Common pathogenetic mechanism involving human chromosome 18 in familial and sporadic ileal carcinoid tumors
Serotonin producing endocrine carcinoma of small intestine (ileal carcinoid) is a clinically distinct endocrine tumor. It is generally considered as a sporadic disease and its molecular etiology is poorly understood. We report comprehensive clinical and molecular studies of 55 sporadic and familial...
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| Published in | Genes chromosomes & cancer Vol. 50; no. 2; pp. 82 - 94 |
|---|---|
| Main Authors | , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Hoboken
Wiley Subscription Services, Inc., A Wiley Company
01.02.2011
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| Subjects | |
| Online Access | Get full text |
| ISSN | 1045-2257 1098-2264 1098-2264 |
| DOI | 10.1002/gcc.20834 |
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| Abstract | Serotonin producing endocrine carcinoma of small intestine (ileal carcinoid) is a clinically distinct endocrine tumor. It is generally considered as a sporadic disease and its molecular etiology is poorly understood. We report comprehensive clinical and molecular studies of 55 sporadic and familial patients diagnosed with this condition. Nine pedigrees encompassing 23 affected subjects were established, consistent with autosomal dominant mode of inheritance. Familial and sporadic patients demonstrated indistinguishable clinical pictures. Molecular analyses of 61 tumors from 45 individuals, including eight familial and 37 sporadic patients, aimed at determination of global copy number aberrations using BAC and Illumina SNP arrays and gene expression profiling by Affymetrix chips. Chromosome 18 aberrations were identified in both sporadic and in familial tumors; 100% vs. 38%, respectively. Other, less frequent aberrations were also common for both groups. Global expression profiles revealed no differentially expressed genes. Frequent gain of chromosome 7 was exclusively observed in metastases, when patient matched primary tumors and metastases were compared. Notably, the latter aberration correlated with solid growth pattern morphology (P < 0.01), a histopathological feature that has previously been related to worse prognosis. The clinical and molecular similarities identified between sporadic and familial cases suggest a common pathogenetic mechanism involved in tumor initiation. The familial variant of ileal carcinoid represents a previously unrecognized autosomal dominant inherited tumor disease, which we propose to call Familial Ileal Endocrine Carcinoma (FIEC). Our findings indicate the location of a FIEC tumor suppressor gene near the telomere of 18q, involved in development of inherited and sporadic tumors. © 2010 Wiley‐Liss, Inc. |
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| AbstractList | Serotonin producing endocrine carcinoma of small intestine (ileal carcinoid) is a clinically distinct endocrine tumor. It is generally considered as a sporadic disease and its molecular etiology is poorly understood. We report comprehensive clinical and molecular studies of 55 sporadic and familial patients diagnosed with this condition. Nine pedigrees encompassing 23 affected subjects were established, consistent with autosomal dominant mode of inheritance. Familial and sporadic patients demonstrated indistinguishable clinical pictures. Molecular analyses of 61 tumors from 45 individuals, including eight familial and 37 sporadic patients, aimed at determination of global copy number aberrations using BAC and Illumina SNP arrays and gene expression profiling by Affymetrix chips. Chromosome 18 aberrations were identified in both sporadic and in familial tumors; 100% vs. 38%, respectively. Other, less frequent aberrations were also common for both groups. Global expression profiles revealed no differentially expressed genes. Frequent gain of chromosome 7 was exclusively observed in metastases, when patient matched primary tumors and metastases were compared. Notably, the latter aberration correlated with solid growth pattern morphology (
P
< 0.01), a histopathological feature that has previously been related to worse prognosis. The clinical and molecular similarities identified between sporadic and familial cases suggest a common pathogenetic mechanism involved in tumor initiation. The familial variant of ileal carcinoid represents a previously unrecognized autosomal dominant inherited tumor disease, which we propose to call Familial Ileal Endocrine Carcinoma (FIEC). Our findings indicate the location of a FIEC tumor suppressor gene near the telomere of 18q, involved in development of inherited and sporadic tumors. © 2010 Wiley‐Liss, Inc. Serotonin producing endocrine carcinoma of small intestine (ileal carcinoid) is a clinically distinct endocrine tumor. It is generally considered as a sporadic disease and its molecular etiology is poorly understood. We report comprehensive clinical and molecular studies of 55 sporadic and familial patients diagnosed with this condition. Nine pedigrees encompassing 23 affected subjects were established, consistent with autosomal dominant mode of inheritance. Familial and sporadic patients demonstrated indistinguishable clinical pictures. Molecular analyses of 61 tumors from 45 individuals, including eight familial and 37 sporadic patients, aimed at determination of global copy number