Coexisting Amplifications of the Chromosome 1p32 Genes (PTPRF and MYCL1) Encoding Protein Tyrosine Phosphatase LAR and L-myc in a Small Cell Lung Cancer Line

Harder, Kenneth W.; Saw, Jacqueline; Miki, N.; Jirik, Frank R.

doi:10.1006/geno.1995.1092

Cited by 12 publications

(7 citation statements)

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“…PPFIBP1 has been proposed to participate in the recruitment and anchoring of LAR (leukocyte antigen-related) family of protein-tyrosine phosphatases (PTPases) at focal adhesions, which are sites of cell-cell contact and of interactions between cells and extracellular matrix (Serra-Pagè s et al, 1998). The gene coding for LAR has previously been found to be coamplified with the MYCL1 gene in a small cell lung cancer line (Harder et al, 1995). Thus, the present study showed four genes/ESTs, in addition to KRAS2, that showed increased expression in the cell lines with amplifications in 12p11-12.…”

Section: Discussionmentioning

confidence: 60%

Detailed genomic mapping and expression analyses of 12p amplifications in pancreatic carcinomas reveal a 3.5‐Mb target region for amplification

Heidenblad

Jonson

Mahlamäki

et al. 2002

Genes Chromosomes & Cancer

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Previous cytogenetic and comparative genomic hybridization (CGH) analyses have shown that the gain of chromosome arm 12p is frequent in pancreatic carcinomas. We investigated 15 pancreatic carcinoma cell lines using CGH, fluorescence in situ hybridization (FISH), and semiquantitative polymerase chain reaction (PCR) to characterize 12p amplifications in detail. The CGH analysis revealed gains of 12p in four of the cell lines and local amplification within 12p11-12 in six cell lines. By FISH analysis, using precisely mapped YAC clones, the commonly amplified region was found to be approximately 5 Mb. The amplified segment extended from YAC 753f12, covering the KRAS2 locus, to YAC 891f1, close to the centromere. A semiquantitative PCR methodology was used to estimate genomic copy numbers of 14 precisely mapped expressed sequence tags (ESTs) and sequence-tagged sites, located within this interval. The level of amplification ranged from two- to 12-fold. The produced gene copy profiles revealed a 3.5-Mb segment with various local amplifications. This region includes KRAS2 and ranges from D12S1617 to sts-N38796. Two of the cell lines (primary and metastatic tumor from the same patient) showed amplification peaks within the distal region of this segment, two had peaks within the proximal region, one showed subpeaks in both regions, and one displayed amplification of the entire region. Chromosome segment-specific cDNA array analysis of 29 expressed sequences within the whole interval between D12S1617 and sts-N38796 indicated overexpression of four ESTs, two corresponding to DEC2 and PPFIBP1, and two to ESTs with unknown function. Expression analysis of these and of KRAS2 showed specific overexpression in the six cell lines with local 12p amplifications. These findings indicate two target regions within the 3.5-Mb segment in 12p11-12, one proximal including PPFIBP1, and one distal including KRAS2.

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Section: Discussionmentioning

confidence: 60%

Detailed genomic mapping and expression analyses of 12p amplifications in pancreatic carcinomas reveal a 3.5‐Mb target region for amplification

Heidenblad

Jonson

Mahlamäki

et al. 2002

Genes Chromosomes & Cancer

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“…For example, PTPRF encoded proteins which are known to be signaling molecules that regulate a variety of cellular processes including cell growth, differentiation, mitotic cycle, and oncogenic transformation. The PTPRF gene also plays important roles in colorectal cancers [ 31 ] and kidney carcinomas [ 32 ]. Therefore, it is reasonable for us to conclude that our predicted MRM modules are really related to human cancers.…”

Section: Resultsmentioning

confidence: 99%

Finding microRNA regulatory modules in human genome using rule induction

Tran

Satou

2008

BMC Bioinformatics

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Background: MicroRNAs (miRNAs) are a class of small non-coding RNA molecules (20-24 nt), which are believed to participate in repression of gene expression. They play important roles in several biological processes (e.g. cell death and cell growth). Both experimental and computational approaches have been used to determine the function of miRNAs in cellular processes. Most efforts have concentrated on identification of miRNAs and their target genes. However, understanding the regulatory mechanism of miRNAs in the gene regulatory network is also essential to the discovery of functions of miRNAs in complex cellular systems. To understand the regulatory mechanism of miRNAs in complex cellular systems, we need to identify the functional modules involved in complex interactions between miRNAs and their target genes.

