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Isabell A Sesterhenn - One of the best experts on this subject based on the ideXlab platform.

  • Mapping of TMPRSS2–ERG fusions in the context of multi-focal prostate Cancer
    Modern Pathology, 2008
    Co-Authors: Bungo Furusato, Lakshmi Ravindranath, Yongmei Chen, Jennifer Cullen, David G Mcleod, Albert Dobi, Shiv Srivastava, Gyorgy Petrovics, Isabell A Sesterhenn
    Abstract:

    TMPRSS2–ERG gene fusion leading to the androgenic induction of the ERG proto-oncogene expression is a highly prevalent oncogenic alteration in prostate tumor cells. Prostate Cancer is a multi-focal disease, and the origins as well as biological contribution of Multiple Cancer foci remain unclear with respect to prostate Cancer onset or progression. To assess the role of TMPRSS2–ERG alteration in prostate Cancer onset and/or progression, we have evaluated the status of fusion transcripts in benign glands, prostatic intraepithelial neoplasia (PIN) and Multiple Cancer foci of each prostate. Quantitative expression of TMPRSS2–ERG fusion type A and C transcripts was analyzed in benign, tumor and PIN areas, selected from whole-mount radical prostatectomy slides. TMPRSS2–ERG expression was correlated with clinicopathological features. Overall, 30 of 45 (67%) patients exhibited TMPRSS2–ERG fusion transcripts in at least one tumor focus. Of 80 tumor foci analyzed, 39 had TMPRSS2–ERG fusion (type A only: 30, type C only: 2, both types A and C: 7), with predominant detection of the TMPRSS2–ERG fusion type A (27/30, 90%) in the index tumors. Of 14 PIN lesions, 2 were positive for type A fusion. Frequent presence of the TMPRSS2–ERG in index tumors suggests critical roles of ERG alterations in the onset and progression of a large subset of prostate Cancer. However, heterogeneity of the TMPRSS2–ERG detection in the context of Multiple Cancer foci and its frequency in PIN also support the role of other genomic alterations in the origins of prostate Cancer.

  • mapping of tmprss2 erg fusions in the context of multi focal prostate Cancer
    Modern Pathology, 2008
    Co-Authors: Bungo Furusato, Lakshmi Ravindranath, Yongmei Chen, Jennifer Cullen, David G Mcleod, Albert Dobi, Shiv Srivastava, Gyorgy Petrovics, Isabell A Sesterhenn
    Abstract:

    TMPRSS2–ERG gene fusion leading to the androgenic induction of the ERG proto-oncogene expression is a highly prevalent oncogenic alteration in prostate tumor cells. Prostate Cancer is a multi-focal disease, and the origins as well as biological contribution of Multiple Cancer foci remain unclear with respect to prostate Cancer onset or progression. To assess the role of TMPRSS2–ERG alteration in prostate Cancer onset and/or progression, we have evaluated the status of fusion transcripts in benign glands, prostatic intraepithelial neoplasia (PIN) and Multiple Cancer foci of each prostate. Quantitative expression of TMPRSS2–ERG fusion type A and C transcripts was analyzed in benign, tumor and PIN areas, selected from whole-mount radical prostatectomy slides. TMPRSS2–ERG expression was correlated with clinicopathological features. Overall, 30 of 45 (67%) patients exhibited TMPRSS2–ERG fusion transcripts in at least one tumor focus. Of 80 tumor foci analyzed, 39 had TMPRSS2–ERG fusion (type A only: 30, type C only: 2, both types A and C: 7), with predominant detection of the TMPRSS2–ERG fusion type A (27/30, 90%) in the index tumors. Of 14 PIN lesions, 2 were positive for type A fusion. Frequent presence of the TMPRSS2–ERG in index tumors suggests critical roles of ERG alterations in the onset and progression of a large subset of prostate Cancer. However, heterogeneity of the TMPRSS2–ERG detection in the context of Multiple Cancer foci and its frequency in PIN also support the role of other genomic alterations in the origins of prostate Cancer.

Martin E Hemler - One of the best experts on this subject based on the ideXlab platform.

  • tetraspanin proteins promote Multiple Cancer stages
    Nature Reviews Cancer, 2014
    Co-Authors: Martin E Hemler
    Abstract:

    This Review discusses recent evidence, particularly from mouse models, showing that some tetraspanin proteins have important roles in tumour initiation, promotion, metastasis and angiogenesis, and that they might therefore be valid therapeutic targets.

