Cristin-resultat-ID: 363825
Sist endret: 25. oktober 2016 14:35
Resultat
Vitenskapelig artikkel
2006

Identification of flat dysplastic aberrant crypt foci in the colon of azoxymethane-treated A/J mice

Bidragsytere:
  • Jan Erik Paulsen
  • Helle Katrine Knutsen
  • Hege Benedikte Asvald Ølstørn
  • Else Marit Løberg og
  • Jan Alexander

Tidsskrift

International Journal of Cancer
ISSN 0020-7136
e-ISSN 1097-0215
NVI-nivå 2

Om resultatet

Vitenskapelig artikkel
Publiseringsår: 2006
Volum: 118
Hefte: 3
Sider: 540 - 546

Importkilder

Isi-ID: 000234443900004

Beskrivelse Beskrivelse

Tittel

Identification of flat dysplastic aberrant crypt foci in the colon of azoxymethane-treated A/J mice

Sammendrag

The role of aberrant crypt foci (ACF) as preneoplastic lesions in colon carcinogenesis is not clear. In Min/+ mice and their wild-type littermates treated with azoxymethane (AOM), we previously identified a subgroup of flat ACF that seem more immediate precursors of tumors than the classical elevated ACF. In the present study, we identified a similar subgroup of flat ACF in AOM-treated A/J mice and compared them with nascent tumors and classical elevated ACF. At week 1 and 2 after birth, A/J mice were injected subcutaneously with AOM (10 mg/kg bw/injection). At weeks 7-14, we examined the luminal surface of unsectioned colon preparations stained with methylene blue in the inverse light microscope. The lesions were also examined by histopathology and immunohistochemistry. Surface examination revealed flat ACF, classical elevated ACF and nascent tumors. Since flat ACF were not observed as elevated structures, their bright blue appearance and compressed pit pattern of crypt openings seen with transillumination were used as criteria for their identification. Flat ACF and nascent tumors displayed a uniform picture of severe dysplasia, compressed pit pattern, overexpression of cytoplasmic/nuclear beta-catenin and nuclear overexpression of cyclin D1. Apparently, flat ACF and tumors represented the same type of dysplastic lesions at different stages of crypt multiplication. In contrast, classical elevated ACF did not seem to be as clearly related to tumorigenesis. They infrequently (1/20) possessed severe dysplasia, overexpression of cytoplasmic/nuclear beta-catenin, or nuclear overexpression of cyclin D1, and they did not have compressed crypt openings. Furthermore, flat ACF grew significantly faster than classical elevated ACF. In conclusion, our data indicate a development from flat ACF to adenoma characterized by aberrant activation of the Wnt signaling pathway and fast crypt multiplication. Classical elevated ACF do not seem to be as closely related to tumorigenesis.

Bidragsytere

Jan Erik Paulsen

  • Tilknyttet:
    Forfatter
    ved Folkehelseinstituttet

Helle Katrine Knutsen

  • Tilknyttet:
    Forfatter
    ved Avdeling for miljøeksponering og -epidemiologi ved Folkehelseinstituttet

Hege Benedikte Ølstørn

Bidragsyterens navn vises på dette resultatet som Hege Benedikte Asvald Ølstørn
  • Tilknyttet:
    Forfatter
    ved Folkehelseinstituttet

Else Marit Løberg

  • Tilknyttet:
    Forfatter
    ved Oslo universitetssykehus HF

Jan Alexander

  • Tilknyttet:
    Forfatter
    ved Smittevern, miljø og helse ved Folkehelseinstituttet
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