Home > Research > Publications & Outputs > Novel markers of cell kinetics to evaluate prog...
View graph of relations

Novel markers of cell kinetics to evaluate progression from cirrhosis to hepatocellular carcinoma

Research output: Contribution to Journal/MagazineJournal articlepeer-review

Published

Standard

Novel markers of cell kinetics to evaluate progression from cirrhosis to hepatocellular carcinoma. / Quaglia, Alberto; McStay, M.; Stoeber, Kai et al.
In: Liver International, Vol. 26, No. 4, 05.2006, p. 424-432.

Research output: Contribution to Journal/MagazineJournal articlepeer-review

Harvard

Quaglia, A, McStay, M, Stoeber, K, Loddo, M, Caplin, M, Fanshawe, T, Williams, G & Dhillon, AP 2006, 'Novel markers of cell kinetics to evaluate progression from cirrhosis to hepatocellular carcinoma', Liver International, vol. 26, no. 4, pp. 424-432. https://doi.org/10.1111/j.1478-3231.2006.01242.x

APA

Quaglia, A., McStay, M., Stoeber, K., Loddo, M., Caplin, M., Fanshawe, T., Williams, G., & Dhillon, A. P. (2006). Novel markers of cell kinetics to evaluate progression from cirrhosis to hepatocellular carcinoma. Liver International, 26(4), 424-432. https://doi.org/10.1111/j.1478-3231.2006.01242.x

Vancouver

Quaglia A, McStay M, Stoeber K, Loddo M, Caplin M, Fanshawe T et al. Novel markers of cell kinetics to evaluate progression from cirrhosis to hepatocellular carcinoma. Liver International. 2006 May;26(4):424-432. doi: 10.1111/j.1478-3231.2006.01242.x

Author

Quaglia, Alberto ; McStay, M. ; Stoeber, Kai et al. / Novel markers of cell kinetics to evaluate progression from cirrhosis to hepatocellular carcinoma. In: Liver International. 2006 ; Vol. 26, No. 4. pp. 424-432.

Bibtex

@article{ab0c127a1e6d4781bb7219e474830cc7,
title = "Novel markers of cell kinetics to evaluate progression from cirrhosis to hepatocellular carcinoma",
abstract = "Background: We investigated cell cycle kinetics of nodular lesions in cirrhosis to differentiate hepatocellular carcinoma (HCC) from its precursor lesions.Methods: Twelve small HCC, 10 regenerative (RN), six large regenerative (LRN), and five dysplastic nodules (DN), identified in explant cirrhotic livers of five consecutive patients transplanted at Royal Free Hospital in 2002. Immunoperoxidase for MCM2, geminin and Ki67 was performed and the percentage of positive cells counted.Results: The proportion of cells expressing MCM2 was more than those expressing Ki67, which in turn was more than those expressing geminin (overall median=16%, 2% and 0.5%, respectively, P<0.001). There was a statistically significant trend of increasing Ki67 expression (P=0.006), from RN to HCC; this trend was not statistically significant for geminin (P=0.18) or MCM2 (P=0.51). The median percentage of cells expressing Ki67 was 1% in RN, 0.5% in LRN, 2.2% in DN and 5.4% in HCC. The combination of these markers identified four different cell kinetics patterns: {\textquoteleft}resting{\textquoteright} (G0 cells: MCM2 −ve, Ki67 −ve, geminin −ve); {\textquoteleft}licensed{\textquoteright} (MCM2 +ve, Ki67 −ve, geminin −ve); {\textquoteleft}slowly growing{\textquoteright} (G1 phase arrest, MCM2 +ve, Ki67 +ve, low (0.4%) geminin) and expanding (MCM2 +ve, Ki67 +ve, geminin +ve) nodules.Conclusions: The combination of MCM2, geminin and Ki67 could represent a valuable tool in the understanding of HCC progression in cirrhosis.",
keywords = "cell cycle, DNA licensing , dysplastic nodule , geminin , hepatocellular carcinoma , Ki67 , large regenerative nodule , MCM2",
author = "Alberto Quaglia and M. McStay and Kai Stoeber and Marco Loddo and M. Caplin and Thomas Fanshawe and Gareth Williams and A.P. Dhillon",
year = "2006",
month = may,
doi = "10.1111/j.1478-3231.2006.01242.x",
language = "English",
volume = "26",
pages = "424--432",
journal = "Liver International",
issn = "1478-3231",
publisher = "Wiley-Blackwell",
number = "4",

}

RIS

TY - JOUR

T1 - Novel markers of cell kinetics to evaluate progression from cirrhosis to hepatocellular carcinoma

AU - Quaglia, Alberto

AU - McStay, M.

