DNA ploidy of liver biopsies from patients with liver cirrhosis and hepatocellular carcinoma: a flow cytometric analysis

Attallah, Abdelfattah M.; Tabll, Ashraf A.; Salem, S.; Elsadany, Mohamed; Ibrahim, Talaat A; Osman, Sanaa; El-Dosoky, Ibrahim

doi:10.1016/s0304-3835(99)00165-2

Cited by 23 publications

(21 citation statements)

References 13 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The difference between the percentage of CD3 T-cells in LC and HCC patients did not reach a significant level. This may be because LC patients showed a high grade of severity, as demonstrated by DNA flow cytometric analysis in our previous study [12].…”

Section: Discussionmentioning

confidence: 94%

Dysregulation of blood lymphocyte subsets and natural killer cells in schistosomal liver cirrhosis and hepatocellular carcinoma

et al. 2003

View full text Add to dashboard Cite

Immunological factors are important in the pathogenesis of a wide spectrum of hepatobiliary diseases. Using flow cytometry, we determined the changes in lymphocyte subsets and natural killer cells in 123 individuals (81 patients with liver disease and 42 healthy volunteers). The liver diseases included periportal fibrosis (PPF, 10 patients), liver cirrhosis (LC, 31 patients), and hepatocellular carcinoma (HCC, 40 patients). Schistosomiasis and viral hepatitis B and C were the putative etiological agents of liver diseases. Immunophenotyping by indirect immunofluorescence was conducted using monoclonal antibodies to CD3 (T-lymphocytes), CD4 (helper/inducer T-cells), CD8 (suppressor/cytotoxic T-cells), and CD57 (natural killer cells) cell surface markers. Immunophenotyping of PPF patients showed no significant changes in all markers compared with the healthy controls. However, there was a significant decrease ( P<0.01) in CD3 and CD4 T-cells, and a highly significant increase ( P<0.001) in CD57 T-cells in patients with LC or HCC. In addition, LC and HCC patients showed no significant change in CD8 T-cells compared with controls. In conclusion, the progression of liver diseases is associated with a dysregulation of cellular immune responses. T-lymphocytes and natural killer cells may play a role in the immunopathogenesis of liver cirrhosis and HCC.

show abstract

Section: Discussionmentioning

confidence: 94%

Dysregulation of blood lymphocyte subsets and natural killer cells in schistosomal liver cirrhosis and hepatocellular carcinoma

et al. 2003

View full text Add to dashboard Cite

show abstract

“…The frequency of aneuploidy also becomes more pronounced as liver lesions take on an increasing resemblance to tumor (Attallah et al, 1999). In some studies, the state of tumor cell di erentiation is inversely correlated with the number of chromosomal aberrations (Ohsawa et al, 1996).…”

Section: Late Events In Hepatocarcinogenesis (Tumor Progression and Mmentioning

confidence: 96%

Genetic mechanisms of hepatocarcinogenesis

et al. 2002

View full text Add to dashboard Cite

The development of hepatocellular carcinoma (HCC) is a multistep process associated with changes in host gene expression, some of which correlate with the appearance and progression of tumor. Preneoplastic changes in gene expression result from altered DNA methylation, the actions of hepatitis B and C viruses, and point mutations or loss of heterozygosity (LOH) in selected cellular genes. Tumor progression is characterized by LOH involving tumor suppressor genes on many chromosomes and by gene ampli®cation of selected oncogenes. The changes observed in di erent HCC nodules are often distinct, suggesting heterogeneity on the molecular level. These observations suggest that there are multiple, perhaps redundant negative growth regulatory pathways that protect cells against transformation. An understanding of the molecular pathogenesis of HCC may provide new markers for tumor staging, for assessment of the relative risk of tumor formation, and open new opportunities for therapeutic intervention.

show abstract

“…These observations indicate that transcriptional failure or promoter dysfunction may be responsible for changes in checkpoint protein levels and thus induce mitotic checkpoint dysfunction and chromosomal instability. Interestingly, hepatocellular carcinoma (HCC) cell lines display high frequencies of impaired mitotic checkpoints, chromosomal instability, and aneuploidy (16,31,32). However, alterations in mitotic checkpoint genes are not associated with HCC tumorigenesis (16), implying that other mechanisms, such as transcriptional failure or promoter methylation, may contribute to impairment of the mitotic checkpoint.…”

Section: Introductionmentioning

confidence: 99%

Transcriptional Abnormality of the hsMAD2 Mitotic Checkpoint Gene Is a Potential Link to Hepatocellular Carcinogenesis

et al. 2004

View full text Add to dashboard Cite

MAD2 is localized to kinetochores of unaligned chromosomes, where it inactivates the anaphase-promoting complex/cyclosome, thus contributing to the production of a diffusible anaphase inhibitory signal. Disruption of MAD2 expression leads to defects in the mitotic checkpoint, chromosome missegregation, and tumorigenesis. However, the mechanism by which deregulation and/or abnormality of hsMAD2 expression remains to be elucidated. Here, we clone and analyze a ϳ0.5 kb fragment upstream of hsMAD2 and show that this fragment acts as a strong promoter. Transcriptional dysfunction of hsMAD2 is frequently observed in hepatocellular carcinoma cells, and down-regulation of hsMAD2 protein expression is correlated with transcriptional silencing of the hsMAD2 promoter by hypermethylation. These results imply a relationship between transcriptional abnormality of this mitotic checkpoint gene and mitotic abnormality in human cancers.

show abstract

DNA ploidy of liver biopsies from patients with liver cirrhosis and hepatocellular carcinoma: a flow cytometric analysis

Cited by 23 publications

References 13 publications

Dysregulation of blood lymphocyte subsets and natural killer cells in schistosomal liver cirrhosis and hepatocellular carcinoma

Dysregulation of blood lymphocyte subsets and natural killer cells in schistosomal liver cirrhosis and hepatocellular carcinoma

Genetic mechanisms of hepatocarcinogenesis

Transcriptional Abnormality of the hsMAD2 Mitotic Checkpoint Gene Is a Potential Link to Hepatocellular Carcinogenesis

Contact Info

Product

Resources

About