Clonal origin and trisomy of chromosome 15 in murine B‐cell malignancies

Pj, Fialkow; Al, Reddy; Ji, Bryant

doi:10.1002/ijc.2910260512

Cited by 23 publications

(6 citation statements)

References 11 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This has been described in spontaneous T-cell lymphomas of the AKR mouse (Dofuku et al, 1975; Herbst et al, 1981), and in a variety of T-cell leukemias induced by RadLV (Wiener et al, 1978a) or dimethylbenzanthracene (Wiener et al, 1978b;Chan et al, 1979;Spira et al, 1980). Other examples in which trisomy 15 has been observed are B-cell lymphomas (Fialkow et al, 1980;Wiener et al, 1981). Rearrangements between chromosome 15,6 and 12 have been described in plasmocytomas (Shepard et al, 1978;Yoshida et al, 1978; al., 1979).…”

Section: Discussionmentioning

confidence: 99%

Chromosome changes in butylnitrosourea (BNU)‐induced mouse leukemia

Carbonell

Seidel

Saks

et al. 1982

Intl Journal of Cancer

View full text Add to dashboard Cite

G-banding analysis was carried out in 45 mice after exposure to the leukemogen butylnitrosourea (BNU). Of 27 animals without clinical signs of leukemia, 2 had chromosomal rearrangements (7%) while, of 18 leukemic mice, 5 showed abnormal karyotypes (28%). The chromosomal abnormalities were not random and showed preferential changes of chromosomes Nos. 14 and 15. The organ distribution of the chromosomal abnormalities showed a preferential involvement of the thymus with a secondary presence of chromosome anomalies in peripheral lymphoid organs and the bone marrow. The findings are discussed in relation to the recent reports on the specificity of trisomy 15 in murine leukemia and lymphoma.

show abstract

Section: Discussionmentioning

confidence: 99%

Chromosome changes in butylnitrosourea (BNU)‐induced mouse leukemia

Carbonell

Seidel

Saks

et al. 1982

Intl Journal of Cancer

View full text Add to dashboard Cite

show abstract

“…Since then it has been found in other spontaneously derived and carcinogen-, virusor irradation-induced T lymphomas (Wiener et al, 1978~1, 1978c(Wiener et al, 1978~1, , 1981Spira et al, 1980Spira et al, , 1981Haran Ghera, 1978;Chang et al, 1977) as well as in cell lines derived from such lymphomas (Berenson et al, 1981;Bregula et al, 1979;Dowjat and Wlodarska 1981). Some B-cell lymphomas Fialkow et al, 1980), mouse sarcoma and adenocarcinoma lines (Pravtcheva et al, 1981;Manolov, 1979) and epithelial cell lines derived from mouse bladder (Cowell, 1980(Cowell, , 1981 have been also shown to contain trisomy 15. That the duplication of chromosome 15 plays an essential role in T-cell leukemogenesis was shown by recent somatic cell hybridization experiments in which high tumorigenic segregants showed amplification of the tumor-derived chromosome No.…”

Section: Discussionmentioning

confidence: 99%

Cytogenetic changes during tumor progression towards invasion, metastasis and immune escape in the Eb/ESb model system

