Relevant bibliographies by topics / Fusion TMPRSS2:ERG

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Fusion TMPRSS2:ERG'

Author: Grafiati
Published: 17 September 2021
Last updated: 5 February 2022

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'Fusion TMPRSS2:ERG.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Journal articles on the topic "Fusion TMPRSS2:ERG"

1

Sung, Ji-Youn, Hwang Gyun Jeon, Byong Chang Jeong, Seong Il Seo, Seong Soo Jeon, Hyun Moo Lee, Han Yong Choi, So Young Kang, Yoon-La Choi, and Ghee Young Kwon. "Correlation of ERG immunohistochemistry with molecular detection of TMPRSS2-ERG gene fusion." Journal of Clinical Pathology 69, no. 7 (December 15, 2015): 586–92. http://dx.doi.org/10.1136/jclinpath-2015-203314.

Full text
Abstract:
AimsTMPRSS2/E26 transformation-specific (ETS) family gene fusion in prostate carcinoma (PCa) can be detected by several methods including immunohistochemistry (IHC) for ETS-related gene (ERG), the diagnostic utility of which has not been clearly defined.MethodsWe explored TMPRSS2-ERG gene rearrangement status in 132 patients with PCa with four detection methods including fluorescence in situ hybridisation for TMPRSS2-ERG fusion, real-time reverse transcription PCR (RT-qPCR) for ERG and TMPRSS-ERG fusion transcript mRNA and IHC for ERG.ResultsConcordant results were found in 126 cases for the four detection methods and the remaining six cases showed discrepancy in one method: two cases in IHC, three cases in RT-qPCR for ERG and one case in RT-qPCR for fusion transcript. In discordant cases, the majority results were determined as final fusion status. Analysis of discrepancy cases for ERG IHC showed that weak immunoreactivity for ERG should be regarded as equivocal and that even strong immunoreactivity can be false positive. The overall incidence of TMPRSS-ERG gene fusion was 24%.ConclusionsERG IHC is a useful surrogate test for the detection of TMPRSS2-ERG gene fusion, but it needs to be interpreted with caution and definite judgement should not be based on IHC alone. A relatively low incidence of TMPRSS2-ERG gene fusion was demonstrated in this Korean cohort.
APA, Harvard, Vancouver, ISO, and other styles
2

He, Wei, Fukang Sun, Juping Zhao, Dai Jun, Le Xu, Chenghe Wang, Chen Fang, et al. "Prevalence and genetic features of TMPRSS2-ERG fusion in Chinese patients with prostate cancer." Journal of Clinical Oncology 38, no. 15_suppl (May 20, 2020): e17529-e17529. http://dx.doi.org/10.1200/jco.2020.38.15_suppl.e17529.

Full text
Abstract:
e17529 Background: Prostate cancer (PCa) is one of the most common malignancies, with rising incidence rate in China. The Cancer Genome Atlas (TCGA) revealed 53% of patients with PCa had ETS family gene fusions. The most frequent fusion type of ETS fusions is TMPRSS2-ERG, which may predicts resistance to taxane and androgen-deprivation therapies. The prevalence of TMPRSS2-ERG fusion in Chinese PCa patients evaluated by fluorescence in situ hybridization (FISH) or immunohistochemistry (IHC) varied from 7.5% to 78.0%. However, the sample sizes were small. In the present study, we investigated the prevalence and genetic features of TMPRSS2-ERG fusion by next generation sequencing (NGS) in a larger Chinese PCa cohort. Methods: Genomic profiling was performed through NGS from Chinese patients with PCa between January, 2017 and November, 2019. Formalin fixed paraffin-embedded (FFPE) tumor specimens or blood samples from participants were collected for NGS. IHC staining for PD-L1 expression was performed using PD-L1 IHC 22C3 pharmDx assay or Ventana PD-L1 SP263 assay. Data analyses were performed using SPSS and R 3.6.1. Results: A total of 526 Chinese PCa patients were included in this study. The median age was 70 (range, 29-90) years old. We observed 13.1% patients with a positive PD-L1 expression, 3.0% patients with MSI-H, and a median TMB of 4.0 muts/Mb (range: 0-72.9). TMPRSS2 fusions were detected in 47 (8.9%) PCa patients, and 6.8% of patients had TMPRSS2-ERG fusion, which is significantly lower than that of Caucasian patients. The PD-L1 expression pattern and TMB distribution of the TMPRSS2-ERG fusion-positive patients were similar with TMPRSS2-ERG fusion-negative patients, however no fusion-positive patients were identified as MSI-H. Among these 36 TMPRSS2-ERG fusion-positive patients, the most frequently somatic mutations were detected in TP53 (38.9%), AR (11.1%), ATM (11.1%), and PTEN (11.1%). 9 (22.2%) patients harbored somatic mutations in PI3K/ AKT/mTOR pathway that has been previously demonstrated to collaborate with ERG to promote prostate cancer progression. Conclusions: This study revealed the prevalence and genetic features of TMPRSS2-ERG fusion in Chinese PCa patients by NGS in the first time. Our results provide a better understanding of molecular features in Chinese TMPRSS2-ERG fusion-positive PCa patients.
APA, Harvard, Vancouver, ISO, and other styles
3

Minner, S., A. Krohn, L. Burkhardt, P. Tennstedt, R. Simon, H. Sirma, H. Huland, G. Sauter, and T. Schlomm. "Chromosomal deletions, tumor phenotype, and prognosis in prostate cancer." Journal of Clinical Oncology 29, no. 7_suppl (March 1, 2011): 37. http://dx.doi.org/10.1200/jco.2011.29.7_suppl.37.

Full text
Abstract:
37 Background: Chromosomal deletions are frequent in prostate cancer (PCa) but target genes and potential clinical significance are often unknown. This project aimed at the identification of frequent and new deletions in PCa and to study their association with tumor phenotype and PSA recurrence. Methods: Array CGH was performed on 77 advanced PCa. Deletions of interest were subsequently analyzed on a tissue microarray containing more than 2000 PCa with clinical follow-up data using fluorescence in situ hybridization (FISH). The FISH probes used included a break-apart probe for TMPRSS2-ERG and dual-labeling probes for centromere 10/PTEN and centromere 3/3p14. Results: The most frequent circumscribed deletions found by array CGH were 3p14 (including FOXP1) in 18%, 5q31 in 16%, 5q21 in 14%, 6q13 in 21%, 6q21 in 19%, 6q26 in 14%, 8p11 in 17%, 10q23 (including PTEN) in 18%, 12p13 in 14%, 13q14 in 14%, 16q24 in 22% and 21q (representing TMPRSS2-ERG fusion) in 18%. TMPRSS2-ERG fusions, PTEN and FOXP1 deletions were selected for FISH analysis. A TMPRSS2-ERG fusion was observed in 394 of 947 interpretable cases (41.6%). TMPRSS2-ERG fusion was unrelated to tumor stage, Gleason grade, and PSA recurrence. PTEN deletions were observed in 8.9% of 1844 interpretable cases and were associated with advanced tumor stage (p<0.0001), high Gleason grade (p<0.0001), and early biochemical recurrence (p<0.0001). FOXP1 deletions were seen in 5.0% of 619 cases. FOXP1 deletions were not significantly linked to tumor phenotype and outcome. Both PTEN and FOXP1 deletions were strongly linked to TMPRSS2-ERG fusions. TMPRSS2-ERG fusion positive tumors had PTEN deletions in 15.4% and FOXP1 deletions in 10.7%, while TMPRSS2-ERG fusion negative cancers had PTEN deletions in only 5.8% and FOXP1 deletions in only 2.0% of cases (p<0.0001 each). Conclusions: The TMPRSS2-ERG fusion determines a genetically distinct subgroup of prostate cancers. Our data provide no evidence for a particular clinical behaviour of TMPRSS2-ERG fusion positive cancers in radically operated patients. PTEN and FOXP1 alterations are preferentially found in TMPRSS2-ERG fusion positive cancers. Both genes may potentially be involved in pathway dysregulation in these cancers. No significant financial relationships to disclose.
APA, Harvard, Vancouver, ISO, and other styles
4

Yoshimoto, M., A. M. Joshua, S. Chilton-Macneill, J. Bayani, M. Prasad, N. Fleshner, A. Finelli, et al. "Detection of novel variant TMPRSS2 /ERG fusion transcripts suggests independent genomic alterations may underlie origin of multi-centric prostate cancer." Journal of Clinical Oncology 24, no. 18_suppl (June 20, 2006): 10029. http://dx.doi.org/10.1200/jco.2006.24.18_suppl.10029.

