Pubmed-entry ::= {
  pmid 22610166,
  medent {
    em std {
      year 2012,
      month 5,
      day 21
    },
    cit {
      title {
        name "S-adenosylmethionine decarboxylase overexpression inhibits mouse
 skin tumor promotion."
      },
      authors {
        names ml {
          "Shi C",
          "Cooper T",
          "McCloskey D",
          "Glick A",
          "Shantz L",
          "Feith D"
        },
        affil str "Penn State College of Medicine, Cellular and Molecular
 Physiology, Hershey, Pennsylvania, United States."
      },
      from journal {
        title {
          iso-jta "Carcinogenesis",
          ml-jta "Carcinogenesis",
          issn "1460-2180",
          name "Carcinogenesis"
        },
        imp {
          date std {
            year 2012,
            month 5,
            day 19
          },
          language "ENG",
          pubstatus aheadofprint,
          history {
            {
              pubstatus other,
              date std {
                year 2012,
                month 5,
                day 22,
                hour 6,
                minute 0
              }
            },
            {
              pubstatus pubmed,
              date std {
                year 2012,
                month 5,
                day 23,
                hour 6,
                minute 0
              }
            },
            {
              pubstatus medline,
              date std {
                year 2012,
                month 5,
                day 23,
                hour 6,
                minute 0
              }
            }
          }
        }
      },
      ids {
        pii "bgs184",
        doi "10.1093/carcin/bgs184",
        pubmed 22610166
      }
    },
    abstract "Neoplastic growth is associated with increased polyamine
 biosynthetic activity and content. Tumor promoter treatment induces the
 rate-limiting enzymes in polyamine biosynthesis, ornithine decarboxylase
 (ODC) and S-adenosylmethionine decarboxylase (AdoMetDC), and targeted ODC
 overexpression is sufficient for tumor promotion in initiated mouse skin. We
 generated a mouse model with doxycycline (Dox)-regulated AdoMetDC expression
 to determine the impact of this second rate-limiting enzyme on epithelial
 carcinogenesis. TetO-AdoMetDC (TAMD) transgenic founders were crossed with
 transgenic mice (K5-tTA) that express the tetracycline-regulated
 transcriptional activator within basal keratinocytes of the skin. Transgene
 expression in TAMD/K5-tTA mice was restricted to keratin 5 (K5) target
 tissues and silenced upon Dox treatment. AdoMetDC activity and its product,
 decarboxylated AdoMet, both increased approximately 8-fold in the skin. This
 enabled a redistribution of the polyamines that led to reduced putrescine,
 increased spermine and an elevated spermine:spermidine ratio. Given the
 positive association between polyamine biosynthetic capacity and neoplastic
 growth, it was somewhat surprising to find that TAMD/K5-tTA mice developed
 significantly fewer tumors than controls in response to
 7,12-dimethylbenz[a]anthracene/12-O-tetradecanoylphorbol-13-acetate
 (DMBA/TPA) chemical carcinogenesis. Importantly, tumor counts in TAMD/K5-tTA
 mice rebounded to nearly equal the levels in the control group upon
 Dox-mediated transgene silencing at a late stage of tumor promotion, which
 indicates that latent viable initiated cells remain in AdoMetDC-expressing
 skin. These results underscore the complexity of polyamine modulation of
 tumor development and emphasize the critical role of putrescine in tumor
 promotion. AdoMetDC-expressing mice will enable more refined spatial and
 temporal manipulation of polyamine biosynthesis during tumorigenesis and in
 other models of human disease.",
    pmid 22610166,
    pub-type {
      "JOURNAL ARTICLE"
    },
    status publisher
  }
}

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