The Experts below are selected from a list of 44661 Experts worldwide ranked by ideXlab platform
M Von Bergen - One of the best experts on this subject based on the ideXlab platform.
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mir 130a mir 203 and mir 205 jointly repress key oncogenic pathways and are downregulated in Prostate Carcinoma
Oncogene, 2013Co-Authors: K Boll, Jack A. Schalken, Kristin Reiche, Katharina Kasack, N Morbt, Antje K Kretzschmar, Janina M Tomm, Gerald W Verhaegh, M Von BergenAbstract:MiR-130a, miR-203 and miR-205 jointly repress key oncogenic pathways and are downregulated in Prostate Carcinoma
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MiR-130a, miR-203 and miR-205 jointly repress key oncogenic pathways and are downregulated in Prostate Carcinoma
Oncogene, 2013Co-Authors: K Boll, Kristin Reiche, Katharina Kasack, N Morbt, Antje K Kretzschmar, Janina M Tomm, Gerald W Verhaegh, M Von Bergen, J Schalken, F HornAbstract:With ∼30 000 deaths annually in the United States, Prostate cancer (PCa) is a major oncologic disease. Here we show that the microRNAs miR-130a, miR-203 and miR-205 jointly interfere with the two major oncogenic pathways in Prostate Carcinoma and are downregulated in cancer tissue. Using transcriptomics we show that the microRNAs repress several gene products known to be overexpressed in this cancer. Argonaute 2 (AGO2) co-immunoprecipitation, reporter assays and western blot analysis demonstrate that the microRNAs directly target several components of the mitogen-activated protein kinase (MAPK) and androgen receptor (AR) signaling pathways, among those several AR coregulators and HRAS (Harvey rat sarcoma viral oncogene homolog), and repress signaling activity. Both pathways are central for the development of the primary tumor and in particular the progression to its incurable castration-resistant form. Reconstitution of the microRNAs in LNCaP PCa cells induce morphological changes, which resemble the effect of androgen deprivation, and jointly impair tumor cell growth by induction of apoptosis and cell cycle arrest. We therefore propose that these microRNAs jointly act as tumor suppressors in Prostate Carcinoma and might interfere with progression to castration resistance.
Kristin Reiche - One of the best experts on this subject based on the ideXlab platform.
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mir 130a mir 203 and mir 205 jointly repress key oncogenic pathways and are downregulated in Prostate Carcinoma
Oncogene, 2013Co-Authors: K Boll, Jack A. Schalken, Kristin Reiche, Katharina Kasack, N Morbt, Antje K Kretzschmar, Janina M Tomm, Gerald W Verhaegh, M Von BergenAbstract:MiR-130a, miR-203 and miR-205 jointly repress key oncogenic pathways and are downregulated in Prostate Carcinoma
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MiR-130a, miR-203 and miR-205 jointly repress key oncogenic pathways and are downregulated in Prostate Carcinoma
Oncogene, 2013Co-Authors: K Boll, Kristin Reiche, Katharina Kasack, N Morbt, Antje K Kretzschmar, Janina M Tomm, Gerald W Verhaegh, M Von Bergen, J Schalken, F HornAbstract:With ∼30 000 deaths annually in the United States, Prostate cancer (PCa) is a major oncologic disease. Here we show that the microRNAs miR-130a, miR-203 and miR-205 jointly interfere with the two major oncogenic pathways in Prostate Carcinoma and are downregulated in cancer tissue. Using transcriptomics we show that the microRNAs repress several gene products known to be overexpressed in this cancer. Argonaute 2 (AGO2) co-immunoprecipitation, reporter assays and western blot analysis demonstrate that the microRNAs directly target several components of the mitogen-activated protein kinase (MAPK) and androgen receptor (AR) signaling pathways, among those several AR coregulators and HRAS (Harvey rat sarcoma viral oncogene homolog), and repress signaling activity. Both pathways are central for the development of the primary tumor and in particular the progression to its incurable castration-resistant form. Reconstitution of the microRNAs in LNCaP PCa cells induce morphological changes, which resemble the effect of androgen deprivation, and jointly impair tumor cell growth by induction of apoptosis and cell cycle arrest. We therefore propose that these microRNAs jointly act as tumor suppressors in Prostate Carcinoma and might interfere with progression to castration resistance.
K Boll - One of the best experts on this subject based on the ideXlab platform.
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mir 130a mir 203 and mir 205 jointly repress key oncogenic pathways and are downregulated in Prostate Carcinoma
Oncogene, 2013Co-Authors: K Boll, Jack A. Schalken, Kristin Reiche, Katharina Kasack, N Morbt, Antje K Kretzschmar, Janina M Tomm, Gerald W Verhaegh, M Von BergenAbstract:MiR-130a, miR-203 and miR-205 jointly repress key oncogenic pathways and are downregulated in Prostate Carcinoma
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MiR-130a, miR-203 and miR-205 jointly repress key oncogenic pathways and are downregulated in Prostate Carcinoma
Oncogene, 2013Co-Authors: K Boll, Kristin Reiche, Katharina Kasack, N Morbt, Antje K Kretzschmar, Janina M Tomm, Gerald W Verhaegh, M Von Bergen, J Schalken, F HornAbstract:With ∼30 000 deaths annually in the United States, Prostate cancer (PCa) is a major oncologic disease. Here we show that the microRNAs miR-130a, miR-203 and miR-205 jointly interfere with the two major oncogenic pathways in Prostate Carcinoma and are downregulated in cancer tissue. Using transcriptomics we show that the microRNAs repress several gene products known to be overexpressed in this cancer. Argonaute 2 (AGO2) co-immunoprecipitation, reporter assays and western blot analysis demonstrate that the microRNAs directly target several components of the mitogen-activated protein kinase (MAPK) and androgen receptor (AR) signaling pathways, among those several AR coregulators and HRAS (Harvey rat sarcoma viral oncogene homolog), and repress signaling activity. Both pathways are central for the development of the primary tumor and in particular the progression to its incurable castration-resistant form. Reconstitution of the microRNAs in LNCaP PCa cells induce morphological changes, which resemble the effect of androgen deprivation, and jointly impair tumor cell growth by induction of apoptosis and cell cycle arrest. We therefore propose that these microRNAs jointly act as tumor suppressors in Prostate Carcinoma and might interfere with progression to castration resistance.