Full text
Abstract:
10029 Background: Most of the early successes in identifying chromosomal translocations in neoplasias came from the study of hematological malignancies and sarcomas, with limited evidence that consistent genomic rearrangements were present in epithelial malignancies. Recently it was reported that ∼75% of prostate cancers carry a genomic rearrangement leading to fusion of the TMPRSS2 locus to either the ERG or ETV1 genes (both ETS transcription factors). In the fusion gene, the androgen-sensitive promoter elements of TMPRSS2 are thought to mediate over-expression of these ETS transcription factors. Over-activity of the ETS family of transcription factors has been suggested to be involved in the transition from pre-neoplasia to carcinoma as they regulate genes involved in processes such as adhesion, motility, invasion and angiogenesis. Methods: Using both RT-PCR and FISH with published primers and BACs respectively we analyzed 15 samples of prostatic carcinoma from radical prostatectomies and sequenced a subset of the TMPRSS2/ERG fusions. Results: We have found ERG-TMPRSS2 fusion transcripts in 6 samples and no ETV1-TMPRSS2 fusions. Of the 6 fusion tumours, 5 were Gleason 7 and 1 was Gleason 9. Tumour stages ranged from T2a-T3b. One sample with multi-centric carcinoma exhibited 2 distinct in-frame rearrangements generating novel TMPRSS2 /ERG fusion transcripts. Variant I TMPRSS2/ERG transcript was 430 bp and it led to fusion of exons 1 and 2 of the TMPRSS2 gene with exons 5 and 6 of the ERG gene. Variant II TMPRSS2/ERG fusion transcript was slightly smaller at 350 bp and it led to fusion of exon 1 of the TMPRSS2 gene to exons 5 and 6 of the ERG gene. These novel transcripts appear to be smaller than the published fusion proteins but preliminary analysis suggests that all known regulatory and functional protein domains are maintained. Conclusions: The demonstration of two new TMPRSS2/ERG variant fusion transcripts in prostate cancer deserves further study to evaluate their functional impact and prognostic and pathological importance. Moreover the presence of two distinct transcripts within a single multi-centric tumor provides genomic evidence that independent clonal neoplasms can arise synchronously in prostate cancer. No significant financial relationships to disclose.
APA, Harvard, Vancouver, ISO, and other styles
5

Lara, Primo N., Andreas M. Heilmann, Julia A. Elvin, Mamta Parikh, Ralph de Vere White, Regina Gandour-Edwards, Christopher P. Evans, et al. "TMPRSS2-ERG Fusions Unexpectedly Identified in Men Initially Diagnosed With Nonprostatic Malignancies." JCO Precision Oncology, no. 1 (November 2017): 1–6. http://dx.doi.org/10.1200/po.17.00065.

Full text
Abstract:
Purpose TMPRSS2-ERG gene fusions are frequently found in prostate cancer and are pathognomonic for prostatic origin. In a series of cancer cases assayed with comprehensive genomic profiling (CGP) in the course of clinical care, we reviewed the frequency of TMPRSS2-ERG fusions in patient tumors of various histologic subtypes. Methods Frequency of TMPRSS2-ERG fusions was determined in CGPs from 64,263 cancer cases submitted to Foundation Medicine to assess genomic alterations suggesting benefit from targeted therapy. Genomic results are presented from an index case of prostate cancer that underwent evolution from adenocarcinoma to pure squamous cell carcinoma. Results TMPRSS2-ERG fusions were identified for 0.86% of male patients (250 of 29,030) and not found for female patients (none of 35,233). TMPRSS2-ERG fusions were detected in six tumors classified as squamous carcinoma, five of which were of unknown primary site. The index case is a patient with a large, left retrovesical mass diagnosed as squamous carcinoma by morphologic examination and a history of Gleason score 9 prostate cancer with prior prostatectomy and salvage radiation therapy. TMPRSS2-ERG was detected by genomic profiling in the squamous cell tumor, the primary adenocarcinoma of the prostate, and in a metachronous prostatic adenocarcinoma metastasis. On the basis of these results, the patient received androgen deprivation therapy. A phylogenetic tree demonstrating clonal and histopathologic evolution of prostate cancer in the index patient was constructed. Conclusion In this large CGP dataset, TMPRSS2-ERG fusion was seen in approximately 30% of prostate cancers regardless of histologic type; on occasion, the fusion was detected in advanced cancers not initially carrying a diagnosis of prostate carcinoma. CGP of advanced cancers in men may reveal prostatic origin by detection of the pathognomonic TMPRSS2-ERG fusion gene.
APA, Harvard, Vancouver, ISO, and other styles
6

Mani, Ram-Shankar, Scott A. Tomlins, Kaitlin Callahan, Aparna Ghosh, Mukesh K. Nyati, Sooryanarayana Varambally, Nallasivam Palanisamy, and Arul M. Chinnaiyan. "Induced Chromosomal Proximity and Gene Fusions in Prostate Cancer." Science 326, no. 5957 (October 29, 2009): 1230. http://dx.doi.org/10.1126/science.1178124.

Full text
Abstract:
Gene fusions play a critical role in cancer progression. The mechanisms underlying their genesis and cell type specificity are not well understood. About 50% of human prostate cancers display a gene fusion involving the 5′ untranslated region of TMPRSS2, an androgen-regulated gene, and the protein-coding sequences of ERG, which encodes an erythroblast transformation–specific (ETS) transcription factor. By studying human prostate cancer cells with fluorescence in situ hybridization, we show that androgen signaling induces proximity of the TMPRSS2 and ERG genomic loci, both located on chromosome 21q22.2. Subsequent exposure of the cells to gamma irradiation, which causes DNA double-strand breaks, facilitates the formation of the TMPRSS2-ERG gene fusion. These results may help explain why TMPRSS2-ERG fusions are restricted to the prostate, which is dependent on androgen signaling.
APA, Harvard, Vancouver, ISO, and other styles
7

KULDA, VLASTIMIL, ONDREJ TOPOLCAN, RADEK KUCERA, MICHAELA KRIPNEROVA, KRISTYNA SRBECKA, MILAN HORA, ONDREJ HES, et al. "Prognostic Significance of TMPRSS2-ERG Fusion Gene in Prostate Cancer." Anticancer Research 36, no. 9 (September 9, 2016): 4787–94. http://dx.doi.org/10.21873/anticanres.11037.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Trifunovski, Aleksandar, Aleksandar Dimovski, Sasho Dohcev, Sotir Stavridis, Oliver Stankov, Skender Saidi, Marija Gjorgjievska, and Zivko Popov. "Detection of TMPRSS2-ERG Fusion Transcript in Biopsy Specimen of Prostate Cancer Patients: A Single Centre Experience." PRILOZI 41, no. 1 (June 1, 2020): 5–14. http://dx.doi.org/10.2478/prilozi-2020-0018.

