PMID- 7624126
OWN - NLM
STAT- MEDLINE
DCOM- 19950829
LR  - 20061115
IS  - 0950-9232 (Print)
IS  - 0950-9232 (Linking)
VI  - 11
IP  - 1
DP  - 1995 Jul 6
TI  - The MMTV/c-myc transgene and p53 null alleles collaborate to induce T-cell 
      lymphomas, but not mammary carcinomas in transgenic mice.
PG  - 181-90
AB  - A number of properties of the cancer-related genes c-myc and p53 suggest that 
      they might collaborate to induce tumorigenesis. To test this notion, we produced 
      doubly heterozygotic mice bearing disrupted p53 alleles and a fusion transgene 
      consisting of the mouse mammary tumor virus (MMTV) LTR and the oncogene c-myc. 
      Mice bearing both the MMT/c-myc transgene and a single p53- allele develop very 
      aggressive pre-T- and T-cell lymphomas with a significantly shorter latency than 
      mice carrying either the p53- allele or the c-myc transgene alone. Moreover, 
      every lymphoma occurring in these animals has lost or suffers an inactivation of 
      its wild type p53 allele indicating that loss of p53 activity is necessary for 
      this c-myc-accelerated lymphomagenesis. Nonetheless, p53 inactivation and 
      expression of the MMTV/c-myc transgene are not sufficient for lymphoid 
      transformation. Tumors that arise in homozygous p53- mice carrying the c-myc 
      transgene are monoclonal, suggesting that at least one additional event is 
      necessary for their transformation. Moreover, since mice bearing only the 
      MMTV/c-myc transgene predominantly develop mammary carcinomas, it was surprising 
      that the p53- allele failed to accelerate the incidence of mammary carcinomas. 
      Further, in contrast to the lymphomas, only one in four mammary tumors that arose 
      in the double heterozygotic mice had lost its wild type p53 allele. Apparently 
      cell context influences the ability of c-myc and p53- to cooperate in inducing 
      oncogenesis.
FAU - Elson, A
AU  - Elson A
AD  - Department of Genetics, Harvard Medical School, Howard Hughes Medical Institute, 
      Boston, Massachusetts 02115, USA.
FAU - Deng, C
AU  - Deng C
FAU - Campos-Torres, J
AU  - Campos-Torres J
FAU - Donehower, L A
AU  - Donehower LA
FAU - Leder, P
AU  - Leder P
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Oncogene
JT  - Oncogene
JID - 8711562
RN  - 0 (Cdkn1a protein, mouse)
RN  - 0 (Cyclin-Dependent Kinase Inhibitor p21)
RN  - 0 (Cyclins)
RN  - 0 (DNA Primers)
RN  - 0 (Protein Kinase Inhibitors)
SB  - IM
GS  - c-myc
GS  - p53
MH  - Alleles
MH  - Animals
MH  - Base Sequence
MH  - Cell Division/genetics
MH  - Cyclin-Dependent Kinase Inhibitor p21
MH  - Cyclins/genetics
MH  - DNA Primers
MH  - Female
MH  - Gene Expression Regulation, Developmental
MH  - *Genes, myc
MH  - *Genes, p53
MH  - Genotype
MH  - Heterozygote
MH  - Lymphoma, T-Cell/*genetics
MH  - Male
MH  - Mammary Glands, Animal/growth & development/metabolism
MH  - Mammary Neoplasms, Experimental/*genetics
MH  - Mammary Tumor Virus, Mouse/*genetics
MH  - Mice
MH  - Mice, Transgenic
MH  - Molecular Sequence Data
MH  - Protein Kinase Inhibitors
EDAT- 1995/07/06 00:00
MHDA- 1995/07/06 00:01
CRDT- 1995/07/06 00:00
PHST- 1995/07/06 00:00 [pubmed]
PHST- 1995/07/06 00:01 [medline]
PHST- 1995/07/06 00:00 [entrez]
PST - ppublish
SO  - Oncogene. 1995 Jul 6;11(1):181-90.