aberrations using BAC and Illumina SNP arrays and gene expression profiling by Affymetrix chips. Chromosome 18 aberrations were identified in both sporadic and in familial tumors; 100% vs. 38%, respectively. Other, less frequent aberrations were also common for both groups. Global expression profiles revealed no differentially expressed genes. Frequent gain of chromosome 7 was exclusively observed in metastases, when patient matched primary tumors and metastases were compared. Notably, the latter aberration correlated with solid growth pattern morphology (P < 0.01), a histopathological feature that has previously been related to worse prognosis. The clinical and molecular similarities identified between sporadic and familial cases suggest a common pathogenetic mechanism involved in tumor initiation. The familial variant of ileal carcinoid represents a previously unrecognized autosomal dominant inherited tumor disease, which we propose to call Familial Ileal Endocrine Carcinoma (FIEC). Our findings indicate the location of a FIEC tumor suppressor gene near the telomere of 18q, involved in development of inherited and sporadic tumors. © 2010 Wiley‐Liss, Inc. Serotonin producing endocrine carcinoma of small intestine (ileal carcinoid) is a clinically distinct endocrine tumor. It is generally considered as a sporadic disease and its molecular etiology is poorly understood. We report comprehensive clinical and molecular studies of 55 sporadic and familial patients diagnosed with this condition. Nine pedigrees encompassing 23 affected subjects were established, consistent with autosomal dominant mode of inheritance. Familial and sporadic patients demonstrated indistinguishable clinical pictures. Molecular analyses of 61 tumors from 45 individuals, including eight familial and 37 sporadic patients, aimed at determination of global copy number aberrations using BAC and Illumina SNP arrays and gene expression profiling by Affymetrix chips. Chromosome 18 aberrations were identified in both sporadic and in familial tumors; 100% vs. 38%, respectively. Other, less frequent aberrations were also common for both groups. Global expression profiles revealed no differentially expressed genes. Frequent gain of chromosome 7 was exclusively observed in metastases, when patient matched primary tumors and metastases were compared. Notably, the latter aberration correlated with solid growth pattern morphology (P < 0.01), a histopathological feature that has previously been related to worse prognosis. The clinical and molecular similarities identified between sporadic and familial cases suggest a common pathogenetic mechanism involved in tumor initiation. The familial variant of ileal carcinoid represents a previously unrecognized autosomal dominant inherited tumor disease, which we propose to call Familial Ileal Endocrine Carcinoma (FIEC). Our findings indicate the location of a FIEC tumor suppressor gene near the telomere of 18q, involved in development of inherited and sporadic tumors. copyright 2010 Wiley-Liss, Inc. Serotonin producing endocrine carcinoma of small intestine (ileal carcinoid) is a clinically distinct endocrine tumor. It is generally considered as a sporadic disease and its molecular etiology is poorly understood. We report comprehensive clinical and molecular studies of 55 sporadic and familial patients diagnosed with this condition. Nine pedigrees encompassing 23 affected subjects were established, consistent with autosomal dominant mode of inheritance. Familial and sporadic patients demonstrated indistinguishable clinical pictures. Molecular analyses of 61 tumors from 45 individuals, including eight familial and 37 sporadic patients, aimed at determination of global copy number aberrations using BAC and Illumina SNP arrays and gene expression profiling by Affymetrix chips. Chromosome 18 aberrations were identified in both sporadic and in familial tumors; 100% vs. 38%, respectively. Other, less frequent aberrations were also common for both groups. Global expression profiles revealed no differentially expressed genes. Frequent gain of chromosome 7 was exclusively observed in metastases, when patient matched primary tumors and metastases were compared. Notably, the latter aberration correlated with solid growth pattern morphology (P < 0.01), a histopathological feature that has previously been related to worse prognosis. The clinical and molecular similarities identified between sporadic and familial cases suggest a common pathogenetic mechanism involved in tumor initiation. The familial variant of ileal carcinoid represents a previously unrecognized autosomal dominant inherited tumor disease, which we propose to call Familial Ileal Endocrine Carcinoma (FIEC). Our findings indicate the location of a FIEC tumor suppressor gene near the telomere of 18q, involved in development of inherited and sporadic tumors. Serotonin producing endocrine carcinoma of small intestine (ileal carcinoid) is a clinically distinct endocrine tumor. It is generally considered as a sporadic disease and its molecular etiology is poorly understood. We report comprehensive clinical and molecular studies of 55 sporadic and familial patients diagnosed with this condition. Nine pedigrees encompassing 23 affected subjects were established, consistent with autosomal dominant mode of inheritance. Familial and sporadic patients demonstrated indistinguishable clinical