Bax accelerates tumorigenesis in p53-deficient mice

Cancer Research

Volumn 61, Issue 2, 2001, Pages 659-665

  Knudson, C Michael ^a   Johnson, Geoffrey M ^a   Lin, Yuan ^a   Korsmeyer, Stanley J ^b  

^a UNIVERSITY OF IOWA   (United States)

^b DANA FARBER CANCER INSTITUTE   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

PROTEIN BAX; PROTEIN P53;

ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; APOPTOSIS; ARTICLE; CANCER; CARCINOGENESIS; CONTROLLED STUDY; FEMALE; MALE; MOUSE; NONHUMAN; PRIORITY JOURNAL; T CELL LYMPHOMA; TRANSGENIC MOUSE; TUMOR GROWTH;

ANIMALS; APOPTOSIS; BCL-2-ASSOCIATED X PROTEIN; BROMODEOXYURIDINE; CELL DIVISION; CELL SURVIVAL; DISEASE-FREE SURVIVAL; FEMALE; GENE EXPRESSION REGULATION; MALE; MICE; MICE, INBRED C3H; MICE, INBRED C57BL; MICE, KNOCKOUT; MICE, TRANSGENIC; NEOPLASMS; PREGNANCY; PROTO-ONCOGENE PROTEINS; PROTO-ONCOGENE PROTEINS C-BCL-2; SURVIVAL ANALYSIS; THYMUS GLAND; TUMOR SUPPRESSOR PROTEIN P53;

EID: 0035863392     PISSN: 00085472     EISSN: None     Source Type: Journal    
DOI: None     Document Type: Article

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3. Nucleotide sequence of a t(14:18) chromosomal breakpoint in follicular lymphoma and demonstration of a breakpoint-cluster region near a transcriptionally active locus on chromosome 18
4. The t(14:18) chromosome translocations involved in B-cell neoplasms result from mistakes in VDJ joining
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7. Clinical implications of the p53 gene
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12. Frequent Bax frameshift mutations in gastric cancer with high but not low microsatellite instability
13. Hematopoietic malignancies demonstrate loss-of-function mutations of BAX
14. Impairment of the proapoptotic activity of Box by missense mutations found in gastrointestinal cancers
15. BAX protein expression and clinical outcome in epithelial ovarian cancer
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17. Prognostic significance of proliferative and apoptotic markers in oral tongue squamous cell carcinomas
18. Increased BAX expression is associated with an increased risk of relapse in childhood acute lymphocytic leukemia
19. Bcl-2 and Bax function independently to regulate cell death
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22. Tumor spectrum analysis in p53-mutant mice
23. Bcl-2 heterodimerizes in vivo with a conserved homolog, Bax, that accelerates programmed cell death
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26. Rapid DNA content analysis by the propidium iodide-hypotonic citrate method
27. Bax is required for neuronal death after trophic factor deprivation and during development
28. Apoptosis-associated signaling pathways are required for chemotherapy-mediated female germ cell destruction
29. The activity of the routine Bax promoter is regulated by Sp1/3 and E-box binding proteins but not by p53
30. Mice deficient for p53 are developmentally normal but susceptible to spontaneous tumours
31. Bax promotes neuronal survival and antagonises the survival effect of neurotrophic factors
32. Inhibition of virus-induced neuronal apoptosis by Bax
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34. Bax α perturbs T cell development and affects cell cycle entry of T cells
35. Novel primitive lymphoid tumours induced in transgenic mice by cooperation between myc and bcl-2
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37. Tumor suppressor p53 is a regulator of bcl-2 and bax gene expression in vitro and in vivo
38. Tumor induction and tissue atrophy in mice lacking E2F-1
39. Bax accelerates staurosporine-induced but suppresses nigericin-induced neuronal cell death
40. The cell death inhibitor Bcl-2 and its homologues influence control of cell cycle entry
41. bcl-2 transgene expression promotes survival and reduces proliferation of CD3-CD4-CD8- T cell progenitors
42. The anti-apoptosis function of Bcl-2 can be genetically separated from its inhibitory effect on cell cycle entry
43. Deletion of a nonconserved region of Bcl-2 confers a novel gain of function-suppression of apoptosis with concomitant cell proliferation
44. A link between cell cycle and cell death: Bax and Bcl-2 modulate Cdk2 activation during thymocyte apoptosis
45. Bcl-2 retards cell cycle entry through p27(Kip1), pRB relative p130, and altered E2F regulation