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“…Previous CGH studies have shown that gains of 1p, 7/7p, 12/12q, 13/13q, and 20 are commonly seen in nodal and other types of extranodal NHLs (Bentz et al, 1996; Knuutila et al, 2000), suggesting that these genetic events may be associated with NHL, including PCBCL. On the other hand, amplifications of MYCL1, SAS, CDK4, CCND2, GLI, AIB1, STK15, CSE1L, and ZNF217 have been observed in a wide range of tumors including lung, breast, ovarian and liver cancers, gliomas, and nodal B‐cell NHLs (Collins, 1995; Harder et al, 1995; Bentz et al, 1996; Reifenberger et al, 1996; Anzick et al, 1997, Barth et al, 1998; Rao et al, 1998; Zhou et al, 1998; Mao and Hamoudi, 2000; Collins et al, 2001). It is likely that the disruptions of the signal transduction and regulation networks formed by these oncogenes and their products are important in the pathogenesis of these malignant diseases including PCBCL.…”

Section: Discussionmentioning

confidence: 99%

Comparative genomic hybridization analysis of primary cutaneous B‐cell lymphomas: Identification of common genomic alterations in disease pathogenesis

Mao

Lillington

Child

et al. 2002

Genes Chromosomes & Cancer

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To investigate genetic alterations in primary cutaneous B-cell lymphomas (PCBCLs), we have analyzed 29 cases of PCBCL. Comparative genomic hybridization showed chromosome imbalances (CIs) in 12 cases (41%). The mean number of CIs per sample was 2.05 +/- 2.97, with gains (1.48 +/- 2.38) more frequent than losses (0.56 +/- 1.40). The common regions of gains were 18/18q (50%), 7/7p (42%), 3/3q (33%), 20 (33%), 1p (25%), 12/12q (25%), and 13/13q (25%), whereas loss of 6q was frequent (42%). Among the different subsets of PCBCLs, CI was seen in 50% of diffuse large-cell lymphomas (DLCLs), 33% of marginal zone lymphomas, and 8% of follicle center cell lymphomas and unclassified lymphomas. A similar pattern of CI was observed in these lymphomas, but loss of 6q and gains of 3/3q were present only in DLCLs. Microarray-based genomic analysis of four DLCL cases identified oncogene gains of SAS/CDK4 (12q13.3) in three cases and MYCL1 (1p34.3), MYC (8q24), FGFR2 (10q26), BCL2 (18q21.3), CSE1L (20q13), and PDGFB (22q12-13) in two cases, whereas losses of AKT1 (14q32.3), IGFR1 (15q25-26), and JUNB (19p13.2) were identified in three cases, and losses of FGR (1p36), ESR (6q25.1), ABL1 (9q34.1), TOP2A (17q21-22), ERBB2 (17q21.2), CCNE1 (19q13.1), and BCR (22q11) were each identified in two cases. In addition, real-time-polymerase chain reaction detected amplification of BCL2 in 5 of 29 cases. These findings suggest that there are complex but consistent genetic alterations associated with the pathogenesis of PCBCLs.

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Coexisting Amplifications of the Chromosome 1p32 Genes (PTPRF and MYCL1) Encoding Protein Tyrosine Phosphatase LAR and L-myc in a Small Cell Lung Cancer Line

Cited by 12 publications

References 0 publications

Detailed genomic mapping and expression analyses of 12p amplifications in pancreatic carcinomas reveal a 3.5‐Mb target region for amplification

Detailed genomic mapping and expression analyses of 12p amplifications in pancreatic carcinomas reveal a 3.5‐Mb target region for amplification

Finding microRNA regulatory modules in human genome using rule induction

Comparative genomic hybridization analysis of primary cutaneous B‐cell lymphomas: Identification of common genomic alterations in disease pathogenesis

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