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For: Wild A, Langer P, Ramaswamy A, Chaloupka B, Bartsch DK. A novel insulinoma tumor suppressor gene locus on chromosome 22q with potential prognostic implications. J Clin Endocrinol Metab 2001;86:5782-7. [PMID: 11739439 DOI: 10.1210/jcem.86.12.8089] [Citation(s) in RCA: 19] [Impact Index Per Article: 0.8] [Reference Citation Analysis] [What about the content of this article? (0)] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 01/13/2023]

For:	Wild A, Langer P, Ramaswamy A, Chaloupka B, Bartsch DK. A novel insulinoma tumor suppressor gene locus on chromosome 22q with potential prognostic implications. J Clin Endocrinol Metab 2001;86:5782-7. [PMID: 11739439 DOI: 10.1210/jcem.86.12.8089] [Citation(s) in RCA: 19] [Impact Index Per Article: 0.8] [Reference Citation Analysis] [What about the content of this article? (0)] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 01/13/2023]

Number

Cited by Other Article(s)

Alterations of chromosome 3p in 24 cases of gastrinomas and their correlations with clinicopathological and prognostic features. JOURNAL OF PANCREATOLOGY 2020. [DOI: 10.1097/jp9.0000000000000034] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/26/2022] Open

Qi C, Duan J, Shi Q, Wang M, Yan C. Two nonsense somatic mutations in MEN1 identified in sporadic insulinomas. FEBS Open Bio 2018;8:295-301. [PMID: 29435419 PMCID: PMC5794469 DOI: 10.1002/2211-5463.12366] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.1] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/29/2017] [Revised: 11/14/2017] [Accepted: 12/06/2017] [Indexed: 11/07/2022] Open

Delle Fave G, Merola E, Capurso G, Festa S, Piciucchi M, Valente R. Molecular Pathology of Pancreatic Endocrine Tumors. PANCREATIC CANCER 2018:209-239. [DOI: 10.1007/978-1-4939-7193-0_7] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 01/06/2025]

Bhatti TR, Ganapathy K, Huppmann AR, Conlin L, Boodhansingh KE, MacMullen C, Becker S, Ernst LM, Adzick NS, Ruchelli ED, Ganguly A, Stanley CA. Histologic and Molecular Profile of Pediatric Insulinomas: Evidence of a Paternal Parent-of-Origin Effect. J Clin Endocrinol Metab 2016;101:914-22. [PMID: 26756113 PMCID: PMC4803165 DOI: 10.1210/jc.2015-2914] [Citation(s) in RCA: 17] [Impact Index Per Article: 1.9] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/17/2022]

Abstract

CONTEXT

Acquired insulinomas are rare causes of hyperinsulinemic hypoglycemia in children and are much less common than focal lesions of congenital hyperinsulinism. The latter are known to be associated with isodisomy for paternally transmitted ATP-sensitive potassium channel mutations on 11p15; however, the molecular basis for pediatric insulinomas is not well characterized.

OBJECTIVE

The purpose of this study was to characterize the histopathological and molecular defects in a large group of 12 pediatric insulinomas seen at The Children's Hospital of Philadelphia.

RESULTS

Twelve children with insulinomas were seen between 1971 and 2013, compared to 201 cases with focal congenital hyperinsulinism seen between 1997 and 2014. The age of insulinoma patients ranged from 4-16 years at the time of surgery. Features of MEN1 syndrome were present in five of the 12, including four cases with heterozygous mutations of MEN1 on 11q. Immunohistochemical analysis revealed nuclear loss of p57 staining consistent with loss of the maternal 11p15 allele in 11 of the 12 insulinomas, including all five MEN1-associated tumors. Imbalance of the paternal 11p allele was confirmed by single nucleotide polymorphism genotyping and methylation assays of the 11p imprinting control loci in four of five MEN1-associated tumors and six of seven sporadic insulinomas. In addition, single nucleotide polymorphism genotyping revealed extensive tumor aneuploidy beyond chromosome 11.