Full text
Abstract:
AbstractIntroduction: Prostate carcinoma is the most frequent malign neoplasm among men with an ever-growing incidence rate. TMPRSS2-ERG fusion transcript leads to the androgen induction of ERG proto-oncogenes expression, representing a high presence of oncogenes alteration among prostate tumour cells.Aim: The aim of this research was to detect and evaluate theTMPRSS2-ERG fuse transcript in the tissues of patients with prostate cancer, and establish a base of material of these samples for further genetic examination.Materials and methods: The research was a prospective clinical study that involved and focused on random sampling of 101 patients (62 with prostate cancer-study group and 39 with benign changes in the prostate-control group). Real time PCR analysis for detection of the TMPRSS2-ERG fusion transcript in prostate tissue was performed and also data from the histopathology results of tissues were used, as well as data for the level of PSA (prostate-specific antigen) in blood.Results: TMPRSS2-ERG fusion transcript was detected in 20 out of 62 (32.2%) patients with prostate carcinoma and among no patients with benign changes whatsoever. There were no significant differences between patients with/without detected TMPRSS2-ERG fusion related to Gleason score. Among 50%, in the study group this score was greater than 7 per/for Median IQR=7 (6-8). Significant difference was recognized, related to the average value of PSA in favour of significantly higher value of PSA in the study group with prostate cancer, but there was also no significant difference between samples with prostate cancer who were with/without detected TMPRSS2-ERG fusion transcript related to PSA level.Discussion: The results from this research are in accordance with the values and results from analyses done in several research centres and oncological institutes.Conclusion: The positive findings in small scale studies encourage the implementation of larger scale studies that will be enriched with results of genetic transcript in blood and urine and will define the positive diagnostic meaning of the TMPRSS-ERG fusion transcript.
APA, Harvard, Vancouver, ISO, and other styles
9

Dal Pra, Alan, Fiona Warde, Adrian Shea Ishkanian, Alice Meng, Chad Malloff, Wan Lam, Jenna Sykes, et al. "TMPRSS2-ERG status and biochemical recurrence following radiotherapy for intermediate-risk prostate cancer." Journal of Clinical Oncology 30, no. 5_suppl (February 10, 2012): 11. http://dx.doi.org/10.1200/jco.2012.30.5_suppl.11.

Full text
Abstract:
11 Background: Approximately 50% of prostate cancers (PC) contain TMPRSS2-ERG gene fusions leading to ERG overexpression. Pre-clinical data suggest that these fusions are due to altered DNA double-strand break repair status which could have therapeutic ramification for the use of radiotherapy (RT) and PARP inhibitors. The aim of this study was to correlate TMPRSS2-ERG status to biochemical failure following clinical induction of DNA breaks in the form of image-guided radiotherapy (IGRT) in intermediate-risk PC. Methods: Pre-treatment biopsies from two separate cohorts of intermediate-risk PC patients (T1/T2, GS < 8, PSA < 20ng/ml) were analyzed: 1) 126 patients assessed by array Comparative Genomic Hybridization (aCGH) for TMPRSS2:ERG fusion; and 2) 121 patients assessed by tissue microarray (TMA) for ERG expression by immunohistochemistry (IHC). All patients received IGRT with a median dose of 79.8 Gy (60-79.8 Gy). TMPRSS2:ERG status was correlated to Gleason score, T stage, initial PSA and biochemical-free relapse rate (bFRR; Phoenix definition: nadir + 2ng/ml). Results: At a median follow-up time of 6.36 years, the biochemical relapse event rate was 37% and 18% in the aCGH and IHC cohorts, respectively. ERG expression by IHC was found in 49.6% of the 121 PC. TMPRSS2-ERG status was not correlated to increased Gleason score, pre-treatment PSA or T stage. On multivariate analyses in models containing clinical factors, TMPRSS2:ERG status (either using aCGH or IHC) was not prognostic for biochemical outcome (ERG expression: HR=0.78, 95% CI: 0.33-1.85; p= 0.568; TMPRSS2-ERG fusion: HR=0.71, 95% CI: 0.35-1.41; p=0.326). Conclusions: In two separate cohorts, TMPRSS2-ERG status was not prognostic for bRFR after IGRT. Although a trend was observed, these clinical data do not support the hypothesis that these cancers have DNA repair defects that render them significantly more radiosensitive when compared to other PC. Further clinical trials are required to understand the utility of TMPRSS2:ERG status and response to DNA damaging agents, including that of PARP inhibitors. The trans-Canadian PROFIT trial is completing accrual of close to 1200 patients allowing for TMPRSS2:ERG studies in a larger RT cohort.
APA, Harvard, Vancouver, ISO, and other styles
10

Klein, E. A., S. M. Falzarano, T. Maddala, D. Cherbavaz, W. F. Novotny, C. Millward, and C. Magi-Galluzzi. "Use of TMPRSS2-ERG gene rearrangement and quantitative ERG expression to predict clinical recurrence after radical prostatectomy." Journal of Clinical Oncology 29, no. 7_suppl (March 1, 2011): 36. http://dx.doi.org/10.1200/jco.2011.29.7_suppl.36.

Full text
Abstract:
36 Background: The association of TMPRSS2-ERG fusions and ERG expression in prostate cancer (PC) with adverse clinical outcomes has been controversial, with mixed results in the literature. We conducted a study to test whether tumor-derived gene expression profiles, including the presence of TMPRSS2-ERG fusions and ERG gene expression, are associated with clinical recurrence (cR) after radical prostatectomy (RP). Methods: All patients with clinical stage T1/T2 prostate cancer treated with RP at CC from 1987 to 2004 were identified (n∼f2,600). A cohort sampling design was used to select 127 patients with cR and 374 patients without cR after RP. For each patient a primary Gleason pattern (GP) sample, secondary (or highest) GP sample, and an adjacent nontumor tissue sample were evaluated. Surgical Gleason Score (GS) and clinical data were centrally reviewed. RNA was extracted from 6 manually dissected 10 μ m formalin-fixed paraffin-embedded sections obtained from RP specimens and expression of TMPRSS2-ERGa, TMPRSS2-ERGb, ERG and reference genes were quantified using RT-PCR. Times to cR, PSA recurrence, and PC death were analyzed using Cox PH regression. Results: Blocks from 441 patients were evaluable. Median F/U was 5.8 years. Patients were mostly Caucasian (83%), clinical stage T1 (66%), had baseline PSA <10 ng/mL (82%), and had surgical Gleason score ≤7 (87%). 848 tumor samples and 410 non-tumor samples were assessed. TMPRSS2-ERGa and/or TMPRSS2-ERGb fusions were present in 51.8% of tumor samples and 7.5% of non-tumor samples. There was 89% concordance (95% CI: 86%, 92%) for TMPRSS2-ERG fusion status between the 2 tumor samples for each patient. High ERG expression was strongly associated with the presence of TMPRSS2-ERG fusions (p <0.01). We did not find an association between TMPRSS2-ERG a/b gene rearrangement or ERG expression with cR, PSA recurrence, PC death, or surgical GS (p > 0.2). Conclusions: This study was notable for the large number of cR events, use of a standardized quantitative assay, and rigorous central review of pathology and clinical data. We did not find an association of TMPRSS2-ERG gene rearrangements or ERG expression with aggressiveness of prostate cancer post RP. [Table: see text]
APA, Harvard, Vancouver, ISO, and other styles
More sources

Dissertations / Theses on the topic "Fusion TMPRSS2:ERG"

1

Coll, Bastus Nuria. "Study of the mechanisms causing the TMPRSS2:ERG gene fusion in prostate cancer." Thesis, Queen Mary, University of London, 2013. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.610967.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Souza, Bruna Ferreira de. "Investigação dos mRNAs de Fusão do Gene TMPRSS2/ERG em Pacientes com Câncer de Próstata." Universidade de São Paulo, 2013. http://www.teses.usp.br/teses/disponiveis/17/17135/tde-11062013-165125/.

