The human CAS (cellular apoptosis susceptibility) gene mapping on chromosome 20q13 is amplified in BT474 breast cancer cells and part of aberrant chromosomes in breast and colon cancer cell lines.

Brinkmann, Ulrich; Gallo, Maria; Polymeropoulos, M H; Pastan, Ira

doi:10.1101/gr.6.3.187

Cited by 93 publications

(60 citation statements)

References 14 publications

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“…The CROC1/UEV1-1 gene is located on chromosome 20q13.2 (Sancho et al, 1998), a region frequently ampli®ed in many types of human cancer . Others have reported that SW480 cells contain aberrant chromosomes harboring large portions of 20q (Brinkmann et al, 1996), a ®nding that may account, at least in part, for the high level of CIR1/CROC1 mRNA present in this cell line.…”

Section: Expression Of Cir1/croc1 In Human Tissues and Tumor-derived mentioning

confidence: 83%

Up-regulation of CIR1/CROC1 expression upon cell immortalization and in tumor-derived human cell lines

Broomfield

Lavery

et al. 1998

Oncogene

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Acquisition of the immortal phenotype by tumor cells represents an essential and potentially rate-limiting step in tumorigenesis. To identify changes in gene expression that are associated with the early stages of cell immortalization, we compared genetically matched pairs of pre-immortal and immortal human cell clones by mRNA di erential display. Two transcripts, denoted CIR1 and CIR2, were identi®ed which were up-regulated in immortal cells. Sequence analysis revealed CIR1 to be identical to the recently cloned CROC1/UEV-1 gene, whereas CIR2 corresponds to an as yet uncharacterized 1.2 kb mRNA. A 5 ± 6-fold elevation in CIR1/CROC1 expression and a 2 ± 3-fold elevation in CIR2 expression were observed in SV40-transformed human enbryonic kidney cells immediately following proliferative crisis, suggesting a potential role for these genes in immortalization. Expression of CIR1/CROC1 was found to be elevated also in a variety of immortal human tumorderived cell lines, as compared to their normal tissue counterparts. These results are compatible with induction of CIR1/CROC1 being an early event in the acquisition of immortality and with a role for this gene in the immortal phenotype of tumor cells.

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Section: Expression Of Cir1/croc1 In Human Tissues and Tumor-derived mentioning

confidence: 83%

Up-regulation of CIR1/CROC1 expression upon cell immortalization and in tumor-derived human cell lines

Broomfield

Lavery

et al. 1998

Oncogene

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“…A similar frequency (85%) of chromosome arm 20q gains in metastases was observed previously. 12 Four different genes, the cellular apoptosis susceptibility gene (CAS), 37 the steroid receptor coactivator gene (AIB1), 38 a putative serine/threonine kinase gene (BTAK/Aurora2) 39 -41 and DcR3, 42 were identified within this amplicon. In addition, a novel zinc finger gene mapped on 20q13.2 was amplified in human breast cancer.…”

Section: Discussionmentioning

confidence: 99%

Chromosomal aberrations in colorectal cancers and liver metastases analyzed by comparative genomic hybridization

et al. 2001

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Comparative genomic hybridization (CGH) was used to screen for changes in the number of DNA sequence copies in 30 primary colorectal cancers and 16 liver metastases, to identify regions that contain genes important for the development and progression of colorectal cancer. In primary colorectal cancer, we found frequent gains at 7p21 (36.7%), 7q31-36 (30%), 8q23-24 (43.0%), 12p (30%) Many detailed reports have been published on the carcinogenesis of colorectal cancer. Several genetic aberrations are required for tumor initiation and progression. 1 These aberrations include activation of the SRC and RAS oncogenes 2,3 along with inactivation of the FAP 4,5 and DCC 6 tumor suppressors and loss of TP53 function. 7 However, genetic changes involved in the progression and metastases of colorectal cancer remain unclear. To investigate differences in chromosomal aberrations between primary colorectal cancer and metastatic liver tumor, we used comparative genomic hybridization (CGH). CGH is based on dual-color fluorescence in situ hybridization (FISH) using differentially labeled tumors and reference DNA as a probe. 8,9 The efficacy of CGH is based on the concept that regions with an increase in the number of copies reveal sites that may contain dominantly acting oncogenes, whereas regions with a reduction may harbor putative tumorsuppressor genes. 8 Our aim was to generate a comprehensive picture of genomic and chromosomal aberrations that occur during the development of metastases of colorectal cancers and to identify those chromosomal regions that contain genes important for the development and progression of colorectal cancer.,Colorectal adenoma and adenocarcinoma have previously been analyzed by CGH, 10 as have primary and metastatic liver tumors. 11,12 These results supported ours; above all, we emphasize that some important genes appear to be contained in 20q and to play an important role in liver metastases. Furthermore, we examined the follow-up surveys of all cases and compared cases with and without loss at 18q and with gains at 8q and 20q to determine the usefulness of these genetic alterations as prognostic markers. MATERIAL AND METHODS Samples and DNA preparationPrimary tumors and metastatic liver tumors from 44 cancer patients with colorectal cancer (Table I) were classified according to the UICC system. These samples were provided by the Department of Digestive Surgery, Kyoto Prefectural University of Medicine (Kyoto, Japan). After surgical resection, tissues were frozen and stored at -80°C and DNA was extracted. CGHCGH was performed as described previously. 13 In brief, tumor DNA was labeled with FITC-dUTP and controlled DNA and extracted from a normal male with the aid of Texas red-dUTP using nick translation. Metaphase spreads were denatured at 75°C for 2.1 min in a formamide solution [70% formamide, 2 ϫ SCC (pH 7.0)] and dehydrated in an ethanol series of 70%, 85% and 100%. Labeled tumor and normal DNAs together with 10 g unlabeled cot-1 DNA was mixed with 50% formamide, 10% dextran sulfate and 2 ϫ SSC...

