Mouse c-myc oncogene is located on chromosome 15 and translocated to chromosome 12 in plasmacytomas

Science ◽  
1982 ◽  
Vol 218 (4579) ◽  
pp. 1319-1321 ◽  
Author(s):  
S Crews ◽  
R Barth ◽  
L Hood ◽  
J Prehn ◽  
K Calame
Keyword(s):  
Chromosome 12 ◽  
Chromosome 15 ◽  
Myc Oncogene

Ring chromosome 12 resulting from nonrandom telomeric associations with the short arm of chromosome 15 in a cerebellar astrocytoma

1993 ◽  
Vol 8 (2) ◽  
pp. 69-73 ◽  
Author(s):  
Jeffrey R. Sawyer ◽  
Gael Sammartino ◽  
M. Husain ◽  
Jane M. Lewis ◽  
Bruce Anderson ◽  
...  
Keyword(s):  
Ring Chromosome ◽  
Chromosome 12 ◽  
Chromosome 15 ◽  
Cerebellar Astrocytoma

scholarly journals A complex translocation at the murine kappa light-chain locus.

1987 ◽  
Vol 7 (11) ◽  
pp. 4130-4133 ◽  
Author(s):  
M A Shapiro ◽  
M Weigert
Keyword(s):  
Light Chain ◽  
Chromosome 12 ◽  
Chromosome 15 ◽  
Chromosome 6 ◽  
Kappa Light Chain ◽  
Complex Translocation ◽  
Immunoglobulin Kappa ◽  
Complex Series ◽  
Chain Locus ◽  
Light Chain Locus

We have previously reported that a segment of DNA from a murine plasmacytoma comprises DNA from three chromosomes, the immunoglobulin kappa light-chain locus on chromosome 6, the S mu locus on chromosome 12, and a region on chromosome 15. We now report that the reciprocal product contains DNA from only the kappa locus and chromosome 15 and not from S mu. We conclude that a complex series of events, including both a transposition of DNA and a translocation between chromosomes, generated these imperfect reciprocal products.

Chromosomal location of the regulator of mouse alpha-fetoprotein, Afr-1.

Genetics ◽  
1988 ◽  
Vol 119 (3) ◽  
pp. 687-691
Author(s):  
E P Blankenhorn ◽  
R Duncan ◽  
K Huppi ◽  
M Potter
Keyword(s):  
Mouse Chromosome ◽  
Chromosomal Location ◽  
Serum Levels ◽  
Alpha Fetoprotein ◽  
Chromosome 15 ◽  
Myc Oncogene ◽  
Close Proximity ◽  
B Mice

Abstract Afr-1 is a gene whose product contributes to the adult regulation of mouse alpha-fetoprotein (AFP). In Afr-1b/b homozygotes, the adult serum levels of AFP are 10- to 20-fold higher than in Afr-1a/a or Afr-1a/b mice. The studies reported here were performed to map the Afr-1 gene. Our results show that Afr-1 resides on mouse chromosome 15, approximately 25 cM from Gdc-1. Afr-1 appears to be located in close proximity to the mouse c-myc oncogene. These results are discussed with respect to the susceptibility or resistance of different BALB/c sublines (which are either Afr-1a or Afr-1b, respectively) to pristane-induced plasmacytomas.

Myc oncogene activation in B and T lymphoid tumours

1985 ◽  
Vol 226 (1242) ◽  
pp. 59-72 ◽  
Keyword(s):  
Chromosome 15 ◽  
Chromosome 6 ◽  
Coding Region ◽  
Chromosome Translocations ◽  
Myc Oncogene ◽  
Chain Locus ◽  
Oncogene Activation ◽  
Selection For ◽  
T Lymphomas ◽  
B Lymphoid

The chromosome translocations characteristic of certain B lymphoid tumours associate the myc oncogene and immunoglobulin loci. The typical t(12;15) in murine plasmacytomas and analogous t(14;8) in Burkitt lyphomas couple the myc coding region to one of the switch recombination regions within the immunoglobulin heavy (H) chain locus; hence the switch machinery may promote some translocations. Significantly, translocation induces constitutive myc expression, the untranslocated myc allele remaining silent. The predilection for breakpoints near the 5´ end of the c -myc gene may reflect selection for altered myc regulation. In most tumours, the stimulatory effect of the H locus context is not understood, but an H locus enhancer participates in some tumours, including one displaying a novel transposition . The variant (6;15) translocations found in about 15 % of plasmacytomas involve the myc band and the region of chromosome 6 where the k locus lies. The t(6;15) is shown here to represent an exchange between C K and a chromosome 15 locus (designated pvt -1) which lies unexpectedly far from c-myc .The association of myc expression with pvt -1 alterations suggest that myc can be activated at a distance. Myc has also been implicated in some T lymphomas by detection of proviral inserts near myc and also surprisingly, within the pvt -1 locus. Inserts near myc appear to activate its expression via the retroviral enhancer.