pictures. Molecular analyses of 61 tumors from 45 individuals, including eight familial and 37 sporadic patients, aimed at determination of global copy number aberrations using BAC and Illumina SNP arrays and gene expression profiling by Affymetrix chips. Chromosome 18 aberrations were identified in both sporadic and in familial tumors; 100% vs. 38%, respectively. Other, less frequent aberrations were also common for both groups. Global expression profiles revealed no differentially expressed genes. Frequent gain of chromosome 7 was exclusively observed in metastases, when patient matched primary tumors and metastases were compared. Notably, the latter aberration correlated with solid growth pattern morphology (P < 0.01), a histopathological feature that has previously been related to worse prognosis. The clinical and molecular similarities identified between sporadic and familial cases suggest a common pathogenetic mechanism involved in tumor initiation. The familial variant of ileal carcinoid represents a previously unrecognized autosomal dominant inherited tumor disease, which we propose to call Familial Ileal Endocrine Carcinoma (FIEC). Our findings indicate the location of a FIEC tumor suppressor gene near the telomere of 18q, involved in development of inherited and sporadic tumors.Serotonin producing endocrine carcinoma of small intestine (ileal carcinoid) is a clinically distinct endocrine tumor. It is generally considered as a sporadic disease and its molecular etiology is poorly understood. We report comprehensive clinical and molecular studies of 55 sporadic and familial patients diagnosed with this condition. Nine pedigrees encompassing 23 affected subjects were established, consistent with autosomal dominant mode of inheritance. Familial and sporadic patients demonstrated indistinguishable clinical pictures. Molecular analyses of 61 tumors from 45 individuals, including eight familial and 37 sporadic patients, aimed at determination of global copy number aberrations using BAC and Illumina SNP arrays and gene expression profiling by Affymetrix chips. Chromosome 18 aberrations were identified in both sporadic and in familial tumors; 100% vs. 38%, respectively. Other, less frequent aberrations were also common for both groups. Global expression profiles revealed no differentially expressed genes. Frequent gain of chromosome 7 was exclusively observed in metastases, when patient matched primary tumors and metastases were compared. Notably, the latter aberration correlated with solid growth pattern morphology (P < 0.01), a histopathological feature that has previously been related to worse prognosis. The clinical and molecular similarities identified between sporadic and familial cases suggest a common pathogenetic mechanism involved in tumor initiation. The familial variant of ileal carcinoid represents a previously unrecognized autosomal dominant inherited tumor disease, which we propose to call Familial Ileal Endocrine Carcinoma (FIEC). Our findings indicate the location of a FIEC tumor suppressor gene near the telomere of 18q, involved in development of inherited and sporadic tumors. Serotonin producing endocrine carcinoma of small intestine (ileal carcinoid) is a clinically distinct endocrine tumor. It is generally considered as a sporadic disease and its molecular etiology is poorly understood. We report comprehensive clinical and molecular studies of 55 sporadic and familial patients diagnosed with this condition. Nine pedigrees encompassing 23 affected subjects were established, consistent with autosomal dominant mode of inheritance. Familial and sporadic patients demonstrated indistinguishable clinical pictures. Molecular analyses of 61 tumors from 45 individuals, including eight familial and 37 sporadic patients, aimed at determination of global copy number aberrations using BAC and Illumina SNP arrays and gene expression profiling by Affymetrix chips. Chromosome 18 aberrations were identified in both sporadic and in familial tumors; 100% vs. 38%, respectively. Other, less frequent aberrations were also common for both groups. Global expression profiles revealed no differentially expressed genes. Frequent gain of chromosome 7 was exclusively observed in metastases, when patient matched primary tumors and metastases were compared. Notably, the latter aberration correlated with solid growth pattern morphology (P < 0.01), a histopathological feature that has previously been related to worse prognosis. The clinical and molecular similarities identified between sporadic and familial cases suggest a common pathogenetic mechanism involved in tumor initiation. The familial variant of ileal carcinoid represents a previously unrecognized autosomal dominant inherited tumor disease, which we propose to call Familial Ileal Endocrine Carcinoma (FIEC). Our findings indicate the location of a FIEC tumor suppressor gene near the telomere of 18q, involved in development of inherited and sporadic tumors. Serotonin producing endocrine carcinoma of small intestine (ileal carcinoid) is a clinically distinct endocrine tumor. It is generally considered as a sporadic disease and its molecular etiology is poorly understood. We report comprehensive clinical and molecular studies of 55 sporadic and familial patients diagnosed with this condition. Nine pedigrees encompassing 23 affected subjects were established, consistent with autosomal