Summary Loss of sequences from human chromosome 10q has been reported in several different cancers. Recently, a second candidate tumour-suppressor gene, DMBT1, was identified in this chromosomal region. We studied the mRNA expression and homozygous deletion of this gene in human oesophageal, gastric and colon cancers. Reverse transcriptase polymerase chain reaction (RT-PCR) amplification demonstrated that 23 (53.5%) of 43 oesophageal, 5 (12.5%) of 40 gastric, and 4 (16.7%) of 24 colorectal cancer cases showed an apparent reduction in DMBT1 mRNA in tumour tissues compared with paired normal tissues. Twelve out of 15 oesophageal cancer cell lines also showed no expression. We next studied homozygous deletions within the DMBT1 gene in oesophageal cancers by using duplex PCR. Consequently, it was recognized in five (11.6%) of the primary tumours and two (13.3%) of the cell lines. These findings suggest that DMBT1 may act as a tumour-suppressor gene not only in brain tumours but also in gastrointestinal cancers, especially in oesophageal cancers.
Cavernous haemangioma of the liver was diagnosed in 33 patients using hepatic angiography between 1978 and 1988. Thirteen of these patients underwent surgery. There were no deaths after operation; morbidity included upper gastrointestinal bleeding in two patients and liver dysfunction in one. The follow-up study showed no evidence of recurrence in any of the 13 patients up to 143 months after operation. In the operated patients, a small haemangioma was left in the liver of two for anatomical reasons, but the size of these tumours showed no change over 3 years. The remaining 20 patients had no specific treatment for haemangioma and were followed up for between 18 months and 8 years. Of these 20 patients, 19 had tumours of less than 5 cm in size. As there was no enlargement or rupture of haemangiomas of less than 5 cm, it was felt that these could be observed. Cases having a potential for exposure to trauma, rapid tumour growth, or displaying severe symptoms should be considered for surgical treatment; this can be justified due to low morbidity and no mortality.
To investigate clinicopathologic characteristics of hepatocellular carcinoma (HCC) in young adults, excised tumors from 21 patients younger than 45 years (young group) were compared with findings in tumors from 204 patients older than 45 (old group). In the young group HCC showed (1) a high incidence of positive hepatitis B virus surface antigen (HBsAg) (young 71.4% versus old 20.1%); (2) relatively well-preserved hepatocellular function (indocyanine green test; young 10.7 +/- 8.8% versus old 20.6 +/- 10.8%); (3) low incidence of histologically verified concomitant cirrhosis (young 52.4% versus old 78.4%); and (4) a more advanced stage of the disease in TNM classification (Stage III; young 52.4% versus old 18.1%). With respect to survival rates achieved by surgery, there was no statistically significant difference between the two groups. Thus, hepatitis B virus may relate to the occurrence of HCC in the young patients. Despite the advanced stage in the young group, survival rate after surgery was comparable with that achieved in the old group. These observations mean that a close periodic surveillance of young adults with a positive HBsAg is required to detect HCC at an early stage. Treatment of patients with HBsAg using interferon or vidarabine and hepatitis B vaccine should be made to convert HBsAg to negative in these individuals.
Abstract. Malignant transformation of hepatocellular adenoma (HA) is relatively rare and has been reported to be associated with dysregulation of the β-catenin pathway. The presence of bone marrow metaplasia in HA is an uncommon histological characteristic. The current report presents the case of a 46-year-old woman with glycogen storage disease type I (von Gierke's disease) who underwent resection of hepatocellular carcinoma (HCC) arising in a HA with associated bone marrow metaplasia producing three series of hematopoietic cells. The serum level of proteins induced by des-gamma-carboxy prothrombin (DCP) gradually increased as the tumors grew; following hepatic resection, DCP levels returned to normal. Nuclear accumulation of β-catenin was shown in HCC by immunohistochemistry; however, no mutation was detected in exon 3 of β-catenin. To the best of our knowledge, this is the first report of HA with absolute bone marrow metaplasia producing three series of hematopoietic cells. This occurrence suggests that elevated DCP may be an indicator of malignant transformation of HA. IntroductionHepatocellular adenoma (HA) is a benign tumor usually associated with oral contraceptive intake, glycogen storage disease (GSD) type I and III, and a history of excess androgen exposure (1-4). Malignant transformation of HA is relatively rare and has been reported to be associated with dysregulation of the β-catenin pathway (2,5,6). Nuclear translocation and accumulation of β-catenin is induced by a dysregulation, such as a mutation of exon 3 (7), and may be detected by immunohistochemistry. The presence of bone marrow metaplasia in HA is an uncommon histological characteristic, with only 2 cases of HA with bone marrow metaplasia reported to date (8,9).We herein report a case with increased levels of proteins induced by des-gamma-carboxy prothrombin (DCP), resected hepatocellular carcinoma (HCC) and HA with bone marrow metaplasia arising in a patient with GSD-I. Case reportHistory. A 46-year-old woman was diagnosed with GSD-I during childhood. From that time onwards, she was followed up in a local hospital and received treatment with atorvastatin and allopurinol. At the age of 42 years, the patient consulted a physician at the Saiseikai Karatsu Hospital (Karatsu, Japan), as she continued to experience developmental disorders, such as short stature (135 cm) and low weight (36 kg), but was asymptomatic, apart from abdominal enlargement. The liver edge was palpable 6-7 cm below the right costal margin. The patient had no other risk factors for liver tumors, such as hepatitis B or C viral infection, alcohol use, or autoimmune disease.Liver function and tumor markers. Laboratory data at the first consult revealed elevated values of aspartate aminotransferase (96 IU/l), alanine aminotransferase (69 IU/l), alkaline phosphatase (700 U/l), gamma-glutamyl transpeptidase (2610 IU/l) and DCP (421 mAU/ml). Serum total bilirubin,
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.