIP-seq analysis uncovered a link between Tcf-1 and RAG2 showing that the two proteins shared binding sites marked by trimethylated histone-3 lysine-4 (H3K4me3) throughout the genome, including near the translocation sites. Pretransformed CAT thymocytes had increased DNA damage at the translocating loci and showed altered repair of RAG-induced DNA double strand breaks. These cells were able to survive despite DNA damage because activated β-catenin promoted an antiapoptosis gene expression profile. Thus, activated β-catenin promotes genomic instability that leads to T-cell lymphomas as a consequence of altered double strand break repair and increased survival of thymocytes with damaged DNA.beta-catenin/Tcf-1 | DNA recombination Tcf7 | Ctnnb1

show abstract

Variant (6;15) translocations in murine plasmacytomas involve a chromosome 15 locus at least 72 kb from the c-myc oncogene.

Cited by 173 publications

References 50 publications

Three breakpoints of variant t(2;8) translocations in Burkitt's lymphoma cells fall within a region 140 kilobases distal from c-myc.

Three breakpoints of variant t(2;8) translocations in Burkitt's lymphoma cells fall within a region 140 kilobases distal from c-myc.

Amplification of PVT1 Contributes to the Pathophysiology of Ovarian and Breast Cancer

β-Catenin induces T-cell transformation by promoting genomic instability

Contact Info

Product

Resources

About