Full text
Abstract:
O interesse científico em rearranjos gênicos relacionados com a etiogênese e progressão do câncer relaciona-se, principalmente, à descoberta da fusão BCR/ABL na Leucemia Mieloide Crônica, sendo que desde então, houve uma evolução no manejo dessa doença, instigando uma série de estudos correlatos em outras neoplasias. Essas pesquisas culminaram no encontro do primeiro rearranjo gênico em tumores sólidos, o gene de fusão TMPRSS2/ERG, envolvendo a região promotora do gene da serina protease, o TMPRSS2, e o gene da família de fatores de transcrição ETS, o ERG. Ele é específico de adenocarcinoma da próstata, o que o torna forte candidato a biomarcador e já demonstra exercer papel de destaque no manejo clínico do câncer de próstata (CaP), tal qual o exercido pela fusão BCR/ABL. Sua frequência têm se mostrado associada a diversos fatores, sobretudo à etnia de origem. Indivíduos portadores de CaP oriundos de diversos países já foram estudados quanto à frequência dessa fusão e o resultado é bastante diversificado. No Brasil, entretanto, ainda não há dados a respeito desse rearranjo, e este trabalho visa contribuir para a identificação da frequência da mesma e sua contribuição para o diagnóstico e o tratamento do CaP no país. Para tal, utilizamos mRNA de 20 indivíduos com CaP provenientes do serviço de atendimento do HCFMRP/USP, e por meio da técnica de RT-PCR, obtivemos o cDNA dos mesmos que foram investigados quanto à presença da fusão TMPRSS2/ERG, e as amostras positivas sequenciadas para determinação do tipo de isoforma envolvida. Identificamos que 35% das amostras continham o rearranjo e que todas correspondiam à isoforma do tipo III, cuja literatura a relaciona com um fenótipo agressivo do CaP, porém não metástico, e é também a mais comumente identificada. Ao confrontarmos essa evidência com os dados clínicos e histopatológicos, constatamos que havia correlação entre eles, sugerindo assim, como em outros trabalhos, o potencial desse rearranjo como marcador de agressividade do CaP. No entanto, não verificamos relação entre a presença da fusão e dados de progressão da doença. Em vista desses resultados, destacamos a necessidade da promoção de outros trabalhos de mesmo caráter, abrangendo outras regiões, a fim de se delinear um perfil mais representativo desse rearranjo no Brasil, uma vez que seu potencial como biomarcador diagnóstico e clínico é enorme e pode influenciar sobremaneira no manejo do CaP.
Scientific interest in gene rearrangements associated with cancer progression and etiogenesis relates mainly to the discovery of BCR/ABL fusion in chronic myelogenous leukemia, and since then there has been an evolution in the management of this disease, prompting a series of related studies in other malignancies. These researches resulted in the meeting of the first gene rearrangement in solid tumors, the fusion gene TMPRSS2/ERG involving the promoter region of the gene of serine protease, TMPRSS2, and the gene family of transcription factors ETS, the ERG. It is specific for adenocarcinoma of the prostate, which makes it a strong candidate biomarker and shows already exert a prominent role in the clinical management of prostate cancer (PCa), as is exercised by the BCR/ABL. Its frequency has been shown to be associated with several factors, especially the ethnic origin. Individuals with CaP from different countries have been studied in the frequency of this merger and the result is quite diverse. In Brazil, however, there is no data about this rearrangement, and this paper aims to contribute to the identification of the same frequency and its contribution to the diagnosis and treatment of PCa in the country. Therefore, we used mRNA from 20 individuals with CaP from the answering service HCFMRP/USP, and by RT-PCR, cDNA obtained from the same people who were investigated for the presence of fusion TMPRSS2/ERG, and positive samples sequenced to determine the type of isoform involved. We found that 35% of the samples contained the rearrangement and that all corresponded to the type III isoform, whose literature relates to an aggressive phenotype of PCa, but not metastatic, and is also the most commonly identified. When we compared this evidence with clinical and histopathological data, we found that there was a correlation between them, suggesting, as in other studies, the potential of this rearrangement as a agressivity marker of PCa. However, no significant association between the presence of data fusion and disease progression. In view of these results, we highlight the need to promote other works of the same character, covering other regions, in order to delineate a more representative profile of this rearrangement in Brazil, since its potential as a biomarker and clinical diagnosis is huge and can influence greatly in the management of PCa.
APA, Harvard, Vancouver, ISO, and other styles
3

Delliaux, Carine. "Rôle du gène de fusion TMPRSS2.ERG dans la formation des métastases osseuses du cancer de la prostate." Thesis, Lille 2, 2017. http://www.theses.fr/2017LIL2S009/document.

