Loss of heterozygosity on chromosomes 1 and 11 in carcinoma of the pancreas

Ding, Shi-Fa; Habib, Nagy; Delhanty, Jda; Bowles, L.; Greco, Laura; Wood, C. B.; Williamson, R. C. N.; Dooley, JS

doi:10.1038/bjc.1992.173

Cited by 29 publications

(16 citation statements)

References 29 publications

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“…For colorectal carcinomas, patients with a higher frequency of allelic losses had a considerably worse prognosis than did the other patients (Vogelstein et al, 1989). A similar correlation was observed in carcinomas of the pancreas (Ding et al, 1992). Thus this study showing a much lower frequency of allele loss in FLC than in HCC is in agreement with the above observations since FLC has a much better prognosis than HCC (Craig et at., 1980).…”

Section: Discussionsupporting

confidence: 81%

Infrequent chromosome allele loss in fibrolamellar carcinoma

Ding

Delhanty²,

Bowles³

et al. 1993

Br J Cancer

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Summary As yet, there is no reported study of chromosome allele loss in fibrolamellar carcinoma (FLC), a distinct, rare variant of hepatocellular carcinoma (HCC). We searched for evidence of allele loss in FLC using 18 DNA probes for 10 chromosomes and compared the pattern of loss with our series of HCC. Two of the probes, AMS32 (lq42-43) and cMS621 (5p) showed allele losses in one tumour, while other probes showed no loss. The frequency of allele loss in FLC was much lower than in HCC, which may be associated with their different prognoses.

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Section: Discussionsupporting

confidence: 81%

Infrequent chromosome allele loss in fibrolamellar carcinoma

Ding

Delhanty²,

Bowles³

et al. 1993

Br J Cancer

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“…A search of UniGene disclosed that these ESTs were located in UniGene cluster Hs.157119T, which was assigned to chromosome 1. This chromosomal assignment was supported by FISH analysis, which mapped SMRZ to chromosome 1p33-34, a region associated with cell proliferation and differentiation (45)(46)(47)(48)(49)(50)(51)(52)(53)(54). This predicted putative role of SMRZ based on the chromosomal assignment was supported by the subcellular localization experiment, which showed that SMRZ is located in the nucleus using C2C12 myoblasts transfected with SMRZ.…”

Section: Discussionsupporting

confidence: 52%

A Novel Human Striated Muscle RING Zinc Finger Protein, SMRZ, Interacts with SMT3b via Its RING Domain