CONCLUSIONS

These data indicate that MEN1 mutations are more common in insulinomas in children than in adults. Aneuploidy of chromosome 11 and other chromosomes is common in both MEN1 and non-MEN1 insulinomas. The novel observation of a paternal parent-of-origin effect in all MEN1 and most non-MEN1 tumors suggests a critical role for imprinted growth-regulatory genes in the 11p region in the genesis of β-cell endocrine tumors in children.

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Affiliation(s)

Tricia R Bhatti Department of Pathology and Laboratory Medicine (T.R.B., A.R.H., L.C., E.D.R.), The Children's Hospital of Philadelphia, Philadelphia, Pennsylvania 19104-4399; Department of Pathology (T.R.B., L.C., E.D.R.), The Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania 19104; Division of Endocrinology and Diabetes (K.G., K.E.B., C.M., S.B., C.A.S.), The Children's Hospital of Philadelphia, Philadelphia, Pennsylvania 19104-4399; Department of Pathology (L.M.E.), Northwestern University Feinberg School of Medicine, Chicago, Illinois 60611; Department of Surgery (N.S.A.), The Children's Hospital of Philadelphia, Philadelphia, Pennsylvania 19104-4399; and Departments of Surgery (N.S.A.), Genetics (A.G.), and Pediatrics (C.A.S.), The Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania 19104
Karthik Ganapathy Department of Pathology and Laboratory Medicine (T.R.B., A.R.H., L.C., E.D.R.), The Children's Hospital of Philadelphia, Philadelphia, Pennsylvania 19104-4399; Department of Pathology (T.R.B., L.C., E.D.R.), The Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania 19104; Division of Endocrinology and Diabetes (K.G., K.E.B., C.M., S.B., C.A.S.), The Children's Hospital of Philadelphia, Philadelphia, Pennsylvania 19104-4399; Department of Pathology (L.M.E.), Northwestern University Feinberg School of Medicine, Chicago, Illinois 60611; Department of Surgery (N.S.A.), The Children's Hospital of Philadelphia, Philadelphia, Pennsylvania 19104-4399; and Departments of Surgery (N.S.A.), Genetics (A.G.), and Pediatrics (C.A.S.), The Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania 19104
Alison R Huppmann Department of Pathology and Laboratory Medicine (T.R.B., A.R.H., L.C., E.D.R.), The Children's Hospital of Philadelphia, Philadelphia, Pennsylvania 19104-4399; Department of Pathology (T.R.B., L.C., E.D.R.), The Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania 19104; Division of Endocrinology and Diabetes (K.G., K.E.B., C.M., S.B., C.A.S.), The Children's Hospital of Philadelphia, Philadelphia, Pennsylvania 19104-4399; Department of Pathology (L.M.E.), Northwestern University Feinberg School of Medicine, Chicago, Illinois 60611; Department of Surgery (N.S.A.), The Children's Hospital of Philadelphia, Philadelphia, Pennsylvania 19104-4399; and Departments of Surgery (N.S.A.), Genetics (A.G.), and Pediatrics (C.A.S.), The Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania 19104
Laura Conlin Department of Pathology and Laboratory Medicine (T.R.B., A.R.H., L.C., E.D.R.), The Children's Hospital of Philadelphia, Philadelphia, Pennsylvania 19104-4399; Department of Pathology (T.R.B., L.C., E.D.R.), The Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania 19104; Division of Endocrinology and Diabetes (K.G., K.E.B., C.M., S.B., C.A.S.), The Children's Hospital of Philadelphia, Philadelphia, Pennsylvania 19104-4399; Department of Pathology (L.M.E.), Northwestern University Feinberg School of Medicine, Chicago, Illinois 60611; Department of Surgery (N.S.A.), The Children's Hospital of Philadelphia, Philadelphia, Pennsylvania 19104-4399; and Departments of Surgery (N.S.A.), Genetics (A.G.), and Pediatrics (C.A.S.), The Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania 19104
