Interphase Cytogenetics of Gastric and Esophageal Adenocarcinomas

Rao, Pulivarthi H.; Mathew, Susan; Lauwers, Gregory Y.; Rodriguez, Eduardo D.; Kelsen, David P.; Chaganti, R. S. K.

doi:10.1097/00019606-199303000-00035

Cited by 9 publications

(15 citation statements)

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“…The prevalence of the ploidy level of chromosome 17 agreed with the studies of Rao et al (1993) and Van Dekken et al (1990), who examined 6 and 10 gastric carcinomas, respectively, by means of FISH. They found quite frequent trisomy and tetrasomy, although they did not compare these results with the histological type.…”

Section: Discussionsupporting

confidence: 83%

Numerical aberration and point mutation ofp53 gene in human gastric intestinal metaplasia and well-differentiated adenocarcinoma: Analysis by fluorescencein situ hybridization (FISH) and PCR-SSCP

et al. 1996

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Section: Discussionsupporting

confidence: 83%

Numerical aberration and point mutation ofp53 gene in human gastric intestinal metaplasia and well-differentiated adenocarcinoma: Analysis by fluorescencein situ hybridization (FISH) and PCR-SSCP

et al. 1996

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“…En este estudio se encontró una alta frecuencia (63%) de aneuploidías del cromosoma 17 en los diversos tumores sólidos, lo que concuerda con lo publicado en otros trabajos similares realizados con FISH (11,(15)(16)(17)(18). Sin embargo, debe mencionarse que los estudios muestran una amplia escala de porcentajes de aneuploidías para el cromosoma 17 (entre 10% y 80%).…”

Section: Discussionunclassified

“…Sin embargo, es similar al encontrado por Risio et al De esta manera, en la literatura se describen dos patrones de alteraciones cromosómicas (uno monosómico y otro trisómico) en tumores gastrointestinales. Estos trabajos también correlacionan la pérdida del cromosoma 17 con tumores malignos, similar a lo observado en los carcinomas de colon (15,16,26).…”

Section: Discussionunclassified

Detección de aneuploidías del cromosoma 17 y deleción del gen TP53 en una amplia variedad de tumores sólidos mediante hibridación in situ fluorescente bicolor

et al. 2010

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Detección de aneuploidías del cromosoma 17 y deleción del genTP53 en una amplia variedad de tumores sólidos mediante hibridación in situ fluorescente bicolor Introducción. El TP53 es un gen supresor de tumores localizado en la región cromosómica 17p13.1; controla el ciclo celular y se encuentra alterado en cerca de 50% de todas las neoplasias. Objetivos. Determinar las aneuploidías del cromosoma 17 y la deleción en el locus 17p13.1 del gen TP53, en diversos tumores sólidos primarios utilizando la técnica FISH-bicolor. Materiales y métodos. Se analizaron 38 muestras de diversos tipos de tumores sólidos primarios. Todas las muestras se disociaron mecánica y enzimáticamente con colagenasa al 0,2%, antes de la obtención de los núcleos interfásicos. La técnica de FISH-bicolor se realizó en núcleos interfásicos, mediante sondas marcadas directamente con fluorocromos para el centrómero del cromosoma 17 (CEP 17; señal verde; VYSIS) y para el locus específico del gen TP53 (LSI 17p13.1; señal naranja; VYSIS). Resultados. Se encontró que 63% (24/38) de las muestras tenían aneuploidías del cromosoma 17. La monosomía fue la aneuploidía más frecuente (75%; 18/24), seguida de la trisomía (17%; 4/24); la nulisomía y la tetrasomía fueron menos frecuentes. El 89,5% (34/38) de los casos presentaron deleción del gen TP53. Sólo cuatro casos fueron normales para el número de copias del cromosoma 17 y del gen TP53. El estudio histopatológico mostró que la mayoría de las muestras eran tumores malignos. Conclusiones. La aneuploidía del cromosoma 17 y la deleción en el locus 17p13.1 del gen TP53 son alteraciones muy frecuentes en los tumores sólidos. La técnica FISH-bicolor permite detectar simultáneamente alteraciones cromosómicas numéricas y estructurales en núcleos interfásicos.Palabras clave: aneuploidía, deleción cromosómica, gen Tp53, hibridación fluorescente in situ, neoplasias, inestabilidad cromosómica, heterogeneidad genética. Detection of chromosome 17 aneuplody and TP53 gene deletion in a broad variety of solid tumors by dual-color fluorescence in situ hybridization (FISH)Introduction. TP53 is a tumor suppressor gene located on chromosome 17p13.1. This gene is essential for the control of cell cycle and has been found altered in about 50% of all tumor types. Objective. The presence of aneuploidy of chromosome 17 and TP53 gene deletion at 17p13.1 locus was determined in primary solid tumors using the dual-color FISH (fluorescence in situ hybridization). Materials and methods. Thirty-eight samples consisted of several types of primary solid tumors. All samples were mechanically and enzymatically disaggregated with 0.2% collagenase prior to obtaining interphase nuclei. The dual-color FISH was performed using direct fluorescent labeling probes for the chromosome 17 centromere (green signal) and for the TP53 gene locus-specific (orange signal).Results. Characteristic aneuploidy on chromosome 17 was found in 63% (24/38) of the samples. Monosomy occurred most frequently (75%, 18/24), followed by trisomy (17%, 4/24); nullisomy and te...

