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G P Dotto - One of the best experts on this subject based on the ideXlab platform.

  • p21waf1 cip1 functions as a suppressor of malignant Skin Tumor formation and a determinant of keratinocyte stem cell potential
    Proceedings of the National Academy of Sciences of the United States of America, 1999
    Co-Authors: G I Topley, R Okuyama, J G Gonzales, Claudio J Conti, G P Dotto
    Abstract:

    p21WAF1/Cip1 is one of the best characterized downstream targets of p53, and the growth suppressing function of this cyclin-dependent kinase inhibitor is well established. However, whether p21 exerts a Tumor-suppressing function of its own remains to be established. We report here that, similarly to loss of p53, disruption of the p21WAF1/Cip1 gene results in a markedly increased susceptibility to chemically induced Skin carcinoma formation, whereas the number of papillomas is reduced. Previous evidence indicates that malignant versus Benign keratinocyte Tumor formation is likely to involve distinct target-cell populations with a different commitment to differentiation. In parallel with the increased susceptibility to carcinoma formation, loss of p21WAF1/Cip1 was found to promote keratinocyte subpopulations with increased growth/differentiation potential, including clonal growth capability, reversible commitment to differentiation, and capability to generate all types of terminally differentiated keratinocytes present in vivo, not only in the interfollicular epidermis but also in hair follicles. Thus, these findings have revealed a function of p21 as a suppressor of malignant but not Benign Skin-Tumor formation and a determinant of the growth/differentiation potential of keratinocyte subpopulations.

  • p21 waf1 cip1 functions as a suppressor of malignant Skin Tumor formation and a determinant of keratinocyte stem cell potential
    Proceedings of the National Academy of Sciences of the United States of America, 1999
    Co-Authors: G I Topley, R Okuyama, J G Gonzales, C Conti, G P Dotto
    Abstract:

    p21WAF1/Cip1 is one of the best characterized downstream targets of p53, and the growth suppressing function of this cyclin-dependent kinase inhibitor is well established. However, whether p21 exerts a Tumor-suppressing function of its own remains to be established. We report here that, similarly to loss of p53, disruption of the p21WAF1/Cip1 gene results in a markedly increased susceptibility to chemically induced Skin carcinoma formation, whereas the number of papillomas is reduced. Previous evidence indicates that malignant versus Benign keratinocyte Tumor formation is likely to involve distinct target-cell populations with a different commitment to differentiation. In parallel with the increased susceptibility to carcinoma formation, loss of p21WAF1/Cip1 was found to promote keratinocyte subpopulations with increased growth/differentiation potential, including clonal growth capability, reversible commitment to differentiation, and capability to generate all types of terminally differentiated keratinocytes present in vivo, not only in the interfollicular epidermis but also in hair follicles. Thus, these findings have revealed a function of p21 as a suppressor of malignant but not Benign Skin-Tumor formation and a determinant of the growth/differentiation potential of keratinocyte subpopulations.

G I Topley - One of the best experts on this subject based on the ideXlab platform.

  • p21waf1 cip1 functions as a suppressor of malignant Skin Tumor formation and a determinant of keratinocyte stem cell potential
    Proceedings of the National Academy of Sciences of the United States of America, 1999
    Co-Authors: G I Topley, R Okuyama, J G Gonzales, Claudio J Conti, G P Dotto
    Abstract:

    p21WAF1/Cip1 is one of the best characterized downstream targets of p53, and the growth suppressing function of this cyclin-dependent kinase inhibitor is well established. However, whether p21 exerts a Tumor-suppressing function of its own remains to be established. We report here that, similarly to loss of p53, disruption of the p21WAF1/Cip1 gene results in a markedly increased susceptibility to chemically induced Skin carcinoma formation, whereas the number of papillomas is reduced. Previous evidence indicates that malignant versus Benign keratinocyte Tumor formation is likely to involve distinct target-cell populations with a different commitment to differentiation. In parallel with the increased susceptibility to carcinoma formation, loss of p21WAF1/Cip1 was found to promote keratinocyte subpopulations with increased growth/differentiation potential, including clonal growth capability, reversible commitment to differentiation, and capability to generate all types of terminally differentiated keratinocytes present in vivo, not only in the interfollicular epidermis but also in hair follicles. Thus, these findings have revealed a function of p21 as a suppressor of malignant but not Benign Skin-Tumor formation and a determinant of the growth/differentiation potential of keratinocyte subpopulations.

  • p21 waf1 cip1 functions as a suppressor of malignant Skin Tumor formation and a determinant of keratinocyte stem cell potential
    Proceedings of the National Academy of Sciences of the United States of America, 1999
    Co-Authors: G I Topley, R Okuyama, J G Gonzales, C Conti, G P Dotto
    Abstract:

    p21WAF1/Cip1 is one of the best characterized downstream targets of p53, and the growth suppressing function of this cyclin-dependent kinase inhibitor is well established. However, whether p21 exerts a Tumor-suppressing function of its own remains to be established. We report here that, similarly to loss of p53, disruption of the p21WAF1/Cip1 gene results in a markedly increased susceptibility to chemically induced Skin carcinoma formation, whereas the number of papillomas is reduced. Previous evidence indicates that malignant versus Benign keratinocyte Tumor formation is likely to involve distinct target-cell populations with a different commitment to differentiation. In parallel with the increased susceptibility to carcinoma formation, loss of p21WAF1/Cip1 was found to promote keratinocyte subpopulations with increased growth/differentiation potential, including clonal growth capability, reversible commitment to differentