Liver cell dysplasia and hepatocellular carcinoma: a histoiogical and immunohistochemical study

Roncalli, Massimo; Borzio, Mauro; Biagi, G. de; Servida, E; Cantaboni, A; Sironi, Maria; Taccagni, G

doi:10.1111/j.1365-2559.1985.tb02436.x

Cited by 41 publications

(14 citation statements)

References 23 publications

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“…We identified two cases of metastatic adenocarcinoma containing small numbers of cells positive for aFP and it is clear that this antibody is not entirely specific for HCC. A further point of interest was the consistent positive staining of non-neoplastic hepatocytes for aFP, similar to the findings in previous studies 1,21 . However, other authors have found aFP positivity to be confined to HCC with no staining of benign liver cell neoplasms or of non-neoplastic hepatocytes 8 .…”

Section: Discussionsupporting

confidence: 82%

Immunohistochemical staining of hepatocellular carcinoma with monoclonal antibody against inhibin

McCluggage¹,

Maxwell²,

Patterson³

et al. 1997

Histopathology

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Inhibin is a peptide hormone produced by ovarian granulosa cells. During a recent study investigating the immunohistochemical staining of ovarian granulosa cell tumours and other neoplasms with an anti-inhibin monoclonal antibody, we identified strong cytoplasmic staining of hepatocytes. In the present study we investigated the immunostaining of hepatocellular carcinoma and other neoplasms involving the liver with anti-inhibin to determine whether the antibody may be of value in the differential diagnosis of hepatic neoplasms. Immunostaining for alpha-fetoprotein was also performed. With anti-inhibin there was positive, generally strong, cytoplasmic staining of 17 of 19 cases of hepatocellular carcinoma, including the pleomorphic and glandular variants. There was positive staining of six of 20 cases of adenocarcinoma. In these, positive staining was generally focal, of weak intensity and involved the luminal surface of neoplastic glands. There was no staining of five cases of neuroendocrine tumour. There was positive staining for alpha-fetoprotein in 13 of 19 cases of hepatocellular carcinoma and in two of 20 cases of adenocarcinoma but no staining of neuroendocrine tumours. Immunostaining with anti-inhibin antibody may be of value in the differentiation of hepatocellular carcinoma from other neoplasms involving the liver. The antibody is a more sensitive, but less specific, immunohistochemical marker for hepatocellular carcinoma than is alpha-fetoprotein.

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Section: Discussionsupporting

confidence: 82%

Immunohistochemical staining of hepatocellular carcinoma with monoclonal antibody against inhibin

McCluggage¹,

Maxwell²,

Patterson³

et al. 1997

Histopathology

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“…Nonneoplastic control cases displayed uniformly diploid stemlines whereas hepatocellular carcinomas had in 8/ I0 cases bimodal or trimodal populations. Thus, LCD is a heterogeneous lesion in terms of ploidy, and the abnormal DNA content observed in some cases supports its pre-neoplastic nature.Liver-cell dysplasia (LCD) is a morphological alteration of hepatocytes (Anthony et al, 1973).Its pre-neoplastic significance has been inferred in several reports because of its frequent association with hepatocellular carcinoma (HCC) and/or chronic hepatitis B virus infection (Bartok et al, 1981; Ho et al, 1981;Akagi et al, 1984;Roncalli et al, 1985Roncalli et al, , 1986. We have observed some morphometric similarities between LCD and HCC (Roncalli et al, 1988).…”

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confidence: 60%

Abnormal DNA content in liver‐cell dysplasia: A flow cytometric study

Roncalli

Borzio

Brando

et al. 1989

Intl Journal of Cancer

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To clarify the true nature of liver-cell dysplasia (LCD), a flow cytometric study has been performed. The DNA content of hepatocytes from 26 cases of cirrhosis with diffuse areas of LCD was investigated and compared to that of hepatocytes from 21 control patients with non-neoplastic and neoplastic liver conditions. Flow cytometric analysis was performed on propidium-stained nuclei from archival paraffin-embedded material. Analysis was directed to assessment of diploid as well as non-diploid peaks by calculation of DNA index (DI), using normal hepatocytes present in each sample as individual and specific references. Since only samples containing at least 10,000 nuclei were considered suitable for analysis, 4 of the 26 LCD cases were discarded. Eight of 22 LCD cases had an abnormal DNA content compared with 0/11 non-neoplastic cases (p less than 0.05) and 8/10 hepatocellular carcinomas (p less than 0.05). Non-neoplastic control cases displayed uniformly diploid stemlines whereas hepatocellular carcinomas had in 8/10 cases bimodal or trimodal populations. Thus, LCD is a heterogeneous lesion in terms of ploidy, and the abnormal DNA content observed in some cases supports its pre-neoplastic nature.