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“…40 However gains of 20q have been observed in solid tumors such as colorectal carcinoma, 41,42 breast, 43 bladder, 44 ovarian, 45 and pancreatic cancer. 46 Several candidate genes have been identified on 20q: the cellular apoptosis susceptibility (CAS) gene; 47 BTAK, a putative serine/threonine kinase gene; 48 AIB1, a steroid receptor co-activator gene; 49 PTPN1, a nonreceptor tyrosine phosphatase involved in growth regulation; 50 as well as MYB12, which encodes a transcription factor and plays an important role in cell cycle progression. 51 Regarding gene amplifications, CGH studies are detecting an increased number of high-level DNA amplifications in lymphomas, which were relatively rare in NHL by cytogenetic studies.…”

Section: Discussionmentioning

confidence: 99%

Novel Genomic Imbalances in B-Cell Splenic Marginal Zone Lymphomas Revealed by Comparative Genomic Hybridization and Cytogenetics

Hernández

Garcı́a

Gutiérrez

et al. 2001

The American Journal of Pathology

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Splenic marginal zone lymphoma (SMZL) has recently been recognized in the World Health Organization classification of hematological diseases as distinct type of non-Hodgkin's lymphoma. In contrast to the well-established chromosomal changes associated with other B-cell non-Hodgkin's lymphoma, few genetic alterations have been found associated with SMZL. The aim of our study was to analyze by comparative genomic hybridization (CGH) the chromosomal imbalances in 29 patients with SMZL and to correlate these findings with clinical and biological characteristics and patient outcome. In 21 cases, cytogenetic studies were simultaneously performed. Most of the patients (83%) displayed genomic imbalances. A total of 111 DNA copy number changes were detected with a median of four abnormalities per case (range, 1 to 12). Gains (n ‫؍‬ 92) were more frequent than losses (n ‫؍‬ 16), while three high-level amplifications (3q26-q29, 5p11-p15, and 17q22-q25) were observed. The most frequent gains involved 3q (31%), 5q (28%), 12q and 20q (24% each), 9q (21%), and 4q (17%). Losses were observed in 7q (14%) and 17p (10%). SMZL patients with genetic losses had a shorter survival than the remaining SMZL patients (P < 0.05). Splenic marginal zone lymphoma (SMZL) has been considered a subtype of B-cell non-Hodgkin's lymphoma (NHL) in the recent classification of hematological diseases.1 SMZL has been recognized as a separate entity on the basis of its morphological, phenotypic, and clinical characteristics.2 Several studies have been performed to assess the genetic abnormalities in marginal lymphomas. Recently, two translocations, t(1;14)(p22;q32) involving BCL10/IgH 3 and t(11;18)(q21;q21) -API2/MLT-4 have been described, associated with high-grade and lowgrade MALT lymphomas, respectively. However, genetic information of SMZL is scanty. Cytogenetic analyses have shown involvement of chromosomes 1, 3, 7, and 8. 5,6 Fluorescence in situ hybridization studies on interphase nuclei have demonstrated the presence of trisomy 3 in a proportion of cases ranging from 18 to 47% of SMZL. 6 -9 In previous studies we have reported that in some SMZL cases, the only cytogenetic abnormality displayed was del(7q) that could suggest that del(7q) is associated with SMZL. 6,10 Recently, loss of heterozygosity studies demonstrated that the frequency of allelic loss in SMZL (40%) is higher than that observed in other B-cell lymphoproliferative syndromes. The most frequently deleted microsatellite was D7S487.11 These results are in accordance with our fluorescence in situ hybridization studies that mapped the commonly deleted region in chronic B-cell lymphoproliferative disorders at 7q31.3.

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The human CAS (cellular apoptosis susceptibility) gene mapping on chromosome 20q13 is amplified in BT474 breast cancer cells and part of aberrant chromosomes in breast and colon cancer cell lines.

Cited by 93 publications

References 14 publications

Up-regulation of CIR1/CROC1 expression upon cell immortalization and in tumor-derived human cell lines

Up-regulation of CIR1/CROC1 expression upon cell immortalization and in tumor-derived human cell lines

Chromosomal aberrations in colorectal cancers and liver metastases analyzed by comparative genomic hybridization

Novel Genomic Imbalances in B-Cell Splenic Marginal Zone Lymphomas Revealed by Comparative Genomic Hybridization and Cytogenetics

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