Dai¹,

Liew

2001

Journal of Biological Chemistry

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The RING domain is a conserved zinc finger motif, which serves as a protein-protein interaction interface. Searches of a human heart expressed sequence tag data base for genes encoding the RING domain identified a novel cDNA, named striated muscle RING zinc finger protein (SMRZ). The SMRZ cDNA is 1.9 kilobase pairs in length and encodes a polypeptide of 288 amino acid residues; analysis of the peptide sequence demonstrated an N-terminal RING domain. Fluorescence in situ hybridization localized SMRZ to chromosome 1p33-34. Northern blots demonstrated that SMRZ is expressed exclusively in striated muscle. In the cardiovascular system, SMRZ is more highly expressed in the fetal heart than in the adult heart (slightly higher expression in the ventricle than in the atrium), suggesting that SMRZ is developmentally regulated. SMRZ was found to interact with SMT3b, a ubiquitin-like protein, through the SMRZ-RING domain. This interaction was abolished by mutagenesis of conserved RING domain residues. Transient transfection of SMRZ into C2C12 myoblasts showed localization of SMRZ to the nucleus. These data suggest that SMRZ may play an important role in striated muscle cell embryonic development and perhaps in cell cycle regulation.The zinc finger proteins (ZFPs) 1 are a group of proteins containing zinc finger domains. The finger-like structures are formed by the coordination of conserved cysteines (C) and histidines (H) with zinc ions (1-3). The discovery of the zinc finger domain in the Xenopus transcription factor IIIA (4), together with ongoing cDNA sequencing projects, has led to a significant acceleration in the discovery of ZFP genes. Combinational diversities among the conserved cysteines and histidines of the domain classifies ZFPs into several types: C 2 H 2 , C 2 C 2, C 2 HC, C 2 HC 4 C(HD), C 3 H, and C 3 HC 4 (3, 5-12). These ZFP types have been described in a human heart EST data base survey as well as in an in silico Northern analysis of a total of 15 different tissues (13).The C 3 HC 4 -type zinc finger domain, also termed RING domain, was first described in the sequence of the human ring 1 gene (14). This domain was subsequently found in a number of virus, yeast, plant, and animal proteins, which have various functions such as oncogenesis, signal transduction, peroxisome biogenesis, viral infection, development, transcriptional repression, and ubiquitination (15, 16). The widespread presence of the RING domain in functionally distinct proteins and in many different species indicates that the domain is essential to basic cellular function and is conserved during evolution. With the aid of sequence alignment, the consensus sequence of this domain was defined as CX 2 CX (9 -39) CX (1-3) HX (2-3) CX 2 CX (4 -48) CX 2 C, where X can be any amino acid. Unlike other zinc finger domains, this domain shows a unique cross-brace arrangement on the conserved residues that coordinate the two zinc ions (15,16).Accumulated evidence suggests that the RING domain is mainly involved in protein-protein interactions (15,16...

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“…Gain of chromosomes 20 and 7 and loss of 18 and Y are among the most common numerical changes also in colorectal adenocarcinomas (Muleris et al, 1990;Bardi et al, 1993), underscoring the karyotypic similarities among the various gastrointestinal cancers. Genetic similarities are evident also at the molecular level, with loss of heterozygosity on Ip, 5q, 1 lq, 17p and 18q being detected not only in colorectal but also in pancreatic adenocarcinomas (Neuman et al, 1991;Ding et al, 1992;Hohne et al, 1992).…”

Section: Discussionmentioning

confidence: 99%

Karyotypic abnormalities in tumours of the pancreas

et al. 1993

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Summary Short-term cultures from 20 pancreatic tumours, three endocrine and 17 exocrine, were cytogenetically analysed. All three endocrine tumours had a normal chromosome complement. Clonal chromosome aberrations were detected in 13 of the 17 exocrine tumours: simple karyotypic changes were found in five carcinomas and numerous numerical and/or structural changes in eight. When the present findings and those previously reported by our group were viewed in conjunction, the most common numerical imbalances among the 22 karyotypically abnormal pancreatic carcinomas thus available for evaluation turned out to be, in order of falling frequency, -18, -Y, + 20, + 7, + 11 and -12. Imbalances brought about by structural changes most frequently affected chromosomes I (losses in lp but especially gains of lq), 8 (in particular 8q gains but also 8p losses), and 17 (mostly 17q gain but also loss of 17p). Chromosomal bands lp32, 1q1O, 6q21, 7p22, 8p2l, 8ql 1, 14pl 1, l5q10-1 1, and 17qll were the most common breakpoint sites affected by the structural rearrangements. Abnormal karyotypes were detected more frequently in poorly differentiated and anaplastic carcinomas than in moderately and well differentiated tumours.Pancreatic carcinoma accounts for about 10% of malignancies of the digestive organs and the outcome is fatal in more than 95% of the cases.

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Loss of heterozygosity on chromosomes 1 and 11 in carcinoma of the pancreas

Cited by 29 publications

References 29 publications

Infrequent chromosome allele loss in fibrolamellar carcinoma

Infrequent chromosome allele loss in fibrolamellar carcinoma

A Novel Human Striated Muscle RING Zinc Finger Protein, SMRZ, Interacts with SMT3b via Its RING Domain

Karyotypic abnormalities in tumours of the pancreas

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