AU - Stoeber, Kai

AU - Loddo, Marco

AU - Caplin, M.

AU - Fanshawe, Thomas

AU - Williams, Gareth

AU - Dhillon, A.P.

PY - 2006/5

Y1 - 2006/5

N2 - Background: We investigated cell cycle kinetics of nodular lesions in cirrhosis to differentiate hepatocellular carcinoma (HCC) from its precursor lesions.Methods: Twelve small HCC, 10 regenerative (RN), six large regenerative (LRN), and five dysplastic nodules (DN), identified in explant cirrhotic livers of five consecutive patients transplanted at Royal Free Hospital in 2002. Immunoperoxidase for MCM2, geminin and Ki67 was performed and the percentage of positive cells counted.Results: The proportion of cells expressing MCM2 was more than those expressing Ki67, which in turn was more than those expressing geminin (overall median=16%, 2% and 0.5%, respectively, P<0.001). There was a statistically significant trend of increasing Ki67 expression (P=0.006), from RN to HCC; this trend was not statistically significant for geminin (P=0.18) or MCM2 (P=0.51). The median percentage of cells expressing Ki67 was 1% in RN, 0.5% in LRN, 2.2% in DN and 5.4% in HCC. The combination of these markers identified four different cell kinetics patterns: ‘resting’ (G0 cells: MCM2 −ve, Ki67 −ve, geminin −ve); ‘licensed’ (MCM2 +ve, Ki67 −ve, geminin −ve); ‘slowly growing’ (G1 phase arrest, MCM2 +ve, Ki67 +ve, low (0.4%) geminin) and expanding (MCM2 +ve, Ki67 +ve, geminin +ve) nodules.Conclusions: The combination of MCM2, geminin and Ki67 could represent a valuable tool in the understanding of HCC progression in cirrhosis.

AB - Background: We investigated cell cycle kinetics of nodular lesions in cirrhosis to differentiate hepatocellular carcinoma (HCC) from its precursor lesions.Methods: Twelve small HCC, 10 regenerative (RN), six large regenerative (LRN), and five dysplastic nodules (DN), identified in explant cirrhotic livers of five consecutive patients transplanted at Royal Free Hospital in 2002. Immunoperoxidase for MCM2, geminin and Ki67 was performed and the percentage of positive cells counted.Results: The proportion of cells expressing MCM2 was more than those expressing Ki67, which in turn was more than those expressing geminin (overall median=16%, 2% and 0.5%, respectively, P<0.001). There was a statistically significant trend of increasing Ki67 expression (P=0.006), from RN to HCC; this trend was not statistically significant for geminin (P=0.18) or MCM2 (P=0.51). The median percentage of cells expressing Ki67 was 1% in RN, 0.5% in LRN, 2.2% in DN and 5.4% in HCC. The combination of these markers identified four different cell kinetics patterns: ‘resting’ (G0 cells: MCM2 −ve, Ki67 −ve, geminin −ve); ‘licensed’ (MCM2 +ve, Ki67 −ve, geminin −ve); ‘slowly growing’ (G1 phase arrest, MCM2 +ve, Ki67 +ve, low (0.4%) geminin) and expanding (MCM2 +ve, Ki67 +ve, geminin +ve) nodules.Conclusions: The combination of MCM2, geminin and Ki67 could represent a valuable tool in the understanding of HCC progression in cirrhosis.

KW - cell cycle

KW - DNA licensing

KW - dysplastic nodule

KW - geminin

KW - hepatocellular carcinoma

KW - Ki67

KW - large regenerative nodule

KW - MCM2

U2 - 10.1111/j.1478-3231.2006.01242.x

DO - 10.1111/j.1478-3231.2006.01242.x

M3 - Journal article

VL - 26

SP - 424

EP - 432

JO - Liver International

JF - Liver International

SN - 1478-3231

IS - 4

ER -