  • tetraspanin proteins promote Multiple Cancer stages
    Nature Reviews Cancer, 2014
    Co-Authors: Martin E Hemler
    Abstract:

    An abundance of evidence shows supporting roles for tetraspanin proteins in human Cancer. Many studies show that the expression of tetraspanins correlates with tumour stage, tumour type and patient outcome. In addition, perturbations of tetraspanins in tumour cell lines can considerably affect cell growth, morphology, invasion, tumour engraftment and metastasis. This Review emphasizes new studies that have used de novo mouse Cancer models to show that select tetraspanin proteins have key roles in tumour initiation, promotion and metastasis. This Review also emphasizes how tetraspanin proteins can sometimes participate in tumour angiogenesis. These recent data build an increasingly strong case for tetraspanins as therapeutic targets.

Bungo Furusato - One of the best experts on this subject based on the ideXlab platform.

  • Mapping of TMPRSS2–ERG fusions in the context of multi-focal prostate Cancer
    Modern Pathology, 2008
    Co-Authors: Bungo Furusato, Lakshmi Ravindranath, Yongmei Chen, Jennifer Cullen, David G Mcleod, Albert Dobi, Shiv Srivastava, Gyorgy Petrovics, Isabell A Sesterhenn
    Abstract:

    TMPRSS2–ERG gene fusion leading to the androgenic induction of the ERG proto-oncogene expression is a highly prevalent oncogenic alteration in prostate tumor cells. Prostate Cancer is a multi-focal disease, and the origins as well as biological contribution of Multiple Cancer foci remain unclear with respect to prostate Cancer onset or progression. To assess the role of TMPRSS2–ERG alteration in prostate Cancer onset and/or progression, we have evaluated the status of fusion transcripts in benign glands, prostatic intraepithelial neoplasia (PIN) and Multiple Cancer foci of each prostate. Quantitative expression of TMPRSS2–ERG fusion type A and C transcripts was analyzed in benign, tumor and PIN areas, selected from whole-mount radical prostatectomy slides. TMPRSS2–ERG expression was correlated with clinicopathological features. Overall, 30 of 45 (67%) patients exhibited TMPRSS2–ERG fusion transcripts in at least one tumor focus. Of 80 tumor foci analyzed, 39 had TMPRSS2–ERG fusion (type A only: 30, type C only: 2, both types A and C: 7), with predominant detection of the TMPRSS2–ERG fusion type A (27/30, 90%) in the index tumors. Of 14 PIN lesions, 2 were positive for type A fusion. Frequent presence of the TMPRSS2–ERG in index tumors suggests critical roles of ERG alterations in the onset and progression of a large subset of prostate Cancer. However, heterogeneity of the TMPRSS2–ERG detection in the context of Multiple Cancer foci and its frequency in PIN also support the role of other genomic alterations in the origins of prostate Cancer.

  • mapping of tmprss2 erg fusions in the context of multi focal prostate Cancer
    Modern Pathology, 2008
    Co-Authors: Bungo Furusato, Lakshmi Ravindranath, Yongmei Chen, Jennifer Cullen, David G Mcleod, Albert Dobi, Shiv Srivastava, Gyorgy Petrovics, Isabell A Sesterhenn
    Abstract:

    TMPRSS2–ERG gene fusion leading to the androgenic induction of the ERG proto-oncogene expression is a highly prevalent oncogenic alteration in prostate tumor cells. Prostate Cancer is a multi-focal disease, and the origins as well as biological contribution of Multiple Cancer foci remain unclear with respect to prostate Cancer onset or progression. To assess the role of TMPRSS2–ERG alteration in prostate Cancer onset and/or progression, we have evaluated the status of fusion transcripts in benign glands, prostatic intraepithelial neoplasia (PIN) and Multiple Cancer foci of each prostate. Quantitative expression of TMPRSS2–ERG fusion type A and C transcripts was analyzed in benign, tumor and PIN areas, selected from whole-mount radical prostatectomy slides. TMPRSS2–ERG expression was correlated with clinicopathological features. Overall, 30 of 45 (67%) patients exhibited TMPRSS2–ERG fusion transcripts in at least one tumor focus. Of 80 tumor foci analyzed, 39 had TMPRSS2–ERG fusion (type A only: 30, type C only: 2, both types A and C: 7), with predominant detection of the TMPRSS2–ERG fusion type A (27/30, 90%) in the index tumors. Of 14 PIN lesions, 2 were positive for type A fusion. Frequent presence of the TMPRSS2–ERG in index tumors suggests critical roles of ERG alterations in the onset and progression of a large subset of prostate Cancer. However, heterogeneity of the TMPRSS2–ERG detection in the context of Multiple Cancer foci and its frequency in PIN also support the role of other genomic alterations in the origins of prostate Cancer.