dominant mode of inheritance. Familial and sporadic patients demonstrated indistinguishable clinical pictures. Molecular analyses of 61 tumors from 45 individuals, including eight familial and 37 sporadic patients, aimed at determination of global copy number aberrations using BAC and Illumina SNP arrays and gene expression profiling by Affymetrix chips. Chromosome 18 aberrations were identified in both sporadic and in familial tumors; 100% vs. 38%, respectively. Other, less frequent aberrations were also common for both groups. Global expression profiles revealed no differentially expressed genes. Frequent gain of chromosome 7 was exclusively observed in metastases, when patient matched primary tumors and metastases were compared. Notably, the latter aberration correlated with solid growth pattern morphology (P < 0.01), a histopathological feature that has previously been related to worse prognosis. The clinical and molecular similarities identified between sporadic and familial cases suggest a common pathogenetic mechanism involved in tumor initiation. The familial variant of ileal carcinoid represents a previously unrecognized autosomal dominant inherited tumor disease, which we propose to call Familial Ileal Endocrine Carcinoma (FIEC). Our findings indicate the location of a FIEC tumor suppressor gene near the telomere of 18q, involved in development of inherited and sporadic tumors. ? 2010 Wiley-Liss, Inc. |
| Author | Dumanski, Jan P. Westin, Gunnar Sjöblom, Tobias Díaz de Ståhl, Teresita Cunningham, Janet L. Janson, Eva T. |
| Author_xml | – sequence: 1 givenname: Janet L. surname: Cunningham fullname: Cunningham, Janet L. organization: Department of Medical Sciences, Section of Endocrine Oncology, Uppsala University, Uppsala, Sweden – sequence: 2 givenname: Teresita surname: Díaz de Ståhl fullname: Díaz de Ståhl, Teresita organization: Department of Genetics and Pathology, Uppsala University, Uppsala, Sweden – sequence: 3 givenname: Tobias surname: Sjöblom fullname: Sjöblom, Tobias organization: Department of Genetics and Pathology, Uppsala University, Uppsala, Sweden – sequence: 4 givenname: Gunnar surname: Westin fullname: Westin, Gunnar organization: Department of Surgical Sciences, Section of Endocrine Surgery, Uppsala University, Uppsala, Sweden – sequence: 5 givenname: Jan P. surname: Dumanski fullname: Dumanski, Jan P. organization: Department of Genetics and Pathology, Uppsala University, Uppsala, Sweden – sequence: 6 givenname: Eva T. surname: Janson fullname: Janson, Eva T. email: Eva.Tiensuu_Janson@medsci.uu.se organization: Department of Medical Sciences, Section of Endocrine Oncology, Uppsala University, Uppsala, Sweden |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/21104784$$D View this record in MEDLINE/PubMed https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-141978$$DView record from Swedish Publication Index |
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| References | Kytölä S, Nord B, Elder EE, Carling T, Kjellman M, Cedermark B, Juhlin C, Höög A, Isola J, Larsson C. 2002. Alterations of the SDHD gene locus in midgut carcinoids, Merkel cell carcinomas, pheochromocytomas, and abdominal paragangliomas. Genes Chromosomes Cancer 34: 325-332. Tanaka T, Watanabe T, Kitayama J, Kanazawa T, Kazama Y, Tanaka J, Kazama S, Nagawa H. 2009. Chromosome 18q deletion as a novel molecular predictor for colorectal cancer with simultaneous hepatic metastasis. Diagn Mol Pathol 18: 219-225. Wood LD, Parsons DW, Jones S, Lin J, Sjöblom T, Leary RJ, Shen D, Boca SM, Barber T, Ptak J, Silliman N, Szabo S, Dezso Z, Ustyanksky V, Nikolskaya T, Nikolsky Y, Karchin R, Wilson PA, Kaminker JS, Zhang Z, Croshaw R, Willis J, Dawson D, Shipitsin M, Willson JK, Sukumar S, Polyak K, Park BH, Pethiyagoda CL, Pant PV, Ballinger DG, Sparks AB, Hartigan J, Smith DR, Suh E, Papadopoulos N, Buckhaults P, Markowitz SD, Parmigiani G, Kinzler KW, Velculescu VE, Vogelstein B. 2007. The genomic landscapes of human breast and colorectal cancers. Science 318: 1108-1113. Klöppel G, Couvelard A, Perren A, Komminoth P, McNicol AM, Nilsson O, Scarpa A, Scoazec JY, Wiedenmann B, Papotti M, Rindi G, Plöckinger U. 2009. ENETS consensus guidelines for the standards of care in neuroendocrine tumors: Towards a standardized approach to the diagnosis of gastroenteropancreatic neuroendocrine tumors and their prognostic stratification. Neuroendocrinology 90: 162-166. Löllgen RM, Hessman O, Szabo E, Westin G, Åkerström G. 2001. Chromosome 18 deletions are common events in classical midgut carcinoid tumors. Int J Cancer 92: 812-815. Järhult J, Landerholm K, Falkmer S, Nordenskjöld M, Sundler F, Wierup N. 2010. First report on metastasizing small bowel carcinoids in first-degree relatives in three generations. Neuroendocrinology 91: 318-323. Pal T, Liede A, Mitchell M, Calender A, Narod SA. 2001. Intestinal carcinoid tumours in a father and daughter. Can J Gastroenterol 15: 405-409. Sjöblom T, Jones S, Wood LD, Parsons DW, Lin J, Barber TD, Mandelker D, Leary RJ, Ptak J, Silliman N, Szabo S, Buckhaults P, Farrell C, Meeh P, Markowitz SD, Willis J, Dawson D, Willson JK, Gazdar AF, Hartigan J, Wu L, Liu C, Parmigiani G, Park BH, Bachman KE, Papadopoulos N, Vogelstein B, Kinzler KW, Velculescu VE. 2006. The consensus coding sequences of human breast and colorectal cancers. Science 314: 268-274. Hemminki K, Li X. 2001. Familial carcinoid