Mark M Goodman - One of the best experts on this subject based on the ideXlab platform.
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detection of recurrent Prostate Carcinoma with anti 1 amino 3 18f fluorocyclobutane 1 carboxylic acid pet ct and 111in capromab pendetide spect ct
Radiology, 2011Co-Authors: David M Schuster, Peter T Nieh, Weiping Yu, Viraj A Master, Dubois F Bowman, Bital Savirbaruch, Raghuveer Halkar, Peter J Rossi, Melinda M Lewis, Mark M GoodmanAbstract:anti-1-amino-3-fluorine 18-fluorocyclobutane-1-carboxylic acid PET/CT is more sensitive than 111In–capromab pendetide SPECT/CT in the detection of recurrent Prostate Carcinoma in the prostatic bed and extraprostatic sites.
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initial experience with the radiotracer anti 1 amino 3 18f fluorocyclobutane 1 carboxylic acid with pet ct in Prostate Carcinoma
The Journal of Nuclear Medicine, 2007Co-Authors: David M Schuster, John R Votaw, Peter T Nieh, Weiping Yu, Viraj A Master, Dubois F Bowman, Muta M Issa, Mark M GoodmanAbstract:Conventional imaging techniques have serious limitations in the detection, staging, and restaging of Prostate Carcinoma. Anti1-amino-3-18F-fluorocyclobutane-1-carboxylicacid(anti-18F-FACBC) is a synthetic L-leucine analog that has excellent in vitro uptake within the DU-145 Prostate Carcinoma cell line and orthotopically implanted Prostate tumor in nude rats. There is little renal excretion compared with 18 F-FDG. The present study examines anti- 18 F-FACBC uptake in patients with newly diagnosed and recurrent Prostate Carcinoma. Methods: Fifteen patients with a recent diagnosis of Prostate Carcinoma (n 5 9) or suspected recurrence (n 5 6) underwent 65-min dynamic PET/CT of the pelvis after intravenous injection of 300‐410 MBq anti-18F-FACBC followed by static body images. Each study wasevaluatedqualitativelyandquantitatively.Maximumstandardized uptake values were recorded in the Prostate or Prostate bed, and within lymph nodes at 4.5 min (early) and 20 min (delayed), and correlated with clinical, imaging and pathologic follow-up. Time‐activity curveswerealsogeneratedforbenignandmalignanttissue.Results:
Gerald W Verhaegh - One of the best experts on this subject based on the ideXlab platform.
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mir 130a mir 203 and mir 205 jointly repress key oncogenic pathways and are downregulated in Prostate Carcinoma
Oncogene, 2013Co-Authors: K Boll, Jack A. Schalken, Kristin Reiche, Katharina Kasack, N Morbt, Antje K Kretzschmar, Janina M Tomm, Gerald W Verhaegh, M Von BergenAbstract:MiR-130a, miR-203 and miR-205 jointly repress key oncogenic pathways and are downregulated in Prostate Carcinoma
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MiR-130a, miR-203 and miR-205 jointly repress key oncogenic pathways and are downregulated in Prostate Carcinoma
Oncogene, 2013Co-Authors: K Boll, Kristin Reiche, Katharina Kasack, N Morbt, Antje K Kretzschmar, Janina M Tomm, Gerald W Verhaegh, M Von Bergen, J Schalken, F HornAbstract:With ∼30 000 deaths annually in the United States, Prostate cancer (PCa) is a major oncologic disease. Here we show that the microRNAs miR-130a, miR-203 and miR-205 jointly interfere with the two major oncogenic pathways in Prostate Carcinoma and are downregulated in cancer tissue. Using transcriptomics we show that the microRNAs repress several gene products known to be overexpressed in this cancer. Argonaute 2 (AGO2) co-immunoprecipitation, reporter assays and western blot analysis demonstrate that the microRNAs directly target several components of the mitogen-activated protein kinase (MAPK) and androgen receptor (AR) signaling pathways, among those several AR coregulators and HRAS (Harvey rat sarcoma viral oncogene homolog), and repress signaling activity. Both pathways are central for the development of the primary tumor and in particular the progression to its incurable castration-resistant form. Reconstitution of the microRNAs in LNCaP PCa cells induce morphological changes, which resemble the effect of androgen deprivation, and jointly impair tumor cell growth by induction of apoptosis and cell cycle arrest. We therefore propose that these microRNAs jointly act as tumor suppressors in Prostate Carcinoma and might interfere with progression to castration resistance.
