Non-alpha-fetoprotein-producing anaplastic hepatoblastoma cell line

Tsunoda, Yuko; Okamatsu, Takao; Iijima, Tadashi; Shibusawa, Miki; Yatsuzuka, Masashi

doi:10.1007/bf02722945

Cited by 6 publications

(2 citation statements)

References 9 publications

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“…Our literature review identified another 29 cases with initially incompletely resected SCU HB. Demographics are shown in Table II 9–22. Patients ranged in age from 2 to 138 months (median 15 months).…”

Section: Resultsmentioning

confidence: 99%

Small cell undifferentiated variant of hepatoblastoma: Adverse clinical and molecular features similar to rhabdoid tumors

Trobaugh‐Lotrario

Tomlinson

Finegold

et al. 2009

Pediatric Blood & Cancer

152

101

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Section: Resultsmentioning

confidence: 99%

Small cell undifferentiated variant of hepatoblastoma: Adverse clinical and molecular features similar to rhabdoid tumors

Trobaugh‐Lotrario

Tomlinson

Finegold

et al. 2009

Pediatric Blood & Cancer

152

101

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“…(REVERSECELL; Yamanouchi Inc., Tokyo, Japan), and only two patients were judged as positive for HBsAg. Of the two cell lines, one (OHR) was established from ascites of a 4-month-old boy with an anaplastic HBL tumor that did not produce a-fetoprotein (Tsunoda et al, 1996). T h e diagnosis as an anaplastic HBL was made based on morphologic features and immunostaining findings, which were positive for a-1-antitrypsin and cytokeratin (Abenoza et al, 1987).…”

mentioning

confidence: 99%

Infrequent mutations of theTP53 gene and no amplification of theMDM2 gene in hepatoblastomas

Ohnìshì

Kawamura

Hanada

et al. 1996

Genes Chromosom. Cancer

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We have investigated the mutation of the TP53 gene in hepatoblastomas (HBLs) by using polymerase chain reaction‐single strand conformation polymorphism and direct sequencing in 38 HBL tumor samples and in two HBL cell lines. We detected the TP53 gene mutation in an anaplastic hepatoblastoma cell line, but no aberration of the TP53 gene (exons 5–9) was found in tumor samples and in the other HBL cell line. The mutation of the cell line was a missense mutation from GAC (asparagine) to CAC (histidine) at codon 281, which was different from the G‐to‐T transversion of codon 249 that is frequently found in adult hepatocellular carcinomas (HCCs). In addition, we performed Southern blot analysis of the MDM2 gene, but we did not find MDM2 gene amplification in 19 cases tested. Our results suggest that, in contrast to the findings in HCCs in adults, TP53 gene aberrations are not involved in the development or progression of HBLs in children. Genes Chromosom Cancer 15:187–190 (1996). © 1996 Wiley‐Liss, Inc.

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Hepatic tumors in childhood

LaQuaglia¹,

LaQuaglia²

2017

Blumgart's Surgery of the Liver, Biliary Tract and Pancreas, 2-Volume Set

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Non-alpha-fetoprotein-producing anaplastic hepatoblastoma cell line

Cited by 6 publications

References 9 publications

Small cell undifferentiated variant of hepatoblastoma: Adverse clinical and molecular features similar to rhabdoid tumors

Small cell undifferentiated variant of hepatoblastoma: Adverse clinical and molecular features similar to rhabdoid tumors

Infrequent mutations of theTP53 gene and no amplification of theMDM2 gene in hepatoblastomas

Hepatic tumors in childhood

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