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633 results on '"Lidereau R"'

131. Ceramide galactosyltransferase (UGT8) is a molecular marker of breast cancer malignancy and lung metastases.

Author

Dzie¸giel, P., Owczarek, T., Plaz`uk, E., Gomułkiewicz, A., Majchrzak, M., Podhorska-Około´w, M., Driouch, K., Lidereau, R., Ugorski, M., Dzięgiel, P, Plazuk, E, Gomułkiewicz, A, and Podhorska-Okołów, M

Subjects
CERAMIDES, GALACTOSYLTRANSFERASES, BREAST cancer, METASTASIS, CELL lines, CANCER prognosis
Abstract

Background: It was shown recently on the level of gene expression that UGT8, coding UDP-galactose:ceramide galactosyltransferase, is one of six genes whose elevated expression correlated with a significantly increased the risk of lung metastases in breast cancer patients. In this study primary tumours and their lung metastases as well as breast cancer cell lines were analysed for UGT8 expression at the protein level.Methods: Expression of UGT8 in breast cancer tissue specimens and breast cancer cell lines was analysed using IHC, real-time PCR and Western blotting.Results: Comparison of the average values of the reaction intensities (IRS scale) showed a significant difference in UGT8 expression between (1) primary and metastatic tumours (Mann-Whitney U, P<0.05), (2) tumours of malignancy grades G3 and G2 (Mann-Whitney U, P<0.01) as well as G3 and G1 (Mann-Whitney U, P<0.001) and (3) node-positive and node-negative tumours (Mann-Whitney U, P<0.001). The predictive ability of increased expression of UGT8 was validated at the mRNA level in three independent cohorts of breast cancer patients (721). Similarly, breast cancer cell lines with the 'luminal epithelial-like' phenotype did not express or weakly expressed UGT8, in contrast to malignant, 'mesenchymal-like,' cells forming metastases in nude mice.Conclusion: Our data suggest that UGT8 is a significant index of tumour aggressiveness and a potential marker for the prognostic evaluation of lung metastases in breast cancer. [ABSTRACT FROM AUTHOR]

Published
2010
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136. Short Report Real-time PCR-based gene dosage assay for detecting BRCA1 rearrangements in breast–ovarian cancer families.

Author

Barrois, M., Bièche, I., Mazoyer, S., Champèm, M. H., Bressac-de Paillerets, B., and Lidereau, R.

Subjects
BREAST cancer, GENETIC disorders, GENETIC mutation, DIAGNOSTIC use of polymerase chain reaction, DNA, FRENCH people
Abstract

Barrois M, Bièche I, Mazoyer S, Champème M-H, Bressac-de Pailleret B, Lidereau R. Real-time PCR-based gene dosage assay for detecting BRCA1 rearrangements in breast–ovarian cancer families. BRCA1 and BRCA2 germline mutations, mainly point mutations and other small alterations, are responsible for most hereditary cases of breast–ovarian cancer. However, the observed frequency of BRCA1 alterations is lower than that predicted by linkage analysis. Several large BRCA1 rearrangements have been identified with a variety of technical approaches in some families. We have developed a gene dosage assay based on real-time quantitative PCR and used it to extensively analyze 91 French families of breast–ovarian cancer in which no BRCA1 or BRCA2 point mutations was identified. This gene dosage method calculates the copy number of each BRCA1 exon to readily detect one, two, and three or more copies of BRCA1 target exons. In the series of 91 families at high risk of carrying BRCA1 mutations, we detected seven large rearrangements of the BRCA1 gene by using this real-time PCR approach. This simple, rapid, and semiautomated real-time quantitative polymerase chain reaction (PCR) assay is a promising alternative technique to Southern blot, bar code analysis on combed DNA, quantitative multiplex PCR of short fluorescent fragments, and cDNA length analysis for the detection of large rearrangements. Therefore, this technique should be considered as a powerful diagnostic method for breast/ovarian cancer susceptibility in clinical and research genetic surveys. [ABSTRACT FROM AUTHOR]

Published
2004
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139. Quantitation of androgen receptor gene expression in sporadic breast tumors by real-time RT-PCR: evidence that MYC is an AR-regulated gene.

Author

Bièche, I, Parfait, B, Tozlu, S, Lidereau, R, and Vidaud, M

Abstract

Little is known of the function and clinical significance of the androgen receptor (AR) in human breast cancer. Paradoxically, synthetic progestins, such as medroxyprogesterone acetate, are used for second line hormone therapy of breast cancer following tamoxifen failure. A sensitive and accurate assay for AR expression in breast tumors is thus required. Here we have developed and validated a real-time RT-PCR assay to quantify AR gene expression at the mRNA level in a series of 131 patients with unilateral invasive primary breast tumors. AR expression varied widely in tumor tissues (by at least 3 orders of magnitude), being underexpressed in 24/131 (18.3%) and overexpressed in 45/131 (34.4%) relative to normal breast tissues. We observed links (or trends) between AR status and age, menopausal status, Scarff-Bloom-Richardson histopathological grade, lymph node status and estrogen receptor alpha and progesterone receptor status. High AR mRNA levels were negatively linked to MYC gene overexpression (P = 8 x 10(-6)), confirming previous in vitro studies. Our results also suggest a role of the ARA70 gene (which encodes a major AR co-activator) in the AR pathway dysregulation observed in breast cancer. This simple, rapid and semi-automated method will be useful for screening cancer patients for altered AR expression and for predicting the response to androgen therapy in AR-related cancer patients.