tumors and subsequent cancers: A nation-wide epidemiologic study from Sweden. Int J Cancer 94: 444-448. Steemers FJ, Chang W, Lee G, Barker DL, Shen R, Gunderson KL. 2006. Whole-genome genotyping with the single-base extension assay. Nat Methods 3: 31-33. Vogelstein B, Kinzler KW. 2002. The genetic basis of human cancer, 2nd ed. New York: McGrawh-Hill. Andersson E, Sward C, Stenman G, Ahlman H, Nilsson O. 2009. High-resolution genomic profiling reveals gain of chromosome 14 as a predictor of poor outcome in ileal carcinoids. Endocr Relat Cancer 16: 953-966. Buckley PG, Mantripragada KK, Benetkiewicz M, Tapia-Paez I, Diaz De Ståhl T, Rosenquist M, Ali H, Jarbo C, De Bustos C, Hirvelä C, Sinder Wilén B, Fransson I, Thyr C, Johnsson BI, Bruder CE, Menzel U, Hergersberg M, Mandajl N, Blennow E, Wedell A, Beare DM, Collins JE, Dunham I, Albertson D, Pinkel D, Bastian BC, Faruqi AF, Lasken RS, Ichimura K, Collins VP, Dumanski JP. 2002. A full-coverage, high-resolution human chromosome 22 genomic microarray for clinical and research applications. Hum Mol Genet 11: 3221-3229. Janson ET, Holmberg L, Stridsberg M, Eriksson B, Theodorsson E, Wilander E, Öberg K. 1997. Carcinoid tumors: analysis of prognostic factors and survival in 301 patients from a referral center. Ann Oncol 8: 685-690. Debelenko LV, Brambilla E, Agarwal SK, Swalwell JI, Kester MB, Lubensky IA, Zhuang Z, Guru SC, Manickam P, Olufemi SE, Chandrasekharappa SC, Crabtree JS, Kim YS, Heppner C, Burns AL, Spiegel AM, Marx SJ, Liotta LA, Collins FS, Travis WD, Emmert-Buck MR. 1997. Identification of MEN1 gene mutations in sporadic carcinoid tumors of the lung. Hum Mol Genet 6: 2285-2290. Nord H, Segersten U, Sandgren J, Wester K, Busch C, Menzel U, Komorowski J, Dumanski JP, Malmström PU, de Ståhl TD. 2010. Focal amplifications are associated with high grade and recurrences in stage Ta bladder carcinoma. Int J Cancer 126: 1390-1402. Kulke MH, Freed E, Chiang DY, Philips J, Zahrieh D, Glickman JN, Shivdasani RA. 2008. High-resolution analysis of genetic alterations in small bowel carcinoid tumors reveals areas of recurrent amplification and loss. Genes Chromosomes Cancer 47: 591-603. Kytölä S, Höög A, Nord B, Cedermark B, Frisk T, Larsson C, Kjellman M. 2001. Comparative genomic hybridization identifies loss of 18q22-qter as an early and specific event in tumorigenesis of midgut carcinoids. Am J Pathol 158: 1803-1808. Smyth GK. 2004. Linear models and empirical bayes methods for assessing differential expression in microarray experiments. Stat Appl Genet Mol Biol 3:Article3. D'Adda T, Pizzi S, Azzoni C, Bottarelli L, Crafa P, Pasquali C, Davoli C, Corleto VD, Delle Fave G, Bordi C. 2002. Different patterns of 11q allelic losses in digestive endocrine tumors. Hum Pathol 33: 322-329. Eschbach J, Rinaldo J. 1962. Metastatic carcinoid, a familial occurrence. Ann Intern Med 57: 647-650. Wale RJ, Williams JA, Beeley AH, Hughes ES. 1983. Familial occurrence in carcinoid tumours. Aust N Z J Surg 53: 325-328. Berge T, Linell F. 1976. Carcinoid tumours. Frequency in a defined population during a 12-year period. Acta Pathol Microbiol Scand A 84: 322-330. Moertel CG, Dockerty MB. 1973. Familial occurrence of metastasizing carcinoid tumors. Ann Intern Med 78: 389-390. Modlin IM, Öberg K, Chung DC, Jensen RT, de Herder WW, Thakker RV, Caplin M, Delle Fave G, Kaltsas GA, Krenning EP, Moss SF, Nilsson O, Rindi G, Salazar R, Ruszniewski P, Sundin A. 2008. Gastroenteropancreatic neuroendocrine tumours. Lancet Oncol 9: 61-72. Otsuka R, Tamakoshi K, Wada K, Matsushita K, Ouyang P, Hotta Y, Takefuji S, Mitsuhashi H, Toyoshima H, Shimokata H, Yatsuya H. 2008. Having more healthy practice was associated with low white blood cell counts in middle-aged Japanese male and female workers. Ind Health 46: 341-347. Sturn A, Quackenbush J, Trajanoski Z. 2002. Genesis: cluster analysis of microarray data. Bioinformatics 18: 207-208. Solcia E, Klöppel G, Sobin LH. 2000. Histological Typing of Endocrine Tumours. WHO International Histological Classification of Tumours, 2nd ed. Berlin: Springer. Babovic-Vuksanovic D, Constantinou CL, Rubin J, Rowland CM, Schaid DJ, Karnes PS. 1999. Familial occurrence of carcinoid tumors and association with other malignant neoplasms. Cancer Epidemiol Biomarkers Prev 8: 715-719. Cunningham JL, Grimelius L, Sundin A, Agarwal S, Janson ET. 2007. Malignant ileocaecal serotonin-producing carcinoid tumours: the presence of a solid growth pattern and/or Ki67 index above 1% identifies patients with a poorer prognosis. Acta Oncol 46: 747-756. Kinova S, Duris I, Kovacova E, Stvrtina S, Galbavy S, Makaiova I. 2001. Malignant carcinoid in two brothers. Bratisl Lek Listy 102: 231-234. de Ståhl TD, Sandgren J, Piotrowski A, Nord H, Andersson R, Menzel U, Bogdan A, Thuresson AC, Poplawski A, von Tell D, Hansson CM, Elshafie AI, Elghazali G, Imreh S, Nordenskjöld M, Upadhyaya M, Komorowski J, Bruder CE, Dumanski JP. 2008. Profiling of copy number variations (CNVs) in healthy individuals from three ethnic groups using a human genome 32 K BAC-clone-based array. Hum Mutat 29: 398-408. Duerr E, Mizukami Y, Warshaw A, Kulke M, Chung C. 2006. Gene expression profiles of pancreatic neuroendocrine tumors and gastrointestinal carcinoids. Gastroenterology 130( Suppl 2): S1887. Zikusoka MN, Kidd M, Eick G, Latich I, Modlin IM. 2005. The molecular genetics of gastroenteropancreatic neuroendocrine tumors. Cancer 104: 2292-2230. Benjamini Y, Drai D, Elmer G, Kafkafi N, Golani I. 2001. Controlling the false discovery rate in behavior genetics research. 