Full text
Abstract:
Les tumeurs locales de la prostate sont associées à une évolution lente et une bonne survie, alors que les stades plus avancés révèlent dans 80% des cas des métastases osseuses incurables. La découverte de gènes de fusion issus de remaniements chromosomiques, tel que TMPRSS2:ERG dans plus de 50% des cas, a ouvert une nouvelle voie dans la compréhension du processus de cancérisation de la prostate. La présence de ce gène de fusion peut être associée à un mauvais pronostic dans de nombreuses études cliniques. Cependant, son rôle précis au cours de la cancérisation et de la progression du cancer de la prostate reste à déterminer. Le gène Erg (Ets related gene) code un facteur de transcription dont l’expression est notamment associée à la mise en place du cartilage, et plus largement du squelette. Ceci suggère un rôle potentiel du gène de fusion impliquant ce facteur, et de ses gènes cibles, dans la formation des métastases osseuses du cancer de la prostate.Pour notre étude, nous avons utilisé des lignées de cellules tumorales prostatiques PC3 et PC3c, exprimant stablement le gène de fusion TMPRSS2:ERG et précédemment établies au laboratoire. Dans un premier temps, en utilisant un modèle d’injections intratibiales chez les souris SCID, nous avons démontré que l’expression ectopique de la fusion améliore la capacité d’induction de lésions ostéocondensantes en inhibant l’ostéolyse dans le modèle PC3 ostéolytique, et en stimulant l’ostéoformation dans le modèle PC3c mixte (ostéolytique et ostéocondensant). Cette expression ectopique de la fusion augmente également l’ostéomimétisme dans les deux modèles cellulaires, c’est-à-dire l’acquisition d’un phénotype semblable aux cellules osseuses leur conférant des avantages de survie et de propagation dans la moelle osseuse. En outre, trois nouveaux gènes cibles de TMPRSS2:ERG ont été mis en évidence : ET-1 (Endothelin-1), stimulant la différenciation ostéoblastique et inhibant la résorption osseuse ostéoclastique, ALPL (Alkaline Phosphatase Liver/Bone/Kidney), marqueur de différenciation des ostéoblastes, et COL1A1 (Collagen Type 1 Alpha 1), composant de la matrice osseuse, témoignant d’un rôle du gène de fusion dans la formation de métastases ostéocondensantes du cancer de la prostate.Par ailleurs, deux autres gènes ont été étudiés, codant soit une protéine impliquée dans la stabilisation de structures particulières appelées invadopodes, soit une protéine impliquée dans le métabolisme des lipides. L’ensemble de ces résultats contribue à mieux comprendre les mécanismes de cancérisation et d’évolution métastatique du cancer de la prostate, en particulier l’influence de l’expression du gène de fusion TMPRSS2:ERG dans les métastases osseuses du cancer de la prostate
Local prostate cancers are associated with slow progression and good survival, while advanced stages reveal incurable bone metastases in 80% of cases. The discovery of fusion genes resulting from chromosomal rearrangements, such as TMPRSS2:ERG in more than 50% of cases, opened a new way in understanding the process of prostate cancer. The presence of this fusion gene may be associated with poor prognosis in many clinical studies. However, its precise role during cancerization and progression of prostate cancer remains to be determined. The Erg gene (Ets related gene) encodes a transcription factor whose expression is associated in particular with embryonic skeleton development. This suggests a potential role of the fusion gene involving this factor, and its target genes, in the formation of prostate cancer bone metastases.In this study, we used prostate cancer cell lines PC3 and PC3c, stably expressing the TMPRSS2:ERG fusion gene and previously established in the laboratory. First, using a model of intratibial injections in SCID mice, we demonstrated that ectopic expression of the fusion enhances the ability to induce osteoblastic lesions by inhibiting osteolysis in the osteolytic PC3 model, and by stimulating osteoformation in the mixed PC3c model (osteolytic and osteoblastic). This ectopic expression of the fusion also increases osteomimicry in both cell models, meaning the acquisition of a bone-cell-like phenotype which gives them advantages of survival and spread in the bone marrow. In addition, three new TMPRSS2:ERG target genes have been described: ET-1 (Endothelin-1), stimulating osteoblastic differentiation and inhibiting osteoclastic bone resorption, ALPL (Alkaline Phosphatase Liver/Bone/Kidney), a marker of the osteoblasts differentiation, and COL1A1 (Collagen Type 1 Alpha 1), a component of the bone matrix, providing novel insights into the role of the fusion gene in the formation of osteoblastic metastases of prostate cancer.In addition, two other genes have been studied, encoding either a protein involved in the stabilization of particular structures called invadopodia, or a protein involved in lipid metabolism.All these results contribute to decipher the mechanisms of cancerization and metastatic progression of prostate cancer, in particular the influence of the expression of TMPRSS2:ERG fusion gene in prostate cancer bone metastases
APA, Harvard, Vancouver, ISO, and other styles
4

Rinckleb, Antje [Verfasser]. "Common germline variants for prostate cancer risk: implication in DNA repair and TMPRSS2-ERG fusion formation / Antje Rinckleb." Ulm : Universität Ulm. Medizinische Fakultät, 2014. http://d-nb.info/1054996709/34.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Ovtcharov, Slav. "Impact of TMPRSS2-ERG fusion gene on prostate cancer cell response to chemotherapy, radiotherapy and androgen deprivation therapy." Thesis, University of Oxford, 2015. http://ora.ox.ac.uk/objects/uuid:f30bf48d-fff5-49e7-8258-107a500c8752.

Full text
Abstract:
Many aspects of the mechanisms by which prostate cancer (PCa) progresses from being a confined tumour to advanced metastatic and castration-resistant disease remain unclear. The aim of this study is to evaluate in vitro the potential role of the fusion gene TMPRSS2-ERG in the response of PCa cells to ionising radiation (IR) and androgen deprivation therapy (ADT). This research focused on assessing the presence of the TMPRSS2-ERG transcript across various PCa cell lines and identifying any correlation between the TMPRSS2-ERG transcript and other genes, particularly genes related to DNA damage repair pathways. Several genes involved in cell metabolism and development were found to correlate with TMPRSS2-ERG but not genes involved in DNA repair. In accordance with previous reports, this research confirmed a proliferative advantage for cells expressing ERG. However this project also tested the role of ERG-status in response to chemotherapy, radiation and ADT. The data showed that VCaP and DuCaP cells exposed to low-dose radiation demonstrated decreased viability irrespective of their ERG-status. Similarly ADT decreased the viability of VCaP cells and seemed to neutralise the proliferative advantage of TMPRSS2-ERG positive cells. Stimulation with dihydrotestosterone caused increased radioresistance of TMPRSS2-ERG positive cells. Treatment with taxanes showed stronger effect on cells with lower ERG expression. This work suggests that the proliferative advantage conferred by ERG overexpression in in vitro models can be neutralised by castration and IR.
APA, Harvard, Vancouver, ISO, and other styles
6

Tian, Tian. "Etudes fonctionnelles du gène de fusion TMPRSS2 : ERG dans le cancer de la prostate et les métastases osseuses associées." Thesis, Lille 2, 2013. http://www.theses.fr/2013LIL2S004.

Full text
Abstract:
Issu de remaniements chromosomiques, le gène de fusion TMPRSS2 :ERG a été identifié dans plus de 50% des cas des cancers de la prostate (CaP). Cette découverte a ouvert une nouvelle voie dans la compréhension du processus de cancérisation. De nombreuses études cliniques démontrent l’association de la présence de ce gène de fusion avec un mauvais pronostic. Erg (Ets-Related-Gene) est un facteur de transcription dont l’expression est associée, en particulier, à la mise en place du cartilage et plus largement du squelette. Une étude transcriptomique, comparant les transcriptomes des chondrocytes embryonnaires de souris sauvages et de souris transgéniques qui expriment une protéine ERG tronquée, à l’effet trans-dominant négatif, nous a permis d’identifier de nombreux marqueurs osseux et gènes associés à la métastase osseuse comme gènes cibles de ce facteur de transcription. Les CaP, lorsqu’ils évoluent, provoquent dans la plupart des cas des métastases osseuses. Ces résultats suggèrent un rôle potentiel du gène de fusion dans la formation de métastases osseuses du CaP.Pour notre étude, nous avons établi des lignées de cellules cancéreuses prostatiques PC3c qui expriment stablement le gène de fusion TMPRSS2 :ERG. Dans un premier temps, nous avons démontré que l’expression ectopique du gène de fusion renforce la migration et l’invasion des cellules PC3c de manière dose-dépendante. Une étude transcriptomique a révélé que l’expression de certains gènes associés à la migration et l’invasion est dérégulée suite à l’expression du gène de fusion. Grâce à cette étude, de nouveaux gènes cibles de TMPRSS2 :ERG ont été mis en évidence dans les CaPs. L’identification de ces nouveaux gènes cibles renforce l’hypothèse d’un rôle du gène de fusion dans les métastases du cancer de la prostate. Par ailleurs, ces lignées de cellules cancéreuses prostatiques qui expriment stablement TMPRSS2 :ERG ont été injectées dans les tibias des souris SCID pour établir un modèle de métastases osseuses induites. Nous avons démontré que les cellules PC3c exprimant stablement le gène de fusion sont capables d’induire des lésions ostéocondensantes, tandis que les cellules témoins induisent des lésions mixtes (ostéolytiques et ostéocondensantes). Ce modèle nous a permis, pour la première fois, d’associer ce gène de fusion avec la formation des métastases osseuses du CaP in vivo.L’ensemble des résultats contribue à comprendre l’influence qualitative et quantitative de l’expression de TMPRSS2 :ERG dans les métastases du CaP
Prostate cancer (PCa) is one of the most common malignancies that affect men in western countries. Recurrent gene fusion, involving the ERG gene and the androgen-regulated TMPRSS2 gene promoter, occurs in over 50% of PCa. The TMPRSS2:ERG gene fusion results in aberrant ERG transcription factor expression in PCa. We and others have shown that the ERG transcription factor, a member of ETS family, is associated with embryonic skeleton development. Interestingly, some of the potential ERG-target genes, identified using high-throughput DNA microarray analysis, have implications in the physiological bone homeostasis or the pathological bone metastases development. Bone metastases are frequent and represent severe complications of PCa. This suggests a potential role of the TMPRSS2:ERG in PCa bone metastases.In this study, we used PC3c cells line (derived from PC3 cell line) to establish TMPRSS2:ERG-expressing clones cells. The ectopic expression of the fusion resulted in significant induction of cell migration and invasion in a dose-dependent manner. In agreement with this phenotype, high-throughput microarray analysis revealed that a set of genes, functionally associated with cell motility and invasiveness, were deregulated in a dose-dependent manner in TMPRSS2:ERG-expressing cells. Importantly, further analyses of these deregulated genes revealed that some of them are direct target genes of TMPRSS2:ERG in PCa. These results provide novel insights into the role of the TMPRSS2:ERG fusion in PCa metastasis. To test the hypothesis of the implication of ERG in bone metastases development, we used an experimental bone metastases induction model. The implantation of the TMPRSS2:ERG-expression PC3c cells in the tibia of the SCID mice induced osteoblastic bone lesions, whereas the control PC3c resulted in mixed bone lesions. Our results show, for the first time, the possible implication of TMPRSS2:ERG in CaP bone metastasis formation.To summarize, this study provided novel evidences of the role of TMPRSS2:ERG fusion in PCa metastasis
APA, Harvard, Vancouver, ISO, and other styles
7

