Comparative genomic hybridization detects novel amplifications in fibroadenomas of the breast

Ojopi, Elida P.B.; Rogatto, Sílvia Regina; Caldeira, José Roberto Fígaro; Barbieri‐Neto, José; Squire, Jeremy A.

doi:10.1002/1098-2264(2000)9999:9999<::aid-gcc1057>3.0.co;2-d

Cited by 29 publications

(20 citation statements)

References 39 publications

(47 reference statements)

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“…Loeb et al (1974) suggested that multiple mutations found in tumor cells result from mutations in genes that ensure DNA synthesis fidelity or its repair (Ojopi and Neto, 2002).…”

Section: Discussionmentioning

confidence: 76%

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Antigenotoxic and antimutagenic effects of glutamine supplementation on mice treated with cisplatin

Pesarini¹,

Sg²,

Ap³

et al. 2014

Genet. Mol. Res.

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ABSTRACT. We evaluated the effects of glutamine on clastogenic and genotoxic damage prevention caused by the administration of cisplatin. 4821©FUNPEC-RP www.funpecrp.com.br Genetics and Molecular Research 13 (3): 4820-4830 (2014) Glutamine prevents DNA damage Forty Swiss mice were divided into 8 experimental groups: G1 and G2, which were control groups; G3, G4, and G5, which were administered [2 doses of glutamine (orally)] separated by a 24-h period (150, 300, and 600 mg/kg, respectively), and a dose of phosphate-buffered saline by intraperitoneal injection; G6, G7, and G8, which were treated in the same manner as the previous groups, but received cisplatin rather than phosphate-buffered saline. The antimutagenicity groups showed damage reduction percentages of 79.05, 80.00, and 94.27% at the time point T1, 53.18, 67.05, and 64.74 at time point T2 for the 150, 300, and 600 mg/kg doses of glutamine, respectively. Antigenotoxic activity was evident for all 3 doses with damage reduction percentages of 115.05, 119.06, and 114.38 for the doses of glutamine of 150, 300, and 600 mg/ kg, respectively. These results suggest that further studies are needed to confirm the clastogenic activity of glutamine. However, our results may lead to rational strategies for supplementation of this antioxidant as an adjuvant in cancer treatment or for preventing genomic lesions.

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“…Loeb et al (1974) suggested that multiple mutations found in tumor cells result from mutations in genes that ensure DNA synthesis fidelity or its repair (Ojopi and Neto, 2002).…”

Section: Discussionmentioning

confidence: 76%

“…These changes consist of the activation of oncogenes and the inactivation of tumor suppressor genes, and it appears that both changes are necessary to cause a neoplastic phenotype (Ojopi and Neto, 2002).…”

Section: Discussionmentioning

confidence: 99%

Antigenotoxic and antimutagenic effects of glutamine supplementation on mice treated with cisplatin

Pesarini¹,

Sg²,

Ap³

et al. 2014

Genet. Mol. Res.

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“…Other sarcomas, in addition to rhabdomyosarcomas, display amplification of 13q31-32, including poor prognosis liposarcomas (7) and other tumor types described with amplification of this region include lymphomas (8), lung carcinomas (9), breast cancers (10), and neurologic tumors (11).…”

Section: Introductionmentioning

confidence: 99%

Role for Amplification and Expression of Glypican-5 in Rhabdomyosarcoma

et al. 2007

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Overexpression of genes, through genomic amplification and other mechanisms, can critically affect the behavior of tumor cells. Genomic amplification of the 13q31-32 region is reported in many tumors, including rhabdomyosarcomas that are primarily pediatric sarcomas resembling developing skeletal muscle. The minimum overlapping region of amplification at 13q31-32 in rhabdomyosarcomas was defined as containing two genes: Glypican-5 (GPC5) encoding a cell surface proteoglycan and C13orf25 encompassing the miR-17-92 micro-RNA cluster. Genomic copy number and gene expression analyses of rhabdomyosarcomas indicated that GPC5 was the only gene consistently expressed and up-regulated in all cases with amplification. Constitutive overexpression and knockdown of GPC5 expression in rhabdomyosarcoma cell lines increased and decreased cell proliferation, respectively. A correlation between expression levels of nascent pre-rRNA and GPC5 (P = 0.001), but not a C13orf25 transcript containing miR-17-92, in primary samples supports an association of GPC5 with proliferative capacity in vivo. We show that GPC5 increases proliferation through potentiating the action of the growth factors fibroblast growth factor 2 (FGF2), hepatocyte growth factor (HGF), and Wnt1A. GPC5 enhanced the intracellular signaling of FGF2 and HGF and altered the cellular distribution of FGF2. The mesoderm-inducing effect of FGF2 and FGF4 in Xenopus blastocysts was also enhanced. Our data are consistent with a role of GPC5, in the context of sarcomagenesis, in enhancing FGF signaling that leads to mesodermal cell proliferation without induction of myogenic differentiation. Furthermore, the properties of GPC5 make it an attractive target for therapeutic intervention in rhabdomyosarcomas and other tumors that amplify and/or overexpress the gene. [Cancer Res 2007;67(1):57-65]

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“…Gene amplification was defined as gain ratios ≥ 1.5. The following regions were excluded from analysis: centromeres, acrocentric p-arms, telomeres, and heterochromatin-rich areas (Kallioniemi et al, 1994;Ojopi et al, 2001). In addition, "reverse labeling" by exchanging biotin and digoxigenin labeling of tumor and normal DNA was used.…”

Section: Comparative Genomic Hybridization (Cgh)mentioning

confidence: 98%

“…Prior to hybridization, the slides were treated with 0.1 µg/mL proteinase K in 20 mM Tris pH7.5, 2mM CaCl 2 . CGH was performed according to a standard protocol (Kallioniemi et al, 1992) with some previously described modifications (Ojopi et al, 2001), using a QuipXL Genetics Workstation (Vysis, Downers Grove, IL, USA). The cut-off values for the fluorescence intensity ratio were set at 1.20 and 0.80, with a 95% confidence limit.…”

Section: Comparative Genomic Hybridization (Cgh)mentioning

confidence: 99%

Chromosomal imbalances detected in primary bone tumors by comparative genomic hybridization and interphase fluorescence in situ hybridization

Baruffi¹,

Engel²,

Squire

et al. 2003

Genet. Mol. Biol.

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We applied a combination of comparative genomic hybridization (CGH) and fluorescence in situ hybridization (FISH), to characterize the genetic aberrations in three osteosarcomas (OS) and one Ewing's sarcoma. CGH identified recurrent chromosomal losses at 10p14-pter and gains at 8q22.3-24.1 in OS. Interphase FISH allowed to confirm 8q gain in two cases. A high amplification level of 11q12-qter was detected in one OS. The Ewing's sarcoma showed gain at 1p32-36.1 as the sole chromosome alteration. These studies demonstrate the value of molecular cytogenetic methods in the characterization of recurrent genomic alterations in bone tumor tissue.

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Comparative genomic hybridization detects novel amplifications in fibroadenomas of the breast

Cited by 29 publications

References 39 publications

Antigenotoxic and antimutagenic effects of glutamine supplementation on mice treated with cisplatin

Antigenotoxic and antimutagenic effects of glutamine supplementation on mice treated with cisplatin

Role for Amplification and Expression of Glypican-5 in Rhabdomyosarcoma

Chromosomal imbalances detected in primary bone tumors by comparative genomic hybridization and interphase fluorescence in situ hybridization

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