Dysplasia in view of the cell cycle
- PMID: 15590411
Dysplasia in view of the cell cycle
Abstract
Dysplasia is linked to altered tissue architecture. The lesion belongs into the diagnostic field of human pathology and is highly relevant for the clinical physician, because it breaks the criteria of hyperplasia and regeneration. Dysplasia is a precancerous disorder leading in all probability to malignant transformation if not treated. However, different descriptions do apply for dysplasia in different human tissues, and conventional pathology cannot arrive at unequivocal stringency. In contrast to the previous situation, now, dysplasia is defined by a unifying concept, which works upon cell cycle criteria. The decisive element for the proposed definition is unbalanced segregation of chromosomes and persistent genomic asymmetry through telophase, leading to aneuploid interphase nuclei. Progress of dysplasia can be estimated from the frequency of pathologic mitoses that directly measure cellular proliferation. In routine work, progress of dysplasia shall be quantified by frequency increase of aneuploidy in the increasing fraction of proliferating interphase nuclei. Thus, dysplasia is defined not only by aberrations from healthy histological architecture and normal cytological differentiation, but also by violations of the DNA standard from mitotic nuclei. The proposed classification of dysplasia measures the frequency of pathologic mitoses and the degree of genomic alterations in interphase nuclei. Both these criteria discriminate between low-grade and high-grade dysplasia and ascertain the malignant potential of a dysplastic lesion.
Similar articles
-
Genome instability in human tumorigenesis: microphotometry of interphase nuclei and pathologic mitoses reveals dysplasia.Eur J Histochem. 2000;44(2):133-42. Eur J Histochem. 2000. PMID: 10968361
-
Imbalance of morphologically addressed telophases reflects interphase DNA aneuploidy in tumorigenesis.Eur J Histochem. 1997;41(4):243-54. Eur J Histochem. 1997. PMID: 9491310
-
The DNA content of chromosome division figures and interphase nuclei classifies ulcerative colitis.Eur J Cancer. 1998 Jan;34(1):175-81. doi: 10.1016/s0959-8049(97)00371-7. Eur J Cancer. 1998. PMID: 9624254
-
The molecular basis of dysplasia.Semin Diagn Pathol. 2002 Feb;19(1):48-53. Semin Diagn Pathol. 2002. PMID: 11936266 Review.
-
[Prevention of cancer and the dose-effect relationship: the carcinogenic effects of ionizing radiations].Cancer Radiother. 2009 Jul;13(4):238-58. doi: 10.1016/j.canrad.2009.03.003. Epub 2009 Jun 17. Cancer Radiother. 2009. PMID: 19539515 Review. French.
Cited by
-
Interplay of Developmental Hippo-Notch Signaling Pathways with the DNA Damage Response in Prostate Cancer.Cells. 2022 Aug 7;11(15):2449. doi: 10.3390/cells11152449. Cells. 2022. PMID: 35954292 Free PMC article. Review.
-
Metaplastic esophageal columnar epithelium without goblet cells shows DNA content abnormalities similar to goblet cell-containing epithelium.Am J Gastroenterol. 2009 Apr;104(4):816-24. doi: 10.1038/ajg.2009.85. Epub 2009 Mar 17. Am J Gastroenterol. 2009. PMID: 19293780 Free PMC article.
-
Prognostic importance of mitosis quantification and PHH3 expression in oral epithelial dysplasia.Virchows Arch. 2024 Jan;484(1):47-59. doi: 10.1007/s00428-023-03668-6. Epub 2023 Oct 26. Virchows Arch. 2024. PMID: 37882821 Free PMC article.
-
Liver repopulation and carcinogenesis: two sides of the same coin?Am J Pathol. 2008 Apr;172(4):857-64. doi: 10.2353/ajpath.2008.070910. Epub 2008 Mar 5. Am J Pathol. 2008. PMID: 18321999 Free PMC article. Review.