Broadhurst, Jessica. "A novel mechanism underlying prostate cancer progression : an investigation into the impact of insulin like growth factors (IGFs), PTEN and IGFBP2 on TMPRSS2:ERG fusion induction." Thesis, University of Bristol, 2014. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.701807.

Full text
Abstract:
Prostate cancer (PC) is the most commonly diagnosed male cancer in the UK. The transmembrane protease serine 2 (TMPRSS2) gene has been found fused to the ETS related gene (ERG), which codes for an oncogenic transcription factor in 50% of PC cases. Fusion puts the coding sequence of ERG under the control of the androgen regulated promoter and enhancer of TMPRSS2, resulting in androgen regulated ERG expression. Androgen is present at high concentrations in the prostate and therefore drives high levels of ERG production, resulting in increase proliferation, metastasis and invasion. Several studies have shown that TMPRSS2:ERG fusion can be achieved in vitro by treating prostate cells with androgen alone or in combination with DNA damaging agents. Here fusion was optimised in LNCaP cells by treatment with the androgen, dihydrotestosterone (DHT) and the double strand break (DSB) inducing agent etoposide and detected at the genomic level using nested PCR. Induction ofTMPRSS2:ERG fusion was shown to be regulated by several different factors. The insulin like growth factor 1 (IGF-I), epidermal growth factor (EGF) and insulin were each found to substantially decrease the rat~ of fusion induction when treatment was combined with DHT and etoposide. Insulin like growth factor binding protein 2 (IGFBP-2) has been shown to function by both sequestering IGFs and by signalling independently of IGF via activation of integrin signalling. IGFBP-2 pre-treatment combined with DHT and etoposide dosing of LN CaP cells, was shown to up regulate the initial expression of the catalytic subunit of the DNA repair protein, DNA protein kinase (DNAPKcs), which was found to be associated with accelerated DSB repair and increased fusion induction. This observation was supported by IGFBP-2 knockdown data, which showed a decrease in the expression of DNAPKcs, associated with a slower rate of DSB repair and decreased fusion induction. These observations suggest that IGFBP-2 increases fusion induction by accelerating DNAPKcs mediated DSB repair. The presence of exogenous IGFBP-2 during fusion induction treatment gave rise to an increase in the expression of the forkhead box protein Al (FOXA1), which functions to open the chromatin allowing enzymes and receptors access to the DNA. This was supported by IGFBP-2 knockdown data, which showed a decrease in FOXAl expression following fusion induction. Previous studies in this laboratory have shown increased IGFBP-2 and FOXAllevels at increased glucose concentrations. Fusion induction was observed to increase at a higher glucose concentration compared to at a physiological glucose concentration, associated with an increase in both FOXAl and IGFBP-2 expression. This suggests that elevated glucose levels triggers increased IGFBP-2 and FOXAl expression resulting in a higher incidence of fusion. Together these data suggest that fusion induction is inhibited by EGF, IGF-I and insulin. Fusion induction is increased by IGFBP-2, potentially mediated by increased levels of FOXAl and accelerated DSB repair.
APA, Harvard, Vancouver, ISO, and other styles
8

Turpin, Anthony. "Étude des gènes réprimés par le récepteur aux androgènes dans les cancers de la prostate résistants à la castration et leur évolution neuroendocrine." Thesis, Lille, 2021. http://www.theses.fr/2021LILUS012.