Kara E Boodhansingh Department of Pathology and Laboratory Medicine (T.R.B., A.R.H., L.C., E.D.R.), The Children's Hospital of Philadelphia, Philadelphia, Pennsylvania 19104-4399; Department of Pathology (T.R.B., L.C., E.D.R.), The Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania 19104; Division of Endocrinology and Diabetes (K.G., K.E.B., C.M., S.B., C.A.S.), The Children's Hospital of Philadelphia, Philadelphia, Pennsylvania 19104-4399; Department of Pathology (L.M.E.), Northwestern University Feinberg School of Medicine, Chicago, Illinois 60611; Department of Surgery (N.S.A.), The Children's Hospital of Philadelphia, Philadelphia, Pennsylvania 19104-4399; and Departments of Surgery (N.S.A.), Genetics (A.G.), and Pediatrics (C.A.S.), The Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania 19104
Courtney MacMullen Department of Pathology and Laboratory Medicine (T.R.B., A.R.H., L.C., E.D.R.), The Children's Hospital of Philadelphia, Philadelphia, Pennsylvania 19104-4399; Department of Pathology (T.R.B., L.C., E.D.R.), The Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania 19104; Division of Endocrinology and Diabetes (K.G., K.E.B., C.M., S.B., C.A.S.), The Children's Hospital of Philadelphia, Philadelphia, Pennsylvania 19104-4399; Department of Pathology (L.M.E.), Northwestern University Feinberg School of Medicine, Chicago, Illinois 60611; Department of Surgery (N.S.A.), The Children's Hospital of Philadelphia, Philadelphia, Pennsylvania 19104-4399; and Departments of Surgery (N.S.A.), Genetics (A.G.), and Pediatrics (C.A.S.), The Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania 19104
Susan Becker Department of Pathology and Laboratory Medicine (T.R.B., A.R.H., L.C., E.D.R.), The Children's Hospital of Philadelphia, Philadelphia, Pennsylvania 19104-4399; Department of Pathology (T.R.B., L.C., E.D.R.), The Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania 19104; Division of Endocrinology and Diabetes (K.G., K.E.B., C.M., S.B., C.A.S.), The Children's Hospital of Philadelphia, Philadelphia, Pennsylvania 19104-4399; Department of Pathology (L.M.E.), Northwestern University Feinberg School of Medicine, Chicago, Illinois 60611; Department of Surgery (N.S.A.), The Children's Hospital of Philadelphia, Philadelphia, Pennsylvania 19104-4399; and Departments of Surgery (N.S.A.), Genetics (A.G.), and Pediatrics (C.A.S.), The Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania 19104
Linda M Ernst Department of Pathology and Laboratory Medicine (T.R.B., A.R.H., L.C., E.D.R.), The Children's Hospital of Philadelphia, Philadelphia, Pennsylvania 19104-4399; Department of Pathology (T.R.B., L.C., E.D.R.), The Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania 19104; Division of Endocrinology and Diabetes (K.G., K.E.B., C.M., S.B., C.A.S.), The Children's Hospital of Philadelphia, Philadelphia, Pennsylvania 19104-4399; Department of Pathology (L.M.E.), Northwestern University Feinberg School of Medicine, Chicago, Illinois 60611; Department of Surgery (N.S.A.), The Children's Hospital of Philadelphia, Philadelphia, Pennsylvania 19104-4399; and Departments of Surgery (N.S.A.), Genetics (A.G.), and Pediatrics (C.A.S.), The Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania 19104
