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Beta Catenin

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Benjamin A Alman – 1st expert on this subject based on the ideXlab platform

  • BetaCatenin Mediates Soft Tissue Contracture in Clubfoot
    Clinical Orthopaedics and Related Research, 2009
    Co-Authors: Raymond Poon, Catherine Li, Benjamin A Alman

    Abstract:

    The contracted tissues from clubfeet resemble tissues from other fibroproliferative disorders such as palmar fibromatosis. BetaCatenin-mediated signaling is a crucial pathway controlling the fibroproliferative response in many fibroproliferative disorders. To determine if BetaCatenin signaling plays a role in clubfoot, contracted and less contracted tissues from clubfeet were studied using Western analysis to determine the protein level of BetaCatenin. Primary cell cultures were established from these tissues, and they were treated with either lithium to increase BetaCatenin or Dickkopf-1 to inhibit BetaCatenin. RNA was extracted from the cells and analyzed to determine how BetaCatenin regulates expression of Type III collagen, an extracellular matrix protein upregulated in contracted clubfoot tissue. There was a more than twofold increase in BetaCatenin protein in the contracted tissues. Treatment with either lithium or Dickkopf-1 showed Type III collagen RNA expression positively correlated with the protein level of BetaCatenin. These data support the concept that BetaCatenin-mediated signaling plays an important role regulating contracture in clubfeet. Because pharmacologic agents are under development to block this signaling pathway, such drugs could be used in cases of severe stiffness to improve range of motion or to decrease the need for radical surgical approaches.

  • BetaCatenin expression in Dupuytren’s disease: potential role for cell-matrix interactions in modulating BetaCatenin levels in vivo and in vitro
    Oncogene, 2003
    Co-Authors: Vincenzo M Varallo, Benjamin A Alman, Shannon Seney, Douglas C. Ross, James H. Roth, Robert S. Richards, Robert M. Mcfarlane, Jeffrey C. Howard

    Abstract:

    Dupuytren’s disease (DD) is a superficial fibromatosis of the hand. Although the molecular mechanisms responsible for this disease are unknown, recent studies suggest that BetaCatenin may be a key factor involved in fibromatosis. In this study, we analysed the in vivo and in vitro expression levels of BetaCatenin in DD, using surgical specimens and primary cell lines. Although no somatic mutations (exon 3) of BetaCatenin were detected, Western blot analysis revealed high levels of BetaCatenin in diseased palmar fascia, and low to undetectable levels of BetaCatenin in patient-matched normal palmar fascia. Immunohistochemistry analysis showed high levels of BetaCatenin expression within the disease fascia, as well as cytoplasmic and nuclear accumulations of the protein. Immunoprecipitation of BetaCatenin from seven patient lesions showed the protein to be tyrosine phosphorylated. Lastly, Western analysis of three patient-matched (disease and normal fascia) primary cell cultures showed significantly elevated levels of BetaCatenin in disease cells cultured in three-dimensional collagen lattices. This is the first extensive in vivo and in vitro characterization of BetaCatenin in DD, and the first to suggest that the extracellular matrix may play an important role in modulating BetaCatenin stability in DD.

  • predominance of Beta Catenin mutations and Beta Catenin dysregulation in sporadic aggressive fibromatosis desmoid tumor
    Oncogene, 1999
    Co-Authors: Sabine Tejpar, Friedel Nollet, Catherine Li, Jay S Wunder, G Michils, Eric Van Cutsem, Bharati Bapat, Jean-jacques Cassiman, Benjamin A Alman

    Abstract:

    Predominance of BetaCatenin mutations and BetaCatenin dysregulation in sporadic aggressive fibromatosis (desmoid tumor)

Sabine Tejpar – 2nd expert on this subject based on the ideXlab platform

  • predominance of Beta Catenin mutations and Beta Catenin dysregulation in sporadic aggressive fibromatosis desmoid tumor
    Oncogene, 1999
    Co-Authors: Sabine Tejpar, Friedel Nollet, Catherine Li, Jay S Wunder, G Michils, Eric Van Cutsem, Bharati Bapat, Jean-jacques Cassiman, Benjamin A Alman

    Abstract:

