PMID- 6292467
OWN - NLM
STAT- MEDLINE
DCOM- 19830107
LR  - 20200724
IS  - 0022-538X (Print)
IS  - 1098-5514 (Electronic)
IS  - 0022-538X (Linking)
VI  - 43
IP  - 3
DP  - 1982 Sep
TI  - Mouse mammary tumor virus proviral sequences congenital to C3H/Sm mice are 
      differentially hypomethylated in chemically induced, virus-induced, and 
      spontaneous mammary tumors.
PG  - 876-84
AB  - C3H/Sm mice have lost the exogenous milk-borne mouse mammary tumor virus (MMTV) 
      characteristic of the C3H strain and have a very low (1.5%) incidence of 
      spontaneous mammary tumors, yet they are highly susceptible to mammary 
      carcinogenesis by either chemical carcinogens or infection with the milk-borne 
      virus. We have analyzed the MMTV proviral DNA content of normal tissues and of 
      spontaneous, virus-induced, and chemically induced mammary tumors by restriction 
      endonuclease digestion and Southern blot analysis. Although the results clearly 
      showed additional MMTV sequences in the virus-induced tumor which are not present 
      in normal liver DNA, none of the spontaneous or chemically induced tumors could 
      be shown to contain either newly acquired exogenous or amplified endogenous MMTV 
      sequences. Interestingly, mammary tumors arising in C3H/Sm mice treated 
      simultaneously with infectious MMTV (C3H) and dimethylbenz[a]anthracene (DMBA) 
      possessed new exogenous MMTV DNA even though no quantitative change in tumor 
      production was observed when these mice were compared with C3H/Sm mice treated 
      with DMBA alone (Smith et al., Int. J. Cancer 26:373-379, 1980). Our data 
      indicate that the endogenous MMTV proviral units are extensively methylated in 
      normal tissues, such as livers and normal nonlactating mammary glands. In the 
      absence of MMTV (C3H), we found that in the rare, spontaneously occurring C3H/Sm 
      mammary tumors, certain endogenous MMTV sequences were specifically 
      hypomethylated. Hypomethylation of endogenous MMTV sequences was also noted in 
      the chemically induced mammary tumors, even though radioimmune competition assays 
      for MMTV gp52 and p28 are negative (Smith et al., Int. J. Cancer 27:81-86, 1981). 
      Our results support the conclusion that amplification of endogenous MMTV 
      sequences is not intrinsic to C3H/Sm mouse mammary tumors arising spontaneously 
      or after induction by chemicals. On the other hand, integration of exogenous MMTV 
      DNA into the genome was a constant feature of mammary tumors developing in MMTV 
      (C3H)-infected C3H/Sm mice, even when DMBA was used as the carcinogen. 
      Hypomethylation of some endogenous MMTV sequences is characteristic of C3H/Sm 
      mammary tumors, whether spontaneous or induced by chemicals, which suggests that 
      these sequences are located in actively transcribing regions of the tumor cell 
      genome.
FAU - Drohan, W N
AU  - Drohan WN
FAU - Benade, L E
AU  - Benade LE
FAU - Graham, D E
AU  - Graham DE
FAU - Smith, G H
AU  - Smith GH
LA  - eng
PT  - Journal Article
PL  - United States
TA  - J Virol
JT  - Journal of virology
JID - 0113724
RN  - 0 (DNA, Neoplasm)
RN  - 0 (DNA, Viral)
RN  - 57-97-6 (9,10-Dimethyl-1,2-benzanthracene)
RN  - 6R795CQT4H (5-Methylcytosine)
RN  - 8J337D1HZY (Cytosine)
RN  - EC 3.1.21.- (DNA Restriction Enzymes)
SB  - IM
MH  - 5-Methylcytosine
MH  - 9,10-Dimethyl-1,2-benzanthracene
MH  - Animals
MH  - Cytosine/*analogs & derivatives/analysis
MH  - DNA Restriction Enzymes
MH  - DNA, Neoplasm/*analysis
MH  - DNA, Viral/*analysis
MH  - Female
MH  - Gene Amplification
MH  - Mammary Neoplasms, Experimental/*analysis/chemically induced
MH  - Mammary Tumor Virus, Mouse/*genetics
MH  - Mice
MH  - Mice, Inbred C3H
PMC - PMC256198
EDAT- 1982/09/01 00:00
MHDA- 1982/09/01 00:01
PMCR- 1982/09/01
CRDT- 1982/09/01 00:00
PHST- 1982/09/01 00:00 [pubmed]
PHST- 1982/09/01 00:01 [medline]
PHST- 1982/09/01 00:00 [entrez]
PHST- 1982/09/01 00:00 [pmc-release]
AID - 10.1128/JVI.43.3.876-884.1982 [doi]
PST - ppublish
SO  - J Virol. 1982 Sep;43(3):876-84. doi: 10.1128/JVI.43.3.876-884.1982.