Full text
Abstract:
Dans le cancer de la prostate, la présence de gènes de fusion, issus de remaniementschromosomiques TMPRSS2:ERG dans plus de 50% des cas, aboutit à une dérégulation dutranscriptome prostatique. Le récepteur aux androgènes (AR), membre de la famille desrécepteurs nucléaires, reste toutefois l’acteur majeur de l’évolution du cancer de la prostate.Notre objectif est d’identifier des gènes pouvant avoir un rôle dans l’évolution du cancerde la prostate, en lien avec la fusion TMPRSS2:ERG et AR.Par une analyse transcriptomique, à partir d’un modèle de surexpression de la fusionTMPRSS2:ERG dans une lignée de cellules tumorales prostatiques humaines (PC3c) capablesd'induire des lésions osseuses in vivo, nous avons identifié deux gènes régulés par la fusionparmi lesquels Plexine A2 (PLXNA2), déjà décrit par l’équipe (Tian et al. Oncogene.2014), etégalement Fascine-1 (FSCN1) codant pour une protéine qui permet de regrouper les filamentsd’actine et impliqué dans les phénomènes de migration et invasion tumorale grâce à laformation d’invadopodes. Nous avons recherché d’une part les partenaires fonctionnels dePLXNA2 en réalisant une étude in silico grâce au logiciel Ingenuity Pathway Analysis®, etavons identifié Neuropiline 1 (NRP1) comme potentiellement dérégulé par la fusion. D’autrepart nous avons évalué l’implication de FSCN1, associé à l’évolution de plusieurs cancers maisencore peu connu dans le cancer de la prostate.Pour chaque gène sélectionné nous avons déterminé, pour la validation clinique, leurexpression dans des échantillons humains de cancers de la prostate primitifs, également enanalysant des données de cohortes publiées et en suivant l’expression in vivo parimmunohistochimie dans des cancers avancés. D’autre part nous avons étudié leur rôlefonctionnel in vitro, dans des modèles cellulaires hormono-indépendants et neuroendocrines.Enfin, nous avons réalisé une analyse bioinformatique et recherché dans les données de ChIPseq-ERG et -AR publiées, l’existence de la fixation des facteurs ERG ou AR sur les 2 gènesNRP1 puis FSCN1. Une fois identifiée, nous avons réalisé des expériences de ChIP in vitro àpartir des modèles cellulaires dont nous disposons et nous avons mis en évidence la régulationdirecte de NRP1 puis de FSCN1 par AR.L’ensemble de nos résultats met en évidence NRP1 et FSCN1 comme gènes répriméspar AR, qui se ré-expriment en phase de résistance à la castration et acteurs potentiels de ladifférenciation neuroendocrine lorsque le niveau d’AR est bas ou inactif. Leur régulation par lafusion TMPRSS2:ERG et les mécanismes précis, en lien avec AR et ses cofacteurs restent àdémontrer. Ces deux gènes pourraient toutefois jouer un rôle dans les mécanismes derésistances aux hormonothérapies, et constituer à l’avenir des cibles thérapeutiques
The presence of fusion genes, resulting from TMPRSS2:ERG chromosomalrearrangements in more than 50% of cases, leads to deregulation of the prostate cancertranscriptome. Androgen receptor (AR), a member of the nuclear receptor family, remains themajor actor in the development of prostate cancer.Our objective is to identify genes that may be involved in the evolution of prostate cancer, in relation to the TMPRSS2:ERG fusion and AR.Using a transcriptomic analysis, derived from a PC3c prostate tumour cells line model over expressing TMPRSS2:ERG fusion, we have identified two genes regulated by the fusion:Plexin A2 (PLXNA2), already described in the literature by the team (Tian et al. Oncogene.2014), and also Fascin-1 (FSCN1) coding for a protein that groups actin filaments together and isinvolved in migration and tumour invasion phenomena through invadopods formation. Wesearched for functional partners of PLXNA2, performing an in silico study with Ingenuity Pathway Analysis® software, and have identified Neuropilin-1 (NRP1) as a potentially deregulated gene by fusion. On the other hand, we have evaluated the involvement of FSCN1,associated with the evolution of several cancers but poorly known in prostate cancer.For each selected gene, we have determined, for clinical validation, their expression inhuman samples of primary prostate cancers, also by analyzing published cohort data andmonitoring their expression in vivo by immunohistochemistry in advanced cancers. We havealso studied their functional role in vitro, in hormone-independent and neuroendocrine cellmodels. Finally, we performed a bioinformatics analysis and searched in the published ChIPseq-ERG and -AR data, the existence of ERG or AR factor binding on the 2 genes NRP1 andFSCN1. Once identified, we have performed in vitro ChIP experiments using the availablecellular models and we have demonstrated the direct regulation of NRP1 and FSCN1 by AR.Together, our results highlight NRP1 and FSCN1 as genes repressed by AR, which arere-expressed in the phase of resistance to castration and are potential actors of neuroendocrinedifferentiation when the level of AR is low or inactive. Their regulation by the TMPRSS2:ERGfusion and its precise mechanisms, in relation to AR and co-factors, need to be furtherdemonstrated. However, these two genes could play a role in the mechanisms of resistance tohormone-based therapies such as androgenic deprivation or selective competitive silentantagonist of AR, and could constitute therapeutic targets in the future
APA, Harvard, Vancouver, ISO, and other styles
9

De, Muga Salleras Silvia. "Estudi dels gens FGFR3, EGFR, PTEN, CXCR4 i del gen de fusió TMPRSS2-ERG en càncer de pròstata." Doctoral thesis, Universitat Autònoma de Barcelona, 2012. http://hdl.handle.net/10803/96816.

Full text
Abstract:
El càncer de pròstata és el tumor maligne no cutani més freqüent i una de les principals causes de mort per càncer en la població masculina. Tot i així, són menys els estudis moleculars realitzats sobre aquest tipus de càncer que en altres càncers (www.ncbi.nih.gov). L’objectiu de la tesi ha estat estudiar quins mecanismes moleculars estan implicats en la iniciació i progressió del càncer de pròstata. En el primer treball es va analitzar la freqüència de mutacions del gen FGFR3 ja que havien estat descrites mutacions d’aquest gen en altres tumors humans, però no en càncer de pròstata. També vam investigar la relació de mutacions de FGFR3 en pacients amb tumor de pròstata i altres tipus de tumors. Els nostres resultats indiquen que la freqüència de mutacions de FGFR3 en càncer de pròstata és baixa, per tant, no sembla ser un gen central en la patogènia del càncer de pròstata, tot i que està significativament associat a un grup de tumors de baix grau, i a pacients amb altres tumors concurrents, principalment bufeta i pell. En el segon treball es va analitzar, per primer cop en càncer de pròstata, les mutacions d’EGFR i PTEN conjuntament en un mateix grup de tumors. També es va analitzar l’expressió proteica i l’amplificació gènica d’EGFR. Vam trobar mutacions d’EGFR i PTEN en un nombre baix de tumors. Una tercera part dels adenocarcinomes prostàtics presentaven algun tipus d’alteració a la via de senyalització d’EGFR-PTEN, principalment en els càncers més avançats, sent la sobreexpressió proteica d’EGFR l’abnormalitat més freqüent. En un tercer article, enviat a la revista Human Pathology, s’ha analitzat la presència del gen de fusió TMPRSS2-ERG en els adenocarcinomes prostàtics, i la seva relació amb l’expressió de la proteïna d’ERG. Algun estudi havia descrit una associació entre el gen CXCR4 i l’expressió d’ERG, relacionada amb la fusió TMPRSS2-ERG. Nosaltres vam trobar que l’expressió d’ARNm de CXCR4 està associada amb tumors de pròstata amb elevat grau de Gleason, però és independent del reordenament TMPRSS2-ERG.
Prostate cancer is the most common non skin cancer in men and the second cause of cancer-related death in men of the Western World. Even so, the number of molecular studies in this type of cancer is lower than other types of cancer (www.ncbi.nih.gov). The aim of this work has been to study the molecular mechanisms that are involved in the initiation and progression of prostate cancer. In the first study, we have analyzed the frequency of FGFR3 mutations, as mutations of this gene have been reported in other human tumors, but not in prostate cancer. We have also investigated the relationship between FGFR3 mutations in patients with prostate cancer and other tumors. Our results show that the frequency of FGFR3 mutations in prostate cancer is low, so it does not seem to be central in the pathogenesis of prostate cancer, but it is statistically associated with a subpopulation of low grade tumors, and also with a subset of prostate carcinomas found incidentally in patients with concurrent bladder cancer or skin tumors. In the second study, we have analyzed, for the first time in prostate cancer, EGFR and PTEN mutations in the same subset of prostate tumors. We have also analyzed EGFR protein expression and amplification. We found EGFR or PTEN mutations in a low number of tumors. A third of prostate adenocarcinomas, mainly the most advanced tumors, showed some kind of alteration in the EGFR-PTEN signalling pathway, being EGFR protein overexpression the most frequent abnormality. In the third article, sent to Human Pathology, we have analyzed the presence of TMPRSS2-ERG fusion in prostate adenocarcinomas, and its relationship with ERG protein expression. Several studies have reported an association between CXCR4 gene and ERG expression, related to the TMPRSS2-ERG fusion. We have found an association between mRNA CXCR4 and high grade prostate tumors, but not between CXCR4 expression and the TMPRSS2-ERG rearrangement.
APA, Harvard, Vancouver, ISO, and other styles
10

Nottelmann, Mariné Andrea [Verfasser]. "Functional relevance of the candidate genes MSMB, NCOA4, TIMM23 and PARG in the prostate cancer risk region 10q11 for the emergence of oncogenic TMPRSS2:ERG fusions / Andrea Nottelmann Mariné." Ulm : Universität Ulm, 2016. http://d-nb.info/1110969481/34.