N Scott Adzick Department of Pathology and Laboratory Medicine (T.R.B., A.R.H., L.C., E.D.R.), The Children's Hospital of Philadelphia, Philadelphia, Pennsylvania 19104-4399; Department of Pathology (T.R.B., L.C., E.D.R.), The Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania 19104; Division of Endocrinology and Diabetes (K.G., K.E.B., C.M., S.B., C.A.S.), The Children's Hospital of Philadelphia, Philadelphia, Pennsylvania 19104-4399; Department of Pathology (L.M.E.), Northwestern University Feinberg School of Medicine, Chicago, Illinois 60611; Department of Surgery (N.S.A.), The Children's Hospital of Philadelphia, Philadelphia, Pennsylvania 19104-4399; and Departments of Surgery (N.S.A.), Genetics (A.G.), and Pediatrics (C.A.S.), The Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania 19104
Eduardo D Ruchelli Department of Pathology and Laboratory Medicine (T.R.B., A.R.H., L.C., E.D.R.), The Children's Hospital of Philadelphia, Philadelphia, Pennsylvania 19104-4399; Department of Pathology (T.R.B., L.C., E.D.R.), The Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania 19104; Division of Endocrinology and Diabetes (K.G., K.E.B., C.M., S.B., C.A.S.), The Children's Hospital of Philadelphia, Philadelphia, Pennsylvania 19104-4399; Department of Pathology (L.M.E.), Northwestern University Feinberg School of Medicine, Chicago, Illinois 60611; Department of Surgery (N.S.A.), The Children's Hospital of Philadelphia, Philadelphia, Pennsylvania 19104-4399; and Departments of Surgery (N.S.A.), Genetics (A.G.), and Pediatrics (C.A.S.), The Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania 19104
Arupa Ganguly Department of Pathology and Laboratory Medicine (T.R.B., A.R.H., L.C., E.D.R.), The Children's Hospital of Philadelphia, Philadelphia, Pennsylvania 19104-4399; Department of Pathology (T.R.B., L.C., E.D.R.), The Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania 19104; Division of Endocrinology and Diabetes (K.G., K.E.B., C.M., S.B., C.A.S.), The Children's Hospital of Philadelphia, Philadelphia, Pennsylvania 19104-4399; Department of Pathology (L.M.E.), Northwestern University Feinberg School of Medicine, Chicago, Illinois 60611; Department of Surgery (N.S.A.), The Children's Hospital of Philadelphia, Philadelphia, Pennsylvania 19104-4399; and Departments of Surgery (N.S.A.), Genetics (A.G.), and Pediatrics (C.A.S.), The Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania 19104
Charles A Stanley Department of Pathology and Laboratory Medicine (T.R.B., A.R.H., L.C., E.D.R.), The Children's Hospital of Philadelphia, Philadelphia, Pennsylvania 19104-4399; Department of Pathology (T.R.B., L.C., E.D.R.), The Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania 19104; Division of Endocrinology and Diabetes (K.G., K.E.B., C.M., S.B., C.A.S.), The Children's Hospital of Philadelphia, Philadelphia, Pennsylvania 19104-4399; Department of Pathology (L.M.E.), Northwestern University Feinberg School of Medicine, Chicago, Illinois 60611; Department of Surgery (N.S.A.), The Children's Hospital of Philadelphia, Philadelphia, Pennsylvania 19104-4399; and Departments of Surgery (N.S.A.), Genetics (A.G.), and Pediatrics (C.A.S.), The Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania 19104