Published
2001
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141. Gene characterization, promoter analysis, and chromosomal localization of human bleomycin hydrolase.

Author

Ferrando, A A, Pendás, A M, Llano, E, Velasco, G, Lidereau, R, and López-Otín, C

Abstract

The human gene encoding bleomycin hydrolase, a cysteine proteinase involved in chemotherapy resistance, has been cloned, and its overall organization has been established. The gene is composed of 12 coding exons and 11 introns and spans more than 30 kilobases. The number and distribution of exons and introns differ from those reported for other human cysteine proteinases, indicating that these genes are only distantly related. Nucleotide sequence analysis of about 1.2 kilobases of the 5'-flanking region of the human bleomycin hydrolase gene revealed a high GC content, a ratio of CpG/GpC close to unity, and the absence of consensus transcriptional sequences such as TATA box or CCAAT box. All these features are characteristic of housekeeping genes and provide an explanation for the widespread expression of bleomycin hydrolase in human tissues. The 5'-flanking region of the gene also contains a polymorphic CCG trinucleotide repeat that may be a target of genetic instability events and affect its transcriptional activity. Chromosomal localization of the human bleomycin hydrolase gene revealed that it maps to chromosome 17q11.2, very close to the locus of the neurofibromatosis type 1 gene. This location is unique for any cysteine proteinase mapped to date. Finally, Southern blot analysis of DNA from leukocytes and autologous breast tumors has shown that the bleomycin hydrolase gene is not a frequent target of amplification in human breast carcinomas.

Published
1997

142. Genetic alteration of the c-myc protooncogene (MYC) in human primary breast carcinomas.

Author

Escot, C, Theillet, C, Lidereau, R, Spyratos, F, Champeme, M H, Gest, J, and Callahan, R

Abstract

We have studied the genomic organization of the c-myc locus (MYC) from 121 human primary breast carcinomas. Two types of alterations were observed: (i) the c-myc protooncogene appeared to be amplified 2- to 15-fold in 38 (32%) of the carcinoma DNAs and (ii) a non-germ-line c-myc-related fragment of variable size was detected in 5 primary breast carcinoma DNAs. With three exceptions, all the tumors containing a genetic alteration of the c-myc locus were invasive ductal carcinomas. A significant correlation (P less than 0.02) was observed between patients more than 50 years old and the presence of a genetically altered c-myc. Enhanced levels of c-myc RNA were observed in 10 of 14 breast carcinomas examined. The c-myc gene was genetically altered in 6 of these 10 tumors. The frequency with which the c-myc gene is altered and its correlation with age suggest that it may play a role in the development of breast carcinomas.

Published
1986
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146. In situ c-myc expression and genomic status of the c-myc locus in infiltrating ductal carcinomas of the breast

Author

Renato Mariani-Costantini, Escot, C., Theillet, C., Gentile, A., Merlo, G., Lidereau, R., and Callahan, R.

Subjects
Carcinoma, Intraductal, Noninfiltrating, Transcription, Genetic, Cell Cycle, Proto-Oncogenes, Gene Amplification, Chromosome Mapping, Humans, Nucleic Acid Hybridization, Breast Neoplasms, Female
Abstract

We have studied the expression of the c-myc protooncogene and the cycle-dependent histone 4 gene at the cellular level by RNA:RNA in situ hybridization in 18 primary breast ductal adenocarcinomas. These tumors have previously been examined by Southern and Northern blot analysis for the genomic status of c-myc and its expression, respectively (Escot et al., Proc. Natl. Acad. Sci. USA, 83: 4834-4838, 1986). Positive c-myc hybridization signals were associated with carcinoma cells in all cases, including tumors which had no apparent alterations of the c-myc locus. Steady-state levels of c-myc mRNA appeared heterogeneous in carcinomas with similar histology. High levels of hybridization were found in four of seven tumors with strong amplification of the c-myc locus. Similarly high levels of c-myc hybridization were detected in two of nine cases which had an apparently normal c-myc locus but comparatively low cellularity. In addition to carcinoma cells, dense clusters of infiltrating lymphocytes, present in three tumors, exhibited c-myc hybridization. The expression of the histone 4 gene failed to correlate with levels of c-myc expression. We conclude that in infiltrating ductal carcinomas: (a) the c-myc protooncogene is transcriptionally activated; (b) c-myc amplification is probably underestimated due to heterogeneous cellularity; (c) high-level c-myc amplification is related to high-level expression, but other unknown factors also may play a role; (d) differences in levels of c-myc expression may not only be attributed to differences in the growth fractions; and (e) c-myc mRNA in total RNA from biopsy samples may be contributed by infiltrating lymphocytes.