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| References_xml | – reference: Klöppel G, Couvelard A, Perren A, Komminoth P, McNicol AM, Nilsson O, Scarpa A, Scoazec JY, Wiedenmann B, Papotti M, Rindi G, Plöckinger U. 2009. ENETS consensus guidelines for the standards of care in neuroendocrine tumors: Towards a standardized approach to the diagnosis of gastroenteropancreatic neuroendocrine tumors and their prognostic stratification. Neuroendocrinology 90: 162-166. – reference: Solcia E, Klöppel G, Sobin LH. 2000. Histological Typing of Endocrine Tumours. WHO International Histological Classification of Tumours, 2nd ed. Berlin: Springer. – reference: de Ståhl TD, Sandgren J, Piotrowski A, Nord H, Andersson R, Menzel U, Bogdan A, Thuresson AC, Poplawski A, von Tell D, Hansson CM, Elshafie AI, Elghazali G, Imreh S, Nordenskjöld M, Upadhyaya M, Komorowski J, Bruder CE, Dumanski JP. 2008. Profiling of copy number variations (CNVs) in healthy individuals from three ethnic groups using a human genome 32 K BAC-clone-based array. Hum Mutat 29: 398-408. – reference: Duerr E, Mizukami Y, Warshaw A, Kulke M, Chung C. 2006. Gene expression profiles of pancreatic neuroendocrine tumors and gastrointestinal carcinoids. Gastroenterology 130( Suppl 2): S1887. – reference: Andersson E, Sward C, Stenman G, Ahlman H, Nilsson O. 2009. High-resolution genomic profiling reveals gain of chromosome 14 as a predictor of poor outcome in ileal carcinoids. Endocr Relat Cancer 16: 953-966. – reference: Janson ET, Holmberg L, Stridsberg M, Eriksson B, Theodorsson E, Wilander E, Öberg K. 1997. Carcinoid tumors: analysis of prognostic factors and survival in 301 patients from a referral center. Ann Oncol 8: 685-690. – reference: Kinova S, Duris I, Kovacova E, Stvrtina S, Galbavy S, Makaiova I. 2001. Malignant carcinoid in two brothers. Bratisl Lek Listy 102: 231-234. – reference: Löllgen RM, Hessman O, Szabo E, Westin G, Åkerström G. 2001. Chromosome 18 deletions are common events in classical midgut carcinoid tumors. Int J Cancer 92: 812-815. – reference: D'Adda T, Pizzi S, Azzoni C, Bottarelli L, Crafa P, Pasquali C, Davoli C, Corleto VD, Delle Fave G, Bordi C. 2002. Different patterns of 11q allelic losses in digestive endocrine tumors. Hum Pathol 33: 322-329. – reference: Otsuka R, Tamakoshi K, Wada K, Matsushita K, Ouyang P, Hotta Y, Takefuji S, Mitsuhashi H, Toyoshima H, Shimokata H, Yatsuya H. 2008. Having more healthy practice was associated with low white blood cell counts in middle-aged Japanese male and female workers. Ind Health 46: 341-347. – reference: Buckley PG, Mantripragada KK, Benetkiewicz M, Tapia-Paez I, Diaz De Ståhl T, Rosenquist M, Ali H, Jarbo C, De Bustos C, Hirvelä C, Sinder Wilén B, Fransson I, Thyr C, Johnsson BI, Bruder CE, Menzel U, Hergersberg M, Mandajl N, Blennow E, Wedell A, Beare DM, Collins JE, Dunham I, Albertson D, Pinkel D, Bastian BC, Faruqi AF, Lasken RS, Ichimura K, Collins VP, Dumanski JP. 2002. A full-coverage, high-resolution human chromosome 22 genomic microarray for clinical and research applications. Hum Mol Genet 11: 3221-3229. – reference: Eschbach J, Rinaldo J. 1962. Metastatic carcinoid, a familial occurrence. Ann Intern Med 57: 647-650. – reference: Cunningham JL, Grimelius L, Sundin A, Agarwal S, Janson ET. 2007. Malignant ileocaecal serotonin-producing carcinoid tumours: the presence of a solid growth pattern and/or Ki67 index above 1% identifies patients with a poorer prognosis. Acta Oncol 46: 747-756. – reference: Kytölä S, Nord B, Elder EE, Carling T, Kjellman M, Cedermark B, Juhlin C, Höög A, Isola J, Larsson C. 2002. Alterations of the SDHD gene locus in midgut carcinoids, Merkel cell carcinomas, pheochromocytomas, and abdominal paragangliomas. Genes Chromosomes Cancer 34: 325-332. – reference: Berge T, Linell F. 1976. Carcinoid tumours. Frequency in a defined population during a 12-year period. Acta Pathol Microbiol Scand A 84: 322-330. – reference: Kytölä S, Höög A, Nord B, Cedermark B, Frisk T, Larsson C, Kjellman M. 2001. Comparative genomic hybridization identifies loss of 18q22-qter as an early and specific event in tumorigenesis of midgut carcinoids. Am J Pathol 158: 1803-1808. – reference: Wale RJ, Williams JA, Beeley AH, Hughes ES. 1983. Familial occurrence in carcinoid tumours. Aust N Z J Surg 53: 325-328. – reference: Debelenko LV, Brambilla E, Agarwal SK, Swalwell JI, Kester MB, Lubensky IA, Zhuang Z, Guru SC, Manickam P, Olufemi SE, Chandrasekharappa SC, Crabtree JS, Kim YS, Heppner C, Burns AL, Spiegel AM, Marx SJ, Liotta LA, Collins FS, Travis WD, Emmert-Buck MR. 1997. Identification of MEN1 gene mutations in sporadic carcinoid tumors of the lung. Hum Mol Genet 6: 2285-2290. – reference: Kulke MH, Freed E, Chiang DY, Philips J, Zahrieh D, Glickman JN, Shivdasani RA. 2008. High-resolution analysis of genetic alterations in small bowel carcinoid tumors reveals areas of recurrent amplification and loss. Genes Chromosomes Cancer 47: 591-603. – reference: Tanaka T, Watanabe T, Kitayama J, Kanazawa T, Kazama Y, Tanaka J, Kazama S, Nagawa H. 2009. Chromosome 18q deletion as a novel molecular predictor for colorectal cancer with simultaneous hepatic metastasis. Diagn Mol Pathol 18: 219-225. – reference: Zikusoka MN, Kidd M, Eick G, Latich