    Predominance of BetaCatenin mutations and BetaCatenin dysregulation in sporadic aggressive fibromatosis (desmoid tumor)

  • predominance of Beta Catenin mutations and Beta Catenin dysregulation in sporadic aggressive fibromatosis desmoid tumor
    Oncogene, 1999
    Co-Authors: Sabine Tejpar, Friedel Nollet, Catherine Li, Jay S Wunder, G Michils, Eric Van Cutsem, Bharati Bapat, Jean-jacques Cassiman, Benjamin A Alman

    Abstract:

    Aggressive fibromatosis (also called desmoid tumor) occurs as a sporadic lesion or as part of Familial Adenomatous Polyposis, which is caused by germ line mutations in the Adenomatous polyposis Coli (APC) gene. APC is involved in the regulation of the cellular level of BetaCatenin, which is a mediator in Wnt signaling. Mutational analysis of the BetaCatenin and APC genes was performed in 42 sporadic aggressive fibromatoses. Nine tumors had mutations in APC, and 22 had a point mutation in BetaCatenin at either codon 45 or codon 41 (producing a stabilized BetaCatenin protein product). Immunohistochemistry showed an elevated BetaCatenin protein level in all tumors, regardless of mutational status. BetaCatenin localized to the nucleus, and was not tyrosine phosphorylated in the six tumors in which this was tested. The demonstration of mutations in two mediators in the Wnt-APC-BetaCatenin pathway implicates BetaCatenin stabilization as the key factor in the pathogenesis of aggressive fibromatosis. This is the first demonstration of somatic BetaCatenin mutations in a locally invasive, but non metastatic lesion composed of spindle cells, illustrating the importance of BetaCatenin stabilization in a variety of cell types and neoplastic processes. Moreover, this tumor has one of the highest reported frequencies of BetaCatenin mutations of any tumor type.

Eric Van Cutsem – 3rd expert on this subject based on the ideXlab platform

  • predominance of Beta Catenin mutations and Beta Catenin dysregulation in sporadic aggressive fibromatosis desmoid tumor
    Oncogene, 1999
    Co-Authors: Sabine Tejpar, Friedel Nollet, Catherine Li, Jay S Wunder, G Michils, Eric Van Cutsem, Bharati Bapat, Jean-jacques Cassiman, Benjamin A Alman

    Abstract:

    Predominance of BetaCatenin mutations and BetaCatenin dysregulation in sporadic aggressive fibromatosis (desmoid tumor)

  • predominance of Beta Catenin mutations and Beta Catenin dysregulation in sporadic aggressive fibromatosis desmoid tumor
    Oncogene, 1999
    Co-Authors: Sabine Tejpar, Friedel Nollet, Catherine Li, Jay S Wunder, G Michils, Eric Van Cutsem, Bharati Bapat, Jean-jacques Cassiman, Benjamin A Alman

    Abstract:

    Aggressive fibromatosis (also called desmoid tumor) occurs as a sporadic lesion or as part of Familial Adenomatous Polyposis, which is caused by germ line mutations in the Adenomatous polyposis Coli (APC) gene. APC is involved in the regulation of the cellular level of BetaCatenin, which is a mediator in Wnt signaling. Mutational analysis of the BetaCatenin and APC genes was performed in 42 sporadic aggressive fibromatoses. Nine tumors had mutations in APC, and 22 had a point mutation in BetaCatenin at either codon 45 or codon 41 (producing a stabilized BetaCatenin protein product). Immunohistochemistry showed an elevated BetaCatenin protein level in all tumors, regardless of mutational status. BetaCatenin localized to the nucleus, and was not tyrosine phosphorylated in the six tumors in which this was tested. The demonstration of mutations in two mediators in the Wnt-APC-BetaCatenin pathway implicates BetaCatenin stabilization as the key factor in the pathogenesis of aggressive fibromatosis. This is the first demonstration of somatic BetaCatenin mutations in a locally invasive, but non metastatic lesion composed of spindle cells, illustrating the importance of BetaCatenin stabilization in a variety of cell types and neoplastic processes. Moreover, this tumor has one of the highest reported frequencies of BetaCatenin mutations of any tumor type.