Published
1988

147. Frequent alteration of the DF3 tumor-associated antigen gene in primary human breast carcinomas

Author

Merlo, Giorgio Roberto, Siddiqui, J., Cropp, C., Liscia, D. S., Lidereau, R., Callahan, R., and Kufe, D.

Subjects
Base Sequence, Carcinoma, Molecular Sequence Data, Chromosome Mapping, Nucleic Acid Hybridization, Breast Neoplasms, DNA, DNA, Neoplasm, Clone Cells, Antigens, Neoplasm, Chromosomes, Human, Pair 1, Biomarkers, Tumor, Humans, Amino Acid Sequence
Abstract

The gene for the human DF3 breast carcinoma-associated antigen contains a conserved (G + C)-rich 60-base pair tandem repeat and maps to chromosome 1q21-24. In the present study we isolated and characterized 1220 base pairs of nonrepetitive adjacent sequences. Multiple alleles were identified by fragment size. Signal intensity of hybrids with the tandem and unique sequence probes indicated that allelic variation is due to different numbers of repeats. Probes for both the tandem and the unique sequences were used to study the DF3 locus in human breast tumor DNAs. Seventy of 110 breast tumor DNAs were informative at the DF3 locus. Of these, 20 (29%) showed a loss of heterozygosity, while eight (11%) had an increased copy number of one allele. In some cases, the loss of heterozygosity or increased copy number did not extend to other markers on chromosome 1q or 1p. These data indicate that the chromosomal region around the DF3 locus is affected by mutations at high frequency.

Published
1989

148. ras gene alterations and enhanced levels of ras p21 expression in a spectrum of benign and malignant human mammary tissues

Author

Thor, A., Ohuchi, N., Horan Hand, P., Callahan, R., Weeks, M. O., Charles Theillet, Lidereau, R., Escot, C., Page, D. L., and Vilasi, V.

Subjects
Polymorphism, Genetic, Histocytochemistry, Gene Amplification, Radioimmunoassay, Breast Neoplasms, DNA, Oncogenes, Proto-Oncogene Proteins p21(ras), Gene Expression Regulation, Proto-Oncogene Proteins, Humans, RNA, Female, Breast, Alleles
Published
1986

150. Quantitation of hTERT gene expression in sporadic breast tumors with a real-time reverse transcription-polymerase chain reaction assay

Author

Ivan Bieche, Noguès C, Paradis V, Olivi M, Bedossa P, Lidereau R, and Vidaud M

Subjects
Adult, Aged, 80 and over, Time Factors, Reverse Transcriptase Polymerase Chain Reaction, Breast Neoplasms, Middle Aged, Prognosis, Survival Analysis, DNA-Binding Proteins, Receptors, Estrogen, Predictive Value of Tests, Lymphatic Metastasis, Humans, RNA, Female, Neoplasm Invasiveness, Lymph Nodes, Menopause, Receptors, Progesterone, Telomerase, Aged, Follow-Up Studies
Abstract

Recent observations support the notion that telomerase expression is essential for the formation of human tumor cells [W-C. Hahn et al., Nature (Lond.), 400: 464-468, 1999]. The expression pattern of hTERT, the human telomerase catalytic subunit gene, is a rate-limiting determinant of the enzymatic activity of human telomerase. We have developed a real-time quantitative RT-PCR assay based on Taq-Man fluorescence methodology to quantify the full range of hTERT mRNA copy numbers. We validated the method on a series of 134 unilateral invasive primary breast cancer patients with known long-term outcome. Three-quarters of the breast tumors (75.4%; 101 of 134) were hTERT positive, i.e., contained detectable and quantifiable hTERT mRNA. hTERT-positive patients had significantly shorter relapse-free survival (P = 0.017) after surgery compared with hTERT-negative patients. The prognostic significance of hTERT status persisted in Cox multivariate regression analysis. When we subdivided hTERT-positive patients (n = 101) into three equal groups (tumors showing small, intermediate, or high increase in hTERT mRNA content), we observed statistical (or a trend toward) links between high hTERT mRNA levels and Scarff-Bloom-Richardson histopathological grade III (P = 0.066), and negative estrogen (P = 0.002) and progesterone (P = 0.048) receptor status, and therefore with higher aggressiveness of breast tumors. High hTERT mRNA levels were also linked to MYC gene overexpression (P = 0.007). These findings show that the quantitative evaluation of hTERT mRNA can have important prognostic significance in human breast cancer. In addition, our simple, rapid, and semiautomated assay method is suitable for routine hTERT mRNA detection and quantification and will be a powerful tool in large, randomized, prospective, cooperative group trials and in the hTERT-based therapy project.

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