Reverse transcription-polymerase chain reaction (RT-PCR) assays of estrogen and progesterone receptors in breast cancer

Chevillard, Sylvie; Müller, A; Levalois, Céline; Laine-Bidron, C.; Vielh, P.; Magdelénat, H.

doi:10.1007/bf01807039

Cited by 19 publications

(15 citation statements)

References 14 publications

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“…19 However, in some samples, contrasting results were obtained, which may be explained by partial proteolysis at epitope sites. 19 Several authors have proposed ER␣ mRNA content as an alternative to the ER cytosolic assay 20,21 or as a valuable additive marker. 22 They found a higher number of ER-positive tumors when assessing by ER␣ mRNA than by EIA or LBA.…”

Section: Discussionmentioning

confidence: 99%

Analysis of the potential contribution of estrogen receptor (ER) ? in ER cytosolic assay of breast cancer

et al. 2001

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Section: Discussionmentioning

confidence: 99%

Analysis of the potential contribution of estrogen receptor (ER) ? in ER cytosolic assay of breast cancer

et al. 2001

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“…16 PCR reactions were performed on an ABI PRISM 7300 sequence detection system (Applied Biosystems) using either the SYBR Green PCR Master Mix kit (Applied Biosystems, Courtaboeuf, France) or the ABsolute QPCR Mix (Abgene, Courtaboeuf, France). Quantification of each gene expression was calibrated using a reference standard curve obtained by serial dilutions of PCR product prepare from a mixture of cDNAs from several rat tissues.…”

Section: Quantitative Real-time Rt-pcr Analysismentioning

confidence: 99%

Gene expression profiling of alpha‐radiation‐induced rat osteosarcomas: Identification of dysregulated genes involved in radiation‐induced tumorigenesis of bone

Daino

Ugolin

Altmeyer-Morel

et al. 2009

Intl Journal of Cancer

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To better understand the molecular basis of radiation-induced osteosarcoma (OS), we performed global gene expression profiling of rat OS tumors induced by the bone-seeking alpha emitter 238 Pu, and the expression profiles were compared with those of normal osteoblasts (OB). The expressions of 72 genes were significantly differentially expressed in the tumors related to OB. These included genes involved in the cell adhesion (e.g., Podxl, Col18a1, Cd93, Emcn and Vcl), differentiation, developmental processes (e.g., Hhex, Gata2, P2ry6, P2rx5, Cited2, Osmr and Igsf10), tumorsuppressor function (e.g., Nme3, Blcap and Rrm1), Src tyrosine kinase signaling (e.g., Hck, Shf, Arhgap29, Cttn and Akap12), and Wnt/b-catenin signaling (e.g., Fzd6, Lzic, Dkk3 and Ctnna1) pathways. Expression changes of several genes were validated by quantitative real-time RT-PCR analysis. Notably, all of the identified genes involved in the Wnt/b-catenin signaling pathway were known or proposed to be negative regulators of this pathway and were downregulated in the tumors, suggesting the activation of bcatenin in radiation-induced OS. By using immunohistochemical and immunoblot analyses, constitutive activation of the Wnt/b-catenin signaling pathway in the tumors was confirmed by observing nuclear and/or cytoplasmic localization of b-catenin and a decrease in its inactive (phosphorylated) form. Furthermore, we found a significant reduction in the levels of glycogen synthase kinase 3b (GSK-3b) protein in the tumors relative to OB. Taken together, these findings provide new insights into the molecular basis of radiation-induced OS. ' UICCKey words: osteosarcoma; osteoblast; ionizing radiation; carcinogenesis; transcriptome Osteosarcoma (OS) is the most common primary tumor of bone in children and adolescents. The peak incidence of OS occurs in the second decade of life, with an additional smaller peak in the elderly population. This tumor is highly aggressive and is thought to arise primarily from osteoblasts (OB), boneforming cells. An increased risk for developing OS is known to be associated with some genetic disorders, such as hereditary retinoblastoma and Li-Fraumeni syndrome with germline mutations in the retinoblastoma (RB1) and TP53 genes, respectively. 1,2 In agreement with this, abnormalities of genes involved in the RB1 and TP53 tumor-suppressor pathways are often found in OS. 3,4 On the other hand, the association between ionizing radiation and the subsequent development of OS has been well documented in prior studies. For example, OS is known as one of the most frequent secondary malignant neoplasms occurring within the radiation field in patients, especially with retinoblastoma, treated with radiation therapy. 1,5 The risk of OS has been reported to be increased following the internal exposure to bone-seeking radioisotopes from occupational or medicinal use. 6-8 Interestingly, some studies have revealed the genetic and cytogenetic changes in radiation-induced OS and suggested the presence of additional tumor-associated genes. ...

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“…For GADD45 detection, the primers used (D, 5Ј-ACGAGGACGACGACAGAGAT-3Ј, and F, 5Ј-TCCCGCCAAAACAAATAAG-3Ј) amplified a 262-bp fragment by using an annealing temperature of 58°C. DNA fragments smaller than 400 bp were amplified as described (31).…”

Section: Dna-repair Analysis Complementation Test and Construction mentioning

confidence: 99%

Global genome repair is required to activate KIN17 , a UVC-responsive gene involved in DNA replication

Masson

Menaa

Pinon‐Lataillade

et al. 2003

Proc. Natl. Acad. Sci. U.S.A.

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UV light provokes DNA lesions that interfere with replication and transcription. These lesions may compromise cell viability and usually are removed by nucleotide excision repair (NER). In humans, inactivation of NER is associated with three rare autosomal recessive inherited disorders: xeroderma pigmentosum (XP), Cockayne syndrome, and trichothiodystrophy. The NER earliest step is lesion recognition by a complex formed by XPC and HHR23B proteins. In a subsequent step, XPA protein becomes associated to the repair complex. Here we investigate whether XPA and XPC proteins, involved in global genome repair, may contribute to a signal transduction pathway regulating the response to UVC-induced lesions. We monitored the expression of several UVC-induced genes in cells deficient in either a transduction pathway or mutated on an NER gene. Expression of the KIN17 gene is induced after UVC irradiation independently of p53 and of activating transcription factor 2. However, in human cells derived from XPA or XPC patients the UVCinduced accumulation of KIN17 RNA and protein is abolished. Our results indicate that the presence of functional XPA and XPC proteins is essential for the up-regulation of the KIN17 gene after UVC irradiation. They also show that the integrity of global genome repair is required to trigger KIN17 gene expression and probably other UVC-responsive genes.melanoma ͉ XPA ͉ XPC ͉ genotoxic stress ͉ nuclear proteins

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Reverse transcription-polymerase chain reaction (RT-PCR) assays of estrogen and progesterone receptors in breast cancer

Cited by 19 publications

References 14 publications

Analysis of the potential contribution of estrogen receptor (ER) ? in ER cytosolic assay of breast cancer

Analysis of the potential contribution of estrogen receptor (ER) ? in ER cytosolic assay of breast cancer

Gene expression profiling of alpha‐radiation‐induced rat osteosarcomas: Identification of dysregulated genes involved in radiation‐induced tumorigenesis of bone

Global genome repair is required to activate KIN17 , a UVC-responsive gene involved in DNA replication

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