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Leal-Lopes C, Velloso FJ, Campopiano JC, Sogayar MC, Correa RG. Roles of Commensal Microbiota in Pancreas Homeostasis and Pancreatic Pathologies. J Diabetes Res 2015;2015:284680. [PMID: 26347203 PMCID: PMC4544440 DOI: 10.1155/2015/284680] [Citation(s) in RCA: 32] [Impact Index Per Article: 3.2] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 03/28/2015] [Accepted: 07/09/2015] [Indexed: 12/12/2022] Open

Frequent loss of TIMP-3 expression in progression of esophageal and gastric adenocarcinomas. Neoplasia 2008;10:563-72. [PMID: 18516293 DOI: 10.1593/neo.08208] [Citation(s) in RCA: 47] [Impact Index Per Article: 2.8] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/23/2008] [Revised: 03/14/2008] [Accepted: 03/20/2008] [Indexed: 12/11/2022] Open

Lubensky IA, Zhuang Z. Molecular genetic events in gastrointestinal and pancreatic neuroendocrine tumors. Endocr Pathol 2007;18:156-62. [PMID: 18041590 DOI: 10.1007/s12022-007-9007-x] [Citation(s) in RCA: 17] [Impact Index Per Article: 0.9] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/08/2023]

Lindberg D, Akerström G, Westin G. Mutational analyses of WNT7A and HDAC11 as candidate tumour suppressor genes in sporadic malignant pancreatic endocrine tumours. Clin Endocrinol (Oxf) 2007;66:110-4. [PMID: 17201809 DOI: 10.1111/j.1365-2265.2006.02694.x] [Citation(s) in RCA: 7] [Impact Index Per Article: 0.4] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 01/17/2023]

Jonkers YMH, Claessen SMH, Veltman JA, Geurts van Kessel A, Dinjens WNM, Skogseid B, Ramaekers FCS, Speel EJM. Molecular parameters associated with insulinoma progression: chromosomal instability versus p53 and CK19 status. Cytogenet Genome Res 2006;115:289-97. [PMID: 17124412 DOI: 10.1159/000095926] [Citation(s) in RCA: 17] [Impact Index Per Article: 0.9] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 02/03/2006] [Accepted: 05/02/2006] [Indexed: 12/22/2022] Open

Abstract

Insulinomas represent the predominant syndromic subtype of endocrine pancreatic tumors (EPTs). Their metastatic potential cannot be predicted reliably using histopathological criteria. In the past few years, several attempts have been made to identify prognostic markers, among them TP53 mutations and immunostaining of p53 and recently cytokeratin 19 (CK19). In a previous study using conventional comparative genomic hybridization (CGH) we have shown that chromosomal instability (CIN) is associated with metastatic disease in insulinomas. It was our aim to evaluate these potential parameters in a single study. For the determination of CIN, we applied CGH to microarrays because it allows a high-resolution detection of DNA copy number changes in comparison with conventional CGH as well as the analysis of chromosomal regions close to the centromeres and telomeres, and at 1pter-->p32, 16p, 19 and 22. These regions are usually excluded from conventional CGH analysis, because they may show DNA gains in negative control hybridizations. Array CGH analysis of 30 insulinomas (15 tumors of benign, eight tumors of uncertain and seven tumors of malignant behavior) revealed that >or=20 chromosomal alterations and >or=6 telomeric losses were the best predictors of malignant progression. A subset of 22 insulinomas was further investigated for TP53 exon 5-8 gene mutations, and p53 and CK19 expression. Only one malignant tumor was shown to harbor an arginine 273 serine mutation and immunopositivity for p53. CK19 immunopositivity was detected in three malignant tumors and one tumor with uncertain behavior. In conclusion, our results indicate that CIN as well as telomeric loss are very powerful indicators for malignant progression in sporadic insulinomas. Our data do not support a critical role for p53 and CK19 as molecular parameters for this purpose.

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Zikusoka MN, Kidd M, Eick G, Latich I, Modlin IM. The molecular genetics of gastroenteropancreatic neuroendocrine tumors. Cancer 2006;104:2292-309. [PMID: 16258976 DOI: 10.1002/cncr.21451] [Citation(s) in RCA: 112] [Impact Index Per Article: 5.9] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/17/2022]

Jonkers YMH, Claessen SMH, Feuth T, van Kessel AG, Ramaekers FCS, Veltman JA, Speel EJM. Novel candidate tumour suppressor gene loci on chromosomes 11q23–24 and 22q13 involved in human insulinoma tumourigenesis. J Pathol 2006;210:450-8. [PMID: 17068744 DOI: 10.1002/path.2072] [Citation(s) in RCA: 24] [Impact Index Per Article: 1.3] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/17/2022]

Yang YM, Liu TH, Chen YJ, Jiang WJ, Qian JM, Lu X, Gao J, Wu SF, Sang XT, Chen J. Chromosome 1q loss of heterozygosity frequently occurs in sporadic insulinomas and is associated with tumor malignancy. Int J Cancer 2005;117:234-40. [PMID: 15900598 DOI: 10.1002/ijc.21175] [Citation(s) in RCA: 20] [Impact Index Per Article: 1.0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/11/2022]