I, Modlin IM. 2005. The molecular genetics of gastroenteropancreatic neuroendocrine tumors. Cancer 104: 2292-2230. – reference: Järhult J, Landerholm K, Falkmer S, Nordenskjöld M, Sundler F, Wierup N. 2010. First report on metastasizing small bowel carcinoids in first-degree relatives in three generations. Neuroendocrinology 91: 318-323. – reference: Sturn A, Quackenbush J, Trajanoski Z. 2002. Genesis: cluster analysis of microarray data. Bioinformatics 18: 207-208. – reference: Modlin IM, Öberg K, Chung DC, Jensen RT, de Herder WW, Thakker RV, Caplin M, Delle Fave G, Kaltsas GA, Krenning EP, Moss SF, Nilsson O, Rindi G, Salazar R, Ruszniewski P, Sundin A. 2008. Gastroenteropancreatic neuroendocrine tumours. Lancet Oncol 9: 61-72. – reference: Nord H, Segersten U, Sandgren J, Wester K, Busch C, Menzel U, Komorowski J, Dumanski JP, Malmström PU, de Ståhl TD. 2010. Focal amplifications are associated with high grade and recurrences in stage Ta bladder carcinoma. Int J Cancer 126: 1390-1402. – reference: Babovic-Vuksanovic D, Constantinou CL, Rubin J, Rowland CM, Schaid DJ, Karnes PS. 1999. Familial occurrence of carcinoid tumors and association with other malignant neoplasms. Cancer Epidemiol Biomarkers Prev 8: 715-719. – reference: Pal T, Liede A, Mitchell M, Calender A, Narod SA. 2001. Intestinal carcinoid tumours in a father and daughter. Can J Gastroenterol 15: 405-409. – reference: Wood LD, Parsons DW, Jones S, Lin J, Sjöblom T, Leary RJ, Shen D, Boca SM, Barber T, Ptak J, Silliman N, Szabo S, Dezso Z, Ustyanksky V, Nikolskaya T, Nikolsky Y, Karchin R, Wilson PA, Kaminker JS, Zhang Z, Croshaw R, Willis J, Dawson D, Shipitsin M, Willson JK, Sukumar S, Polyak K, Park BH, Pethiyagoda CL, Pant PV, Ballinger DG, Sparks AB, Hartigan J, Smith DR, Suh E, Papadopoulos N, Buckhaults P, Markowitz SD, Parmigiani G, Kinzler KW, Velculescu VE, Vogelstein B. 2007. The genomic landscapes of human breast and colorectal cancers. Science 318: 1108-1113. – reference: Sjöblom T, Jones S, Wood LD, Parsons DW, Lin J, Barber TD, Mandelker D, Leary RJ, Ptak J, Silliman N, Szabo S, Buckhaults P, Farrell C, Meeh P, Markowitz SD, Willis J, Dawson D, Willson JK, Gazdar AF, Hartigan J, Wu L, Liu C, Parmigiani G, Park BH, Bachman KE, Papadopoulos N, Vogelstein B, Kinzler KW, Velculescu VE. 2006. The consensus coding sequences of human breast and colorectal cancers. Science 314: 268-274. – reference: Smyth GK. 2004. Linear models and empirical bayes methods for assessing differential expression in microarray experiments. Stat Appl Genet Mol Biol 3:Article3. – reference: Steemers FJ, Chang W, Lee G, Barker DL, Shen R, Gunderson KL. 2006. Whole-genome genotyping with the single-base extension assay. Nat Methods 3: 31-33. – reference: Benjamini Y, Drai D, Elmer G, Kafkafi N, Golani I. 2001. Controlling the false discovery rate in behavior genetics research. Behav Brain Res 125: 279-284. – reference: Hemminki K, Li X. 2001. Familial carcinoid tumors and subsequent cancers: A nation-wide epidemiologic study from Sweden. Int J Cancer 94: 444-448. – reference: Vogelstein B, Kinzler KW. 2002. The genetic basis of human cancer, 2nd ed. New York: McGrawh-Hill. – reference: Moertel CG, Dockerty MB. 1973. Familial occurrence of metastasizing carcinoid tumors. Ann Intern Med 78: 389-390. – volume: 15 start-page: 405 year: 2001 end-page: 409 article-title: Intestinal carcinoid tumours in a father and daughter publication-title: Can J Gastroenterol – volume: 29 start-page: 398 year: 2008 end-page: 408 article-title: Profiling of copy number variations (CNVs) in healthy individuals from three ethnic groups using a human genome 32 K BAC‐clone‐based array publication-title: Hum Mutat – volume: 102 start-page: 231 year: 2001 end-page: 234 article-title: Malignant carcinoid in two brothers publication-title: Bratisl Lek Listy – volume: 92 start-page: 812 year: 2001 end-page: 815 article-title: Chromosome 18 deletions are common events in classical midgut carcinoid tumors publication-title: Int J Cancer – volume: 16 start-page: 953 year: 2009 end-page: 966 article-title: High‐resolution genomic profiling reveals gain of chromosome 14 as a predictor of poor outcome in ileal carcinoids publication-title: Endocr Relat Cancer – volume: 18 start-page: 207 year: 2002 end-page: 208 article-title: Genesis: cluster analysis of microarray data publication-title: Bioinformatics – volume: 125 start-page: 279 year: 2001 end-page: 284 article-title: Controlling the false discovery rate in behavior genetics research publication-title: Behav Brain Res – volume: 84 start-page: 322 year: 1976 end-page: 330 article-title: Carcinoid tumours. Frequency in a defined population during a 12‐year period publication-title: Acta Pathol Microbiol Scand A – volume: 91 start-page: 318 year: 2010 end-page: 323 article-title: First report on metastasizing small bowel carcinoids in first‐degree relatives in three generations publication-title: Neuroendocrinology – volume: 158 start-page: 1803 year: 2001 end-page: 1808 article-title: Comparative genomic hybridization identifies loss of 18q22‐qter as an early and specific event in tumorigenesis of midgut carcinoids publication-title: Am J Pathol – volume: 18 start-page: 219 year: 2009 end-page: 225 article-title: Chromosome 18q deletion as a novel molecular predictor for colorectal cancer with simultaneous hepatic metastasis publication-title: Diagn Mol Pathol – volume: 46 start-page: 747 year: 2007 end-page: 756 article-title: Malignant ileocaecal serotonin‐producing carcinoid tumours: the presence of a solid growth pattern and/or Ki67 index above 1% identifies patients with a poorer prognosis publication-title: Acta Oncol – volume: 6 start-page: 2285 year: 1997 end-page: 2290 article-title: Identification of MEN1 gene mutations in sporadic carcinoid tumors of the lung publication-title: Hum Mol Genet – volume: 34 start-page: 325 year: 2002 end-page: 332 article-title: Alterations of the SDHD gene locus in midgut carcinoids, Merkel cell carcinomas, pheochromocytomas, and abdominal paragangliomas publication-title: Genes Chromosomes Cancer – year: 2000 – volume: 8 start-page: 685 year: 1997 end-page: 690 article-title: Carcinoid tumors: analysis of prognostic factors and survival in 301 patients from a referral center publication-title: Ann Oncol – volume: 9 start-page: 61 year: 2008 end-page: 72 article-title: Gastroenteropancreatic neuroendocrine tumours publication-title: Lancet Oncol – volume: 8 start-page: 715 year: 1999 end-page: 719 article-title: Familial occurrence of carcinoid tumors and association with other malignant neoplasms publication-title: Cancer Epidemiol Biomarkers Prev – volume: 318 start-page: 1108 year: 2007 end-page: 1113 article-title: The genomic landscapes of human breast and colorectal cancers publication-title: Science – volume: 104 start-page: 2292 year: 2005 end-page: 2230 article-title: The molecular genetics of gastroenteropancreatic neuroendocrine tumors publication-title: Cancer – volume: 33 start-page: 322 year: 2002 end-page: 329 article-title: Different patterns of 11q allelic losses in digestive endocrine tumors publication-title: Hum Pathol – volume: 46 start-page: 341 year: 2008 end-page: 347 article-title: Having more healthy practice was associated with low white blood cell counts in middle‐aged Japanese male and female workers publication-title: Ind Health – volume: 53 start-page: 325 year: 1983 end-page: 328 article-title: Familial occurrence in carcinoid tumours publication-title: Aust N Z J Surg – volume: 3 year: 2004 article-title: Linear models and empirical bayes methods for assessing differential expression in microarray experiments publication-title: Stat Appl Genet Mol Biol – year: 2002 – volume: 11 start-page: 3221 year: 2002 end-page: 3229 article-title: A full‐coverage, high‐resolution human chromosome 22 genomic microarray for clinical and research applications publication-title: Hum Mol Genet – start-page: 397 year: 2005 end-page: 420 – volume: 3 start-page: 31 year: 2006 end-page: 33 article-title: Whole‐genome genotyping with the single‐base extension assay publication-title: Nat Methods – volume: 126 start-page: 1390 year: 2010 end-page: 1402 article-title: Focal amplifications are associated with high grade and recurrences in stage Ta bladder carcinoma publication-title: Int J Cancer – volume: 314 start-page: 268 year: 2006 end-page: 274 article-title: The consensus coding sequences of human breast and colorectal cancers publication-title: Science – volume: 57 start-page: 647 year: 1962 end-page: 650 article-title: Metastatic carcinoid, a familial occurrence publication-title: Ann Intern Med – volume: 130 start-page: S1887 issue: Suppl 2 year: 2006 article-title: Gene expression profiles of pancreatic neuroendocrine tumors and gastrointestinal carcinoids publication-title: Gastroenterology – volume: 94 start-page: 444 year: 2001 end-page: 448 article-title: Familial carcinoid tumors and subsequent cancers: A nation‐wide epidemiologic study from Sweden publication-title: Int J Cancer – volume: 90 start-page: 162 year: 2009 end-page: 166 article-title: ENETS consensus guidelines for the standards of care in neuroendocrine tumors: Towards a standardized approach to the diagnosis of gastroenteropancreatic neuroendocrine tumors and their prognostic stratification publication-title: Neuroendocrinology – volume: 47 start-page: 591 year: 2008 end-page: 603 article-title: High‐resolution analysis of genetic alterations in small bowel carcinoid tumors reveals areas of recurrent amplification and loss publication-title: Genes Chromosomes 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| Snippet | Serotonin producing endocrine carcinoma of small intestine (ileal carcinoid) is a clinically distinct endocrine tumor. It is generally considered as a sporadic... |
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| SubjectTerms | Adult Aged Aged, 80 and over Bacterial artificial chromosomes Carcinoid Tumor - genetics Carcinoid Tumor - metabolism Carcinoid Tumor - pathology Carcinoma chromosome 18 chromosome 7 Chromosomes, Human, Pair 14 - genetics Chromosomes, Human, Pair 18 Chromosomes, Human, Pair 7 - genetics copy number Etiology Female Gene expression Gene Expression Profiling Gene Expression Regulation, Neoplastic Growth patterns Heredity Humans Ileal Neoplasms - genetics Ileal Neoplasms - metabolism Ileal Neoplasms - pathology Male MEDICIN MEDICINE Metastases Middle Aged Mutation Neoplasm Metastasis - genetics Pedigree Prognosis Sequence Analysis Serotonin Single-nucleotide polymorphism Small intestine Telomeres Tumor suppressor genes Tumors Young Adult |
| Title | Common pathogenetic mechanism involving human chromosome 18 in familial and sporadic ileal carcinoid tumors |
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