Shiv Srivastava - One of the best experts on this subject based on the ideXlab platform.

  • Mapping of TMPRSS2–ERG fusions in the context of multi-focal prostate Cancer
    Modern Pathology, 2008
    Co-Authors: Bungo Furusato, Lakshmi Ravindranath, Yongmei Chen, Jennifer Cullen, David G Mcleod, Albert Dobi, Shiv Srivastava, Gyorgy Petrovics, Isabell A Sesterhenn
    Abstract:

    TMPRSS2–ERG gene fusion leading to the androgenic induction of the ERG proto-oncogene expression is a highly prevalent oncogenic alteration in prostate tumor cells. Prostate Cancer is a multi-focal disease, and the origins as well as biological contribution of Multiple Cancer foci remain unclear with respect to prostate Cancer onset or progression. To assess the role of TMPRSS2–ERG alteration in prostate Cancer onset and/or progression, we have evaluated the status of fusion transcripts in benign glands, prostatic intraepithelial neoplasia (PIN) and Multiple Cancer foci of each prostate. Quantitative expression of TMPRSS2–ERG fusion type A and C transcripts was analyzed in benign, tumor and PIN areas, selected from whole-mount radical prostatectomy slides. TMPRSS2–ERG expression was correlated with clinicopathological features. Overall, 30 of 45 (67%) patients exhibited TMPRSS2–ERG fusion transcripts in at least one tumor focus. Of 80 tumor foci analyzed, 39 had TMPRSS2–ERG fusion (type A only: 30, type C only: 2, both types A and C: 7), with predominant detection of the TMPRSS2–ERG fusion type A (27/30, 90%) in the index tumors. Of 14 PIN lesions, 2 were positive for type A fusion. Frequent presence of the TMPRSS2–ERG in index tumors suggests critical roles of ERG alterations in the onset and progression of a large subset of prostate Cancer. However, heterogeneity of the TMPRSS2–ERG detection in the context of Multiple Cancer foci and its frequency in PIN also support the role of other genomic alterations in the origins of prostate Cancer.

  • mapping of tmprss2 erg fusions in the context of multi focal prostate Cancer
    Modern Pathology, 2008
    Co-Authors: Bungo Furusato, Lakshmi Ravindranath, Yongmei Chen, Jennifer Cullen, David G Mcleod, Albert Dobi, Shiv Srivastava, Gyorgy Petrovics, Isabell A Sesterhenn
    Abstract:

    TMPRSS2–ERG gene fusion leading to the androgenic induction of the ERG proto-oncogene expression is a highly prevalent oncogenic alteration in prostate tumor cells. Prostate Cancer is a multi-focal disease, and the origins as well as biological contribution of Multiple Cancer foci remain unclear with respect to prostate Cancer onset or progression. To assess the role of TMPRSS2–ERG alteration in prostate Cancer onset and/or progression, we have evaluated the status of fusion transcripts in benign glands, prostatic intraepithelial neoplasia (PIN) and Multiple Cancer foci of each prostate. Quantitative expression of TMPRSS2–ERG fusion type A and C transcripts was analyzed in benign, tumor and PIN areas, selected from whole-mount radical prostatectomy slides. TMPRSS2–ERG expression was correlated with clinicopathological features. Overall, 30 of 45 (67%) patients exhibited TMPRSS2–ERG fusion transcripts in at least one tumor focus. Of 80 tumor foci analyzed, 39 had TMPRSS2–ERG fusion (type A only: 30, type C only: 2, both types A and C: 7), with predominant detection of the TMPRSS2–ERG fusion type A (27/30, 90%) in the index tumors. Of 14 PIN lesions, 2 were positive for type A fusion. Frequent presence of the TMPRSS2–ERG in index tumors suggests critical roles of ERG alterations in the onset and progression of a large subset of prostate Cancer. However, heterogeneity of the TMPRSS2–ERG detection in the context of Multiple Cancer foci and its frequency in PIN also support the role of other genomic alterations in the origins of prostate Cancer.