Full text
APA, Harvard, Vancouver, ISO, and other styles

Books on the topic "Fusion TMPRSS2:ERG"

1

Alves, Ines Teles, Jan Trapman, and Guido Jenster. Molecular biology of prostate cancer. Edited by James W. F. Catto. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199659579.003.0059.

Full text
Abstract:
Prostate cancer is a heterogeneous disease that arises through the acquisition of key malignant hallmarks. At the molecular level, prostate tumours are dependent upon the androgen receptor pathway, which affects cell function, growth, and behaviour through downstream androgen-regulated genes. Prostate cancer requires this activity and manipulates the AR pathway to maintain signalling. For example, mutation of the AR (to bind ligands other than androgens) or amplification/duplication of the AR allows signalling to continue in the absence of testosterone. Around 50% of prostate cancers have a gene fusion between the androgen-regulated component of the TMPRSS2 gene and a transcription factor (e.g. ETS family members ERG and ETV1). This results in aberrant androgen stimulated cell growth. Current research is using molecular knowledge to identify biomarkers, such as PCA3, and new therapies, such as enzalutamide or abiraterone acetate.
APA, Harvard, Vancouver, ISO, and other styles

Book chapters on the topic "Fusion TMPRSS2:ERG"

1

Wang, Jianghua, Michael Ittmann, and Yi Cai. "TMPRSS2/ERG Fusions." In Encyclopedia of Cancer, 3706–8. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-16483-5_5839.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Wang, Jianghua, Yi Cai, and Michael Ittmann. "TMPRSS2/ERG Fusions." In Encyclopedia of Cancer, 1–3. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-27841-9_5839-2.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Wang, Jianghua, Yi Cai, and Michael Ittmann. "TMPRSS2/ERG Fusions." In Encyclopedia of Cancer, 4563–65. Berlin, Heidelberg: Springer Berlin Heidelberg, 2017. http://dx.doi.org/10.1007/978-3-662-46875-3_5839.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Rathinavelu, Appu, and Arkene Levy. "Key Genes in Prostate Cancer Progression: Role of MDM2, PTEN, and TMPRSS2-ERG Fusions." In Prostate Cancer - Leading-edge Diagnostic Procedures and Treatments. InTech, 2016. http://dx.doi.org/10.5772/64337.

Full text
APA, Harvard, Vancouver, ISO, and other styles

Conference papers on the topic "Fusion TMPRSS2:ERG"

1

Delliaux, Carine, Tian V. Tian, Mathilde Bouchet, Anaïs Fradet, Nathalie Vanpouille, Anne Flourens, Rachel Deplus, et al. "Abstract 1691: TMPRSS2:ERG fusion enhances osteoblastic phenotype of prostate cancer bone metastases." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-1691.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Ahearn, Thomas, Rebecca E. Graff, Andreas Pettersson, Claire Pernar, Sarah C. Markt, Kathryn M. Wilson, Michelangelo Fiorentino, Massimo Loda, Edward L. Giovannucci, and Lorelei A. Mucci. "Abstract 1763: Body size and incidence of TMPRSS2:ERG fusion-positive and fusion-negative prostate cancer." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-1763.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Yamoah, Kosj, Shivanshu Awasthi, Priti Lal, Arash O. Naghavi, Shelly Mahajan, Jong Y. Park, Rob Rounbehler, et al. "Abstract 1568: Clinical implications of tmprss2-erg fusion and tumor location in prostate cancer." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-1568.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Yamoah, Kosj, Shivanshu Awasthi, Priti Lal, Arash O. Naghavi, Shelly Mahajan, Jong Y. Park, Rob Rounbehler, et al. "Abstract 1568: Clinical implications of tmprss2-erg fusion and tumor location in prostate cancer." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-1568.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Graff, Rebecca E., Azra H. Ligon, Catherine Suppan, Richard Flavin, Howard D. Sesso, Jennifer R. Rider, Christopher Sweeney, et al. "Abstract A29: The TMPRSS2:ERG gene fusion, ERG expression and prostate cancer outcomes: A cohort study and meta-analysis." In Abstracts: AACR International Conference on Frontiers in Cancer Prevention Research‐‐ Oct 22-25, 2011; Boston, MA. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1940-6207.prev-11-a29.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Almami, Amal A. "Abstract 1686: Identification of potential prostate cancer biomarkers associated with TMPRSS2-ERG fusion and PTEN deletions." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-1686.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Bhasin, Manoj, Bin Lu, and M. Simo Arredouani. "Abstract A31: Human prostate cancer transcriptome reveals distinct signaling pathway dysregulations associated with TMPRSS2:ERG fusion." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Nov 15-19, 2009; Boston, MA. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/1535-7163.targ-09-a31.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Zammarchi, Francesca, George Boutsalis, William Gerald, and Luca Cartegni. "Abstract A70: Oncogenic potential of multiple splicing isoforms of the prostate‐cancer specific TMPRSS2‐ERG gene fusion product." In Abstracts: First AACR International Conference on Frontiers in Basic Cancer Research--Oct 8–11, 2009; Boston MA. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/0008-5472.fbcr09-a70.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Minner, Sarah Jane Pauline, Hueseyin Sirma, Ronald Simon, Antje Krohn, Eike Burandt, Pierre Tennstedt, Michael Becker, et al. "Abstract 3809: TMPRSS2-ERG gene fusion is strongly associated with elevated androgen receptor expression in early prostate cancer." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-3809.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Bastus, Nuria Coll, Yong-Jie Lu, Lara K. Boyd, Xueying Mao, Elzbieta Stankiewicz, Sakunthala C. Kudahetti, Tim D. Oliver, and Daniel M. Berney. "Abstract 3048: Enhanced androgen signalling pathway increases the risk of prostate cancer through induction of TMPRSS2:ERG fusion." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-3048.

Full text
APA, Harvard, Vancouver, ISO, and other styles

Reports on the topic "Fusion TMPRSS2:ERG"

1

Wang, Jianghua. Biological Effects of TMPRSS2/ERG Fusion Isoforms in Human Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, February 2009. http://dx.doi.org/10.21236/ada499922.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Ozpolat, Bulent, and Michael Ittmann. Highly Specific Targeting of the TMPRSS2/ERG Fusion Gene in Prostate Cancer Using Liposomal Nanotechnology. Fort Belvoir, VA: Defense Technical Information Center, June 2013. http://dx.doi.org/10.21236/ada585108.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Ozpolat, Bulent, and Michael Ittmann. Highly Specific Targeting of the TMPRSS2/ERG Fusion Gene in Prostate Cancer Using Liposomal Nanotechnology. Fort Belvoir, VA: Defense Technical Information Center, June 2011. http://dx.doi.org/10.21236/ada549160.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Ozpolat, Bulent, and Michael Ittmann. Highly Specific Targeting of the TMPRSS2/ERG Fusion Gene In Prostate Cancer Using Liposomal Nanotechnology. Fort Belvoir, VA: Defense Technical Information Center, June 2011. http://dx.doi.org/10.21236/ada549484.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Litovchick, Larisa. Functional Characterization of the Protein Product of the Prostate Carcinoma Gene Fusion TMPRSS2:ERG Using the Proteomic and Microarray Analyses. Fort Belvoir, VA: Defense Technical Information Center, July 2009. http://dx.doi.org/10.21236/ada509751.

Full text
APA, Harvard, Vancouver, ISO, and other styles
You might also be interested in the extended bibliographies on the topic 'Fusion TMPRSS2:ERG' for particular source types:
Journal articles
We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!

To the bibliography