Engineering de novo reciprocal chromosomal translocations associated with Mll to replicate primary events of human cancer.
The etiology of human tumors often involves chromosomal translocations. Models that emulate translocations are essential to understanding the determinants of frank malignancy, those dictating the restriction of translocations to specific lineages, and as a basis for development of rational therapeut...
| Main Authors: | , , , , , , |
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| Format: | Journal article |
| Language: | English |
| Published: |
2003
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| _version_ | 1826300414529634304 |
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| author | Forster, A Pannell, R Drynan, L McCormack, M Collins, E Daser, A Rabbitts, T |
| author_facet | Forster, A Pannell, R Drynan, L McCormack, M Collins, E Daser, A Rabbitts, T |
| author_sort | Forster, A |
| collection | OXFORD |
| description | The etiology of human tumors often involves chromosomal translocations. Models that emulate translocations are essential to understanding the determinants of frank malignancy, those dictating the restriction of translocations to specific lineages, and as a basis for development of rational therapeutic methods. We demonstrate that developmentally regulated Cre-loxP-mediated interchromosomal recombination between the Mll gene, whose human counterpart is involved in a spectrum of leukemias, and the Enl gene creates reciprocal chromosomal translocations that cause myeloid tumors. There is a rapid onset and high penetrance of leukemogenesis in these translocator mice, and high proportions of cells carrying chromosomal translocations can be found in bone marrow as early as 12 days after birth. This de novo strategy is a direct recapitulation of naturally occurring human cancer-associated translocations. |
| first_indexed | 2024-03-07T05:16:49Z |
| format | Journal article |
| id | oxford-uuid:dd7da1ea-ad81-47f4-a504-a058c72e6c30 |
| institution | University of Oxford |
| language | English |
| last_indexed | 2024-03-07T05:16:49Z |
| publishDate | 2003 |
| record_format | dspace |
| spelling | oxford-uuid:dd7da1ea-ad81-47f4-a504-a058c72e6c302022-03-27T09:25:23ZEngineering de novo reciprocal chromosomal translocations associated with Mll to replicate primary events of human cancer.Journal articlehttp://purl.org/coar/resource_type/c_dcae04bcuuid:dd7da1ea-ad81-47f4-a504-a058c72e6c30EnglishSymplectic Elements at Oxford2003Forster, APannell, RDrynan, LMcCormack, MCollins, EDaser, ARabbitts, TThe etiology of human tumors often involves chromosomal translocations. Models that emulate translocations are essential to understanding the determinants of frank malignancy, those dictating the restriction of translocations to specific lineages, and as a basis for development of rational therapeutic methods. We demonstrate that developmentally regulated Cre-loxP-mediated interchromosomal recombination between the Mll gene, whose human counterpart is involved in a spectrum of leukemias, and the Enl gene creates reciprocal chromosomal translocations that cause myeloid tumors. There is a rapid onset and high penetrance of leukemogenesis in these translocator mice, and high proportions of cells carrying chromosomal translocations can be found in bone marrow as early as 12 days after birth. This de novo strategy is a direct recapitulation of naturally occurring human cancer-associated translocations. |
| spellingShingle | Forster, A Pannell, R Drynan, L McCormack, M Collins, E Daser, A Rabbitts, T Engineering de novo reciprocal chromosomal translocations associated with Mll to replicate primary events of human cancer. |
| title | Engineering de novo reciprocal chromosomal translocations associated with Mll to replicate primary events of human cancer. |
| title_full | Engineering de novo reciprocal chromosomal translocations associated with Mll to replicate primary events of human cancer. |
| title_fullStr | Engineering de novo reciprocal chromosomal translocations associated with Mll to replicate primary events of human cancer. |
| title_full_unstemmed | Engineering de novo reciprocal chromosomal translocations associated with Mll to replicate primary events of human cancer. |
| title_short | Engineering de novo reciprocal chromosomal translocations associated with Mll to replicate primary events of human cancer. |
| title_sort | engineering de novo reciprocal chromosomal translocations associated with mll to replicate primary events of human cancer |
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