David G Mcleod - One of the best experts on this subject based on the ideXlab platform.

  • Mapping of TMPRSS2–ERG fusions in the context of multi-focal prostate Cancer
    Modern Pathology, 2008
    Co-Authors: Bungo Furusato, Lakshmi Ravindranath, Yongmei Chen, Jennifer Cullen, David G Mcleod, Albert Dobi, Shiv Srivastava, Gyorgy Petrovics, Isabell A Sesterhenn
    Abstract:

    TMPRSS2–ERG gene fusion leading to the androgenic induction of the ERG proto-oncogene expression is a highly prevalent oncogenic alteration in prostate tumor cells. Prostate Cancer is a multi-focal disease, and the origins as well as biological contribution of Multiple Cancer foci remain unclear with respect to prostate Cancer onset or progression. To assess the role of TMPRSS2–ERG alteration in prostate Cancer onset and/or progression, we have evaluated the status of fusion transcripts in benign glands, prostatic intraepithelial neoplasia (PIN) and Multiple Cancer foci of each prostate. Quantitative expression of TMPRSS2–ERG fusion type A and C transcripts was analyzed in benign, tumor and PIN areas, selected from whole-mount radical prostatectomy slides. TMPRSS2–ERG expression was correlated with clinicopathological features. Overall, 30 of 45 (67%) patients exhibited TMPRSS2–ERG fusion transcripts in at least one tumor focus. Of 80 tumor foci analyzed, 39 had TMPRSS2–ERG fusion (type A only: 30, type C only: 2, both types A and C: 7), with predominant detection of the TMPRSS2–ERG fusion type A (27/30, 90%) in the index tumors. Of 14 PIN lesions, 2 were positive for type A fusion. Frequent presence of the TMPRSS2–ERG in index tumors suggests critical roles of ERG alterations in the onset and progression of a large subset of prostate Cancer. However, heterogeneity of the TMPRSS2–ERG detection in the context of Multiple Cancer foci and its frequency in PIN also support the role of other genomic alterations in the origins of prostate Cancer.

  • mapping of tmprss2 erg fusions in the context of multi focal prostate Cancer
    Modern Pathology, 2008
    Co-Authors: Bungo Furusato, Lakshmi Ravindranath, Yongmei Chen, Jennifer Cullen, David G Mcleod, Albert Dobi, Shiv Srivastava, Gyorgy Petrovics, Isabell A Sesterhenn
    Abstract:

    TMPRSS2–ERG gene fusion leading to the androgenic induction of the ERG proto-oncogene expression is a highly prevalent oncogenic alteration in prostate tumor cells. Prostate Cancer is a multi-focal disease, and the origins as well as biological contribution of Multiple Cancer foci remain unclear with respect to prostate Cancer onset or progression. To assess the role of TMPRSS2–ERG alteration in prostate Cancer onset and/or progression, we have evaluated the status of fusion transcripts in benign glands, prostatic intraepithelial neoplasia (PIN) and Multiple Cancer foci of each prostate. Quantitative expression of TMPRSS2–ERG fusion type A and C transcripts was analyzed in benign, tumor and PIN areas, selected from whole-mount radical prostatectomy slides. TMPRSS2–ERG expression was correlated with clinicopathological features. Overall, 30 of 45 (67%) patients exhibited TMPRSS2–ERG fusion transcripts in at least one tumor focus. Of 80 tumor foci analyzed, 39 had TMPRSS2–ERG fusion (type A only: 30, type C only: 2, both types A and C: 7), with predominant detection of the TMPRSS2–ERG fusion type A (27/30, 90%) in the index tumors. Of 14 PIN lesions, 2 were positive for type A fusion. Frequent presence of the TMPRSS2–ERG in index tumors suggests critical roles of ERG alterations in the onset and progression of a large subset of prostate Cancer. However, heterogeneity of the TMPRSS2–ERG detection in the context of Multiple Cancer foci and its frequency in PIN also support the role of other genomic alterations in the origins of prostate Cancer.