Research article
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INK4a/ARF mutations accelerate lymphomagenesis and promote chemoresistance by disabling p53
genes & development, vol. 13, no. 20, pp. –, 1999
Abstract
The INK4a/ARF locus encodes upstream regulators of the retinoblastoma and p53 tumor suppressor gene products. To compare the impact of these loci on tumor development and treatment response, the Emu-myc transgenic lymphoma model was used to generate genetically defined tumors with mutations in the I …
Keywords
- National Center for Biotechnology Information
- NCBI
- NLM
- MEDLINE
- genetic
- Mice
- Inbred C57BL
- animals
- humans
- pubmed abstract
- nih
- national institutes of health
- national library of medicine
- research support
- non-u.s. gov't
- u.s. gov't
- female
- male
- P.H.S.
- Genes
- enhancer elements
- Knockout
- lymphoma
- proteins / genetics*
- transgenic
- mutation*
- apoptosis / genetics
- antineoplastic agents / pharmacology
- p53*
- Tumor Suppressor Protein p14ARF
- myc
- p16*
- b-cell / etiology*
- b-cell / genetics*
- c a schmitt
- s w lowe
- immunoglobulin heavy chains / genetics
- pmid:10541553
- pmc317110
- doi:10.1101/gad.13.20.2670
- m e mccurrach
- drug resistance / genetics
- b-cell / drug therapy
How to cite
Schmitt CA; McCurrach ME; de Stanchina E; Wallace-Brodeur RR; Lowe SW. (1999). INK4a/ARF mutations accelerate lymphomagenesis and promote chemoresistance by disabling p53. genes & development, 13(20), –. http://www.ncbi.nlm.nih.gov/pubmed/10541553
Ref key
ca1999genesink4a/arf
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