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“…In endometrial cases, deletion of chromosome 3, the most frequent structural alteration observed, was found in 13 cells of cases E5, E6 and E9, while no deletion of chromosome 3 was found in ovarian cancers. Deletions generally cause the loss of tumor suppressor genes [15][16][17][18][19]. Molecular studies have shown loss of heterozygosity (LOH) on 3p, which seems to be a common event in endo metrial tumors and related to LOH in the FHIT (fragile histidine triad) and the hMLH1 locus [13].…”

Section: Discussionmentioning

confidence: 99%

“…In another study [14], various deletions (3p13, 21, 22, 26) of chromosome 3p were associated with the development of uterine cervical carcinoma in Indian patients. Del(3)(q13q23) was the most consistent aberration observed in six of nine gastric and esophageal adenocarcinomas [15]. Through positional cloning of the 3q21 breakpoint, a novel gene, DIRC2, reported to encode a multi membrane-spanning protein that represents a new member of the major facilitator superfamily (MFS) of transporters, and these fragilities associated with sporadic and familial renal cell carcinomas [16].…”

Section: Discussionmentioning

confidence: 99%

Chromosomal Abnormalities in Endometrial and Ovarian Carcinomas

Pazarbaşı

Kasap

Demırhan

et al. 2007

Balkan Journal of Medical Genetics

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Development and progression of human malignancies involve multiple genetic changes including chromosomal instabilities such as translocations, deletions, and inversions. Chromosomal abnormalities were observed in 23 cases with ovarian and endometrial cancer by cytogenetic studies using a GTG (G bands by trypsin using Giemsa) banding technique. Specific chromosome bands were frequently involved, and were most frequent on chromosomes 1, 2, 3, 5, 12 and 17. Clonal alterations were observed at the cancer breakpoints, such as 1q21, 1q32, 3p21, 7q22, 11q23 in ovarian and 1p36, 1q32, 2p12, 3p21, 7q22, 9q34, 11p15, 11q23, 12q13, 14q11, 14q32, 16p13, 21q22 in endometrial cases. These findings provide evidence that multiple genetic lesions are associated with the patho genesis of endometrial and ovarian cancer.

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Interphase Cytogenetics of Gastric and Esophageal Adenocarcinomas

Cited by 9 publications

References 0 publications

Numerical aberration and point mutation ofp53 gene in human gastric intestinal metaplasia and well-differentiated adenocarcinoma: Analysis by fluorescencein situ hybridization (FISH) and PCR-SSCP

Numerical aberration and point mutation ofp53 gene in human gastric intestinal metaplasia and well-differentiated adenocarcinoma: Analysis by fluorescencein situ hybridization (FISH) and PCR-SSCP

Detección de aneuploidías del cromosoma 17 y deleción del gen TP53 en una amplia variedad de tumores sólidos mediante hibridación in situ fluorescente bicolor

Chromosomal Abnormalities in Endometrial and Ovarian Carcinomas

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