Laigle-Donadey F, Crinière E, Benouaich A, Lesueur E, Mokhtari K, Hoang-Xuan K, Sanson M. Loss of 22q Chromosome is Related to Glioma Progression and Loss of 10q. J Neurooncol 2005;76:265-8. [PMID: 16283437 DOI: 10.1007/s11060-005-7019-2] [Citation(s) in RCA: 8] [Impact Index Per Article: 0.4] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 10/25/2022]

Fendrich V, Slater EP, Heinmöller E, Ramaswamy A, Celik I, Nowak O, Chaloupka B, Gerdes B, Bartsch DK. Alterations of the tissue inhibitor of metalloproteinase-3 (TIMP3) gene in pancreatic adenocarcinomas. Pancreas 2005;30:e40-5. [PMID: 15714128 DOI: 10.1097/01.mpa.0000153325.62192.8a] [Citation(s) in RCA: 31] [Impact Index Per Article: 1.6] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/10/2022]

Hartmann C, Nümann A, Mueller W, Holtkamp N, Simon M, von Deimling A. Fine mapping of chromosome 22q tumor suppressor gene candidate regions in astrocytoma. Int J Cancer 2003;108:839-44. [PMID: 14712485 DOI: 10.1002/ijc.11638] [Citation(s) in RCA: 26] [Impact Index Per Article: 1.2] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 02/06/2023]

Velasco G, Cal S, Quesada V, Sánchez LM, López-Otín C. Matriptase-2, a membrane-bound mosaic serine proteinase predominantly expressed in human liver and showing degrading activity against extracellular matrix proteins. J Biol Chem 2002;277:37637-46. [PMID: 12149247 DOI: 10.1074/jbc.m203007200] [Citation(s) in RCA: 133] [Impact Index Per Article: 5.8] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/06/2022] Open

Zhou CZ, Peng ZH, Zhang F, Qiu GQ, He L. Loss of heterozygosity on long arm of chromosome 22 in sporadic colorectal carcinoma. World J Gastroenterol 2002;8:668-73. [PMID: 12174376 PMCID: PMC4656318 DOI: 10.3748/wjg.v8.i4.668] [Citation(s) in RCA: 28] [Impact Index Per Article: 1.2] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/06/2023] Open

Abstract

AIM: The loss of heterozygosity (LOH) on tumor suppressor genes is believed to play a key role in carcinogenesis of colorectal cancer. In this study, we analyzed the LOH at 5 loci on the long arm of chromosome 22 in sporadic colorectal cancer to identify additional loci involved in colorectal tumorigenesis.

METHODS: Five polymorphic microsatellite markers were analyzed in 83 cases of colorectal and normal DNA by PCR. PCR products were eletrophoresed on an ABI 377 DNA sequencer; Genescan 3.1 and Genotype 2.1 software were used for LOH scanning and analysis. Comparison between LOH frequency and clinicopathological data were performed by χ² test. P < 0.05 was considered as statistically significant.

RESULTS: The average LOH frequency on chromosome 22q was 28.38%. The region between markers D22S280 and D22S274 (22q12.2-q13.33) exhibited relatively high LOH frequency. The two highest LOH loci with frequencies of 35.09% and 34.04% was identified on D22S280 (22q12.2-12.3) and D22S274 (22q13.32-13.33).8 cases showed LOH at all informative loci, suggesting that one chromosome 22q had been completely lost. On D22S274 locus, LOH frequency of rectal cancer was 50% (9/18), which was higher than that of proximal colon cancer (12%, 2/17) (P = 0.018). The frequency of distal colon cancer was 42% (5/12), also higher than that of proximal colon cancer. But there was no statistical significance. Putting both the tumors in distal colon and rectum together into consideration, the frequency, 47% (14/30), was higher than that of proximal colon cancer (P = 0.015), suggesting the mechanism of carcinogenisis was different in both groups.

CONCLUSIONS: This study provided evidence for the involvement of putative tumor suppressor genes related to the sporadic colorectal carcinoma on chromosome 22q. The tumor-suppressor-gene (s) might locate on the 22q12.2-12.3 and/or 22q13.32-13.33.

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