Dzarlieva

Schirrmacher

Fusenig

1982

Intl Journal of Cancer

View full text Add to dashboard Cite

Related tumor lines which represent different stages in their progression towards metastatic capacity were investigated and compared at the chromosomal level. The parental low-metastatic tumor line (L5178Y/Eb) was derived from a long-term transplanted, chemically induced T-cell lymphoma of the DBA/2 mouse. The cytogenetic analysis included this Eb line, a spontaneous high metastatic variant thereof which expressed a distinct tumor-associated transplantation antigen (ESb TATA+), and an immunoresistant TATA-negative variant of the latter (ESb TATA-). All three cell lines were characterized by a near-diploid chromosome count and by some common chromosomal markers derived from Nos. 6, 13 and 16 Large-scale chromosomal rearrangments resulted in the formation of eight marker chromosomes in Eb cells, 16 in ESb TATA+ cells and 18 in ESb TATA- cells. Tumor progression in this system showed a tendency to monosomies, which could bring the corresponding genes to a hemizygous state and possibly to a release from repression. Chromosome 15 was trisomic in Eb cells, monosomic in ESb TATA+ cells and hardly detectable in ESb TATA- cells. The Ig heavy-chain gene-carrying region of both chromosomes No. 12 was found in translocation with chromosomes Nos. 5, 13 and 14 (Eb cells) and with Nos. 1 and 17 (ESb cells). ESb TATA- cells differed from ESb TATA+ cells at four different chromosomes (Nos. 5, 8, 14 and 15).

show abstract

“…[1][2][3][4][5][6] X-inactivation-based analysis of women with myeloproliferative disease (MPD) and karyotypic analysis have demonstrated that these MPDs are clonal stem cell disorders characterized by acquired somatic mutation in hematopoietic progenitors. [7][8][9][10][11][12] Clinical features of PV include polycythemia in the absence of any cause of secondary erythrocytosis and splenomegaly caused by extramedullary hematopoiesis. Most patients with PV also have varying degrees of leukocytosis and thrombocytosis and variable bone marrow fibrosis that may progress with time.…”

Section: Introductionmentioning

confidence: 99%

Expression of Jak2V617F causes a polycythemia vera–like disease with associated myelofibrosis in a murine bone marrow transplant model

Wernig

Mercher

Okabe

et al. 2006

Blood

448

415

View full text Add to dashboard Cite

An acquired somatic mutation, Jak2V617F, was recently discovered in most patients with polycythemia vera (PV), chronic idiopathic myelofibrosis (CIMF), and essential thrombocythemia (ET). To investigate the role of this mutation in vivo, we transplanted bone marrow (BM) transduced with a retrovirus expressing either Jak2 wild-type (wt) or Jak2V617F into lethally irradiated syngeneic recipient mice. Expression of Jak2V617F, but not Jak2wt, resulted in clinicopathologic features that closely resembled PV in humans. These included striking elevation in hemoglobin level/hematocrit, leukocytosis, megakaryocyte hyperplasia, extramedullary hematopoiesis resulting in splenomegaly, and reticulin fibrosis in the bone marrow. Histopathologic and flow cytometric analyses showed an increase in maturing myeloid lineage progenitors, although megakaryocytes showed decreased polyploidization and staining for acetylcholinesterase. In vitro analysis of primary cells showed constitutive activation of Stat5 and cytokine-independent growth of erythroid colony-forming unit (CFU-E) and erythropoietin hypersensitivity, and Southern blot analysis for retroviral integration indicated that the disease was oligoclonal. Furthermore, we observed strain-specific differences in phenotype, with Balb/c mice demonstrating markedly elevated leukocyte counts, splenomegaly, and reticulin fibrosis compared with C57Bl/6 mice. We conclude that Jak2V617F expression in bone marrow progenitors results in a PV-like syndrome with myelofibrosis and that there are strain-specific modifiers that may in part explain phenotypic pleiotropy of Jak2V617F-associated myeloproliferative disease in humans. (Blood. 2006;107: 4274-4281)

show abstract

Clonal origin and trisomy of chromosome 15 in murine B‐cell malignancies

Cited by 23 publications

References 11 publications

Chromosome changes in butylnitrosourea (BNU)‐induced mouse leukemia

Chromosome changes in butylnitrosourea (BNU)‐induced mouse leukemia

Cytogenetic changes during tumor progression towards invasion, metastasis and immune escape in the Eb/ESb model system

Expression of Jak2V617F causes a polycythemia vera–like disease with associated myelofibrosis in a murine bone marrow transplant model

Contact Info

Product

Resources

About