Abnormal rearrangement within the α/δ T-cell receptor locus in lymphomas from Atm-deficient mice

Blood ◽  
2000 ◽  
Vol 96 (5) ◽  
pp. 1940-1946 ◽  
Author(s):  
Marek Liyanage ◽  
Zoë Weaver ◽  
Carrolee Barlow ◽  
Allen Coleman ◽  
Daniel G. Pankratz ◽  
...  
Keyword(s):  
T Cell ◽  
Tumor Development ◽  
Cell Receptor ◽  
Chromosome 15 ◽  
Dna Breaks ◽  
Chromosome 14 ◽  
Myc Oncogene ◽  
Double Stranded Dna ◽  
Receptor Locus ◽  
Deficient Mice

Atm-deficient mice (Atm−/−) recapitulate many aspects of the ataxia telangiectasia (AT) syndrome, including the susceptibility to tumors of lymphoid origin. To investigate the mechanism of tumorigenesis, we have examined a panel of 8 thymic lymphomas from Atm−/− mice. AllAtm−/− tumors are of thymic lymphoblastoid origin, display an immature CD3− and CD4+/CD8+ phenotype, and arise coincident with V(D)J recombination. Cytogenetically, all tumors are diploid or near diploid but exhibit multiple chromosome aberrations with an average of 4 abnormal chromosomes per tumor. All the tumors revealed chromosome 14 rearrangements precisely at the T-cell receptorα/δ(Tcrα/δ) locus, suggesting the involvement of V(D)J recombination in these translocations. In addition, 11.5% ofAtm−/− peripheral T cells showed chromosome 14 translocations, suggesting that rearrangements at theTcrα/δ locus occur early during tumor development in the absence of ATM. However, additional genetic aberrations are required for tumorigenesis. For example, translocations involving chromosome 12, often with chromosome 14 (more than 60%), and partial or complete trisomy of chromosome 15, with copy number increases of the c-myc oncogene were frequently observed. These observations suggest that ATM is required for normal rearrangement of the Tcrα/δ locus but not for V(D)J recombination at other loci. The mechanisms that lead to tumorigenesis may be due to the involvement of ATM in monitoring double-stranded DNA breaks.

scholarly journals The c-myc oncogene is translocated to the involved chromosome 12 in mouse plasmacytoma.

1985 ◽  
Vol 82 (12) ◽  
pp. 4212-4216 ◽  
Author(s):  
J. Erikson ◽  
D. A. Miller ◽  
O. J. Miller ◽  
P. W. Abcarian ◽  
R. M. Skurla ◽  
...  
Keyword(s):  
Chromosome 12 ◽  
Myc Oncogene

Abnormal rearrangement within the α/δ T-cell receptor locus in lymphomas from Atm-deficient mice

Blood ◽  
2000 ◽  
Vol 96 (5) ◽  
pp. 1940-1946 ◽  
Author(s):  
Marek Liyanage ◽  
Zoë Weaver ◽  
Carrolee Barlow ◽  
Allen Coleman ◽  
Daniel G. Pankratz ◽  
...  
Keyword(s):  
T Cell ◽  
Tumor Development ◽  
Cell Receptor ◽  
Chromosome 15 ◽  
Dna Breaks ◽  
Chromosome 14 ◽  
Myc Oncogene ◽  
Double Stranded Dna ◽  
Receptor Locus ◽  
Deficient Mice

Abstract Atm-deficient mice (Atm−/−) recapitulate many aspects of the ataxia telangiectasia (AT) syndrome, including the susceptibility to tumors of lymphoid origin. To investigate the mechanism of tumorigenesis, we have examined a panel of 8 thymic lymphomas from Atm−/− mice. AllAtm−/− tumors are of thymic lymphoblastoid origin, display an immature CD3− and CD4+/CD8+ phenotype, and arise coincident with V(D)J recombination. Cytogenetically, all tumors are diploid or near diploid but exhibit multiple chromosome aberrations with an average of 4 abnormal chromosomes per tumor. All the tumors revealed chromosome 14 rearrangements precisely at the T-cell receptorα/δ(Tcrα/δ) locus, suggesting the involvement of V(D)J recombination in these translocations. In addition, 11.5% ofAtm−/− peripheral T cells showed chromosome 14 translocations, suggesting that rearrangements at theTcrα/δ locus occur early during tumor development in the absence of ATM. However, additional genetic aberrations are required for tumorigenesis. For example, translocations involving chromosome 12, often with chromosome 14 (more than 60%), and partial or complete trisomy of chromosome 15, with copy number increases of the c-myc oncogene were frequently observed. These observations suggest that ATM is required for normal rearrangement of the Tcrα/δ locus but not for V(D)J recombination at other loci. The mechanisms that lead to tumorigenesis may be due to the involvement of ATM in monitoring double-stranded DNA breaks.

A complex translocation at the murine kappa light-chain locus

1987 ◽  
Vol 7 (11) ◽  
pp. 4130-4133
Author(s):  
M A Shapiro ◽  
M Weigert
Keyword(s):  
Light Chain ◽  
Chromosome 12 ◽  
Chromosome 15 ◽  
Chromosome 6 ◽  
Kappa Light Chain ◽  
Complex Translocation ◽  
Immunoglobulin Kappa ◽  
Complex Series ◽  
Chain Locus ◽  
Light Chain Locus

We have previously reported that a segment of DNA from a murine plasmacytoma comprises DNA from three chromosomes, the immunoglobulin kappa light-chain locus on chromosome 6, the S mu locus on chromosome 12, and a region on chromosome 15. We now report that the reciprocal product contains DNA from only the kappa locus and chromosome 15 and not from S mu. We conclude that a complex series of events, including both a transposition of DNA and a translocation between chromosomes, generated these imperfect reciprocal products.

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