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“…This agreement among separate among studies. 23,[26][27][28][29][30] One recent report has proposed that studies using different methodologies and patient popula-LCC represents a response to prolonged cholestasis. 31 tions strongly suggests that the two lesions are linked in To help untangle this controversy, we assessed the prog-some underlying pathogenetic fashion and argues against nostic value of LCC for HCC through a matched case-control LCC representing merely a degenerative or regenerative alterstudy that compared the occurrence of LCC between cir-ation.…”

Section: Discussionmentioning

confidence: 99%

Large cell change (liver cell dysplasia) and hepatocellular carcinoma in cirrhosis: Matched case-control study, pathological analysis, and pathogenetic hypothesis

1997

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Liver cell dysplasia is the term originally applied by AnLarge cell change (LCC), characterized by cellular enthony et al. 1 in 1973 to cytologically atypical hepatocytes largement, nuclear pleomorphism and hyperchromasia, showing cellular enlargement, nuclear pleomorphism with and multinucleation of hepatocytes, is a common lesion hyperchromasia, and multinucleation. In their study, this in cirrhotic livers, but its nature, significance, and pathoalteration was uncommon in normal livers and occasionally genesis remain uncertain. Therefore, we assessed the noted in cirrhotic livers, particularly with chronic hepatitis prognostic value of LCC as a marker of subsequent hepato-B infection, but was most prevalent in cirrhotic livers bearing cellular carcinoma (HCC) through a case-control study hepatocellular carcinoma (HCC). Because of this relationthat compared pretransplant liver biopsy specimens from ship, liver cell dysplasia, later termed large cell dysplasia, 37 cirrhotic liver transplant recipients with HCC to speciwas proposed to represent a premalignant change.1 mens from a control group of recipients without HCC, Over the succeeding 25 years, however, this proposal has matched for sex, age ({5 years), and cause of cirrhosis.been contested, and other workers have concluded that large LCC was identified in 16 (43%) of the study and 7 (19%) cell dysplasia instead represents a regenerative or degeneraof the control group biopsy specimens. By matched-pair tive phenomenon. Evidence has been marshalled to support analysis, LCC conveyed a moderately increased risk of both sides of this controversy, but much of the data are later HCC with an estimated odds ratio of 3.3 (95% CI, conflicting or circumstantial in nature, and no consensus has 1.2-15; P Å .038). However, a pathology review of 45 been reached as to the nature or significance of the alteration. HCCs showed adjoining LCC in only 12 (27%) and didBecause of this lingering uncertainty, the pathogenetically not suggest a morphological transition or a histogenetic noncommittal term large cell change (LCC) is now recomassociation between the two lesions. LCC hepatocytes dismended as an alternative designation.2 played a low proliferative rate by Ki-67 or proliferating The controversy over LCC poses a practical conundrum: cell nuclear antigen immunostaining (labeling indices of Should it receive special notice as a potential precursor of 0.27 and 0.73) but showed a greater degree of apoptosis malignancy, or should it be dismissed as an inconsequential than normal hepatocytes (labeling indices of 1.9 and 0.23; marker of chronic liver injury? To address this issue, we P Å .03) To reconcile these findings, we propose that LCC evaluated three different aspects of LCC. First, we performed derives from derangements in the hepatocyte's normal a case-control study to evaluate whether the presence of LCC process of polyploidization. Such derangements, possibly presaged any increased risk for the subsequent presence of caused by chronic inflammation-induced DNA damage, HCC...

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Liver cell dysplasia and hepatocellular carcinoma: a histoiogical and immunohistochemical study

Cited by 41 publications

References 23 publications

Immunohistochemical staining of hepatocellular carcinoma with monoclonal antibody against inhibin

Immunohistochemical staining of hepatocellular carcinoma with monoclonal antibody against inhibin

Abnormal DNA content in liver‐cell dysplasia: A flow cytometric study

Large cell change (liver cell dysplasia) and hepatocellular carcinoma in cirrhosis: Matched case-control study, pathological analysis, and pathogenetic hypothesis

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