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Human epidermal cancer and accompanying precursors have identical p53 mutations different from p53 mutations in adjacent areas of clonally expanded non-neoplastic keratinocytes.
Oncogene. 1996 Feb 15; 12(4):765-73.O

Abstract

Microdissection of biopsies with sequencing of exons 4-8 of the p53 gene permitted precise morphological identification of correlation between mutations and/or loss of heterozygosity, immunoreactivty of p53 and type of squamous neoplasia. Seventy-two specimens from ten lesions of sun-exposed sites including normal epidermis were analysed. Irrespective of p53 immunoreactivity and morphological grade dysplasia, in situ or invasive cancer, in each case, carried the identical mutation indicating that invasive skin cancer and its precursors derive from the same original neoplastic clone. Additionally, morphologically normal epidermis showed some sharply demarcated immunoreactive areas. These never had the same p53 mutation as that of the adjacent tumor, indicating that their mutations were separate events and ruling them out as common precursors of cancer. Non-immunoreactive normal epidermis did not show p53 mutations. Our findings indicate that a large fraction of keratinocytes in sun-exposed human skin carry mutations of p53 and suggest that at least two options exist for such cells (i) innocuous clonal expansion with preserved morphology and normal differentiation or (ii) malignant transformation with the p53 mutation as an early event. Suggestive evidence existed that the p53 mutations were qualitatively different in the two respective groups of lesions.

Authors+Show Affiliations

Department of Pathology, University Hospital of Uppsala, Sweden.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

8632898

Citation

Ren, Z P., et al. "Human Epidermal Cancer and Accompanying Precursors Have Identical P53 Mutations Different From P53 Mutations in Adjacent Areas of Clonally Expanded Non-neoplastic Keratinocytes." Oncogene, vol. 12, no. 4, 1996, pp. 765-73.
Ren ZP, Hedrum A, Pontén F, et al. Human epidermal cancer and accompanying precursors have identical p53 mutations different from p53 mutations in adjacent areas of clonally expanded non-neoplastic keratinocytes. Oncogene. 1996;12(4):765-73.
Ren, Z. P., Hedrum, A., Pontén, F., Nistér, M., Ahmadian, A., Lundeberg, J., Uhlén, M., & Pontén, J. (1996). Human epidermal cancer and accompanying precursors have identical p53 mutations different from p53 mutations in adjacent areas of clonally expanded non-neoplastic keratinocytes. Oncogene, 12(4), 765-73.
Ren ZP, et al. Human Epidermal Cancer and Accompanying Precursors Have Identical P53 Mutations Different From P53 Mutations in Adjacent Areas of Clonally Expanded Non-neoplastic Keratinocytes. Oncogene. 1996 Feb 15;12(4):765-73. PubMed PMID: 8632898.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Human epidermal cancer and accompanying precursors have identical p53 mutations different from p53 mutations in adjacent areas of clonally expanded non-neoplastic keratinocytes. AU - Ren,Z P, AU - Hedrum,A, AU - Pontén,F, AU - Nistér,M, AU - Ahmadian,A, AU - Lundeberg,J, AU - Uhlén,M, AU - Pontén,J, PY - 1996/2/15/pubmed PY - 1996/2/15/medline PY - 1996/2/15/entrez SP - 765 EP - 73 JF - Oncogene JO - Oncogene VL - 12 IS - 4 N2 - Microdissection of biopsies with sequencing of exons 4-8 of the p53 gene permitted precise morphological identification of correlation between mutations and/or loss of heterozygosity, immunoreactivty of p53 and type of squamous neoplasia. Seventy-two specimens from ten lesions of sun-exposed sites including normal epidermis were analysed. Irrespective of p53 immunoreactivity and morphological grade dysplasia, in situ or invasive cancer, in each case, carried the identical mutation indicating that invasive skin cancer and its precursors derive from the same original neoplastic clone. Additionally, morphologically normal epidermis showed some sharply demarcated immunoreactive areas. These never had the same p53 mutation as that of the adjacent tumor, indicating that their mutations were separate events and ruling them out as common precursors of cancer. Non-immunoreactive normal epidermis did not show p53 mutations. Our findings indicate that a large fraction of keratinocytes in sun-exposed human skin carry mutations of p53 and suggest that at least two options exist for such cells (i) innocuous clonal expansion with preserved morphology and normal differentiation or (ii) malignant transformation with the p53 mutation as an early event. Suggestive evidence existed that the p53 mutations were qualitatively different in the two respective groups of lesions. SN - 0950-9232 UR - https://www.unboundmedicine.com/medline/citation/8632898/Human_epidermal_cancer_and_accompanying_precursors_have_identical_p53_mutations_different_from_p53_mutations_in_adjacent_areas_of_clonally_expanded_non_neoplastic_keratinocytes_ L2 - https://medlineplus.gov/skincancer.html DB - PRIME DP - Unbound Medicine ER -