Loss of heterozygosity and microsatellite instability in human non‐neoplastic hepatic lesions

Tsopanomichalou, Maria; Kouroumalls, Elias; Ergazaki, M.; Spandldos, Demetrios A.

doi:10.1111/j.1478-3231.1999.tb00054.x

Cited by 17 publications

(14 citation statements)

References 18 publications

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“…[19][20][21][22] However, genetic changes have been very rarely documented in hepatocellular dysplastic nodules. Yamada et al 23 found the same insulinlike growth factor receptor II gene allelic loss in both dysplastic nodules and the adjacent cirrhotic tissue.…”

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confidence: 99%

Molecular Changes in Hepatocellular Dysplastic Nodules on Microdissected Liver Biopsies

et al. 2000

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The genetic profile of dysplastic hepatocellular nodules arising in cirrhosis is poorly understood. We assessed loss of heterozygosity (LOH) and microsatellite instability (MI) in 10 dysplastic nodules (4 low-grade and 6 high-grade) with surrounding cirrhosis and in 10 hepatocellular carcinomas (HCC). Six microsatellite loci were selected and investigated on microdissected needle biopsies. Twenty-four (24.4%) informative loci showed allelic loss, while MI was seen in 3 loci only (3%). The most involved sites were located on chromosomes 4q (54.5%) and 8p (50%). LOH was documented in 16.6%, cirrhotic, 50% low-grade dysplastic nodules (LGDN), 83% high-grade dysplastic nodules (HGDN), and 70% malignant nodules. LOH at multiple loci was increasingly seen from cirrhotic to HGDN, but not from the latter to HCC. The fractional allelic loss (FAL) was significantly increased in dysplastic and neoplastic nodules as compared with cirrhosis (P < .01). The progressive accumulation of genetic changes in cirrhotic, dysplastic, and malignant hepatocellular nodules is in keeping with a multistep process of carcinogenesis; within this spectrum, HGDN can be considered advanced precursors of HCC. (HEPATOLOGY 2000;32:942-946.)

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Molecular Changes in Hepatocellular Dysplastic Nodules on Microdissected Liver Biopsies

et al. 2000

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“…For the HCC-specific transcripts, some of the corresponding genes are associated with pathways related to fatty acid metabolism (APOA2, HAO2, ECH1), signal transduction (DOK1, DYRK1B) and ion transport (CATSPER2, SFXN2). Two of the genes identified by mSSH have also been previously reported to be related to HCC: SIP1 identified by quantitative RT-PCR (Comijin et al, 2001), and APOA2 identified by microsatellite DNA studies (Tsopanomichalou et al, 1999). Several of the genes identified, including SERPI-NA1, ALB, AZGP1, APOA2 and CYP8B1, are known to be regulated by the liver-specific transcription factor HNF4a (Odom et al, 2004), while the transcripts SEC14L2, DDR2 and ZYX identified by mSSH are reported to be regulated by p53.…”

Section: Discussionmentioning

confidence: 96%

Identification of unique and common low abundance tumour-specific transcripts by suppression subtractive hybridization and oligonucleotide probe array analysis

et al. 2008

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“…Some of the microsatellite sequences used for these examinations are located on chromosome arms known to harbor tumor suppressor genes, Rauh/Rickes/Fleischhacker but alterations in these sequences are generally not 'tumor markers' per se. This is underlined by the observation that microsatellite alterations (MA) are not only found in tumor cells [7], but also in morphologically normal appearing cells next to a tumor [8][9][10]. In addition, MA has been described in benign diseases such as asthma [11], chronic obstructive pulmonary disease [12], and in patients with myotonic dystrophy [13] as well.…”

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confidence: 99%

Microsatellite Alterations in Free-Circulating Serum DNA in Patients with Ulcerative Colitis

Rauh

Rickes²,

Fleischhacker³

2003

Dig Dis

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Background/Aims: The aim of this study was to find out whether there is free-circulating DNA in the serum of patients with ulcerative colitis and whether it is possible to establish a panel of genetic alterations which might be useful markers for diagnostic purposes, staging, or follow up. Methods: A set of 11 microsatellite markers located on different chromosomes were analyzed in a group of 59 patients with ulcerative colitis. Radiolabeled PCR products from serum and white blood cell DNA were analyzed by autoradiography and correlated with the clinical data from these patients. Results: Seven of 59 patients showed one or more microsatellite alteration(s) in their serum DNA. Six patients had an alteration in one marker, and two patients had changes in 4 markers, respectively. There was no correlation between the frequency of microsatellite alterations and the clinical data. Conclusion: From the panel of 11 microsatellite markers used for these studies, 6 of them seem to be well suited for the detection of ulcerative colitis-associated alterations in free circulating serum DNA. In order to increase the specificity of this assay, it is necessary to increase the number of patients to be analyzed and to use a different set of markers.

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Loss of heterozygosity and microsatellite instability in human non‐neoplastic hepatic lesions

Abstract: Microsatellite APOA2 located on chromosome 1, shows a statistically significant increase in the rate of loss of heterozygosity as liver lesions become more severe, indicating the presence of tumor suppressor genes which may be involved in the development of these lesions.

Cited by 17 publications

References 18 publications

Molecular Changes in Hepatocellular Dysplastic Nodules on Microdissected Liver Biopsies

Molecular Changes in Hepatocellular Dysplastic Nodules on Microdissected Liver Biopsies

Identification of unique and common low abundance tumour-specific transcripts by suppression subtractive hybridization and oligonucleotide probe array analysis

Microsatellite Alterations in Free-Circulating Serum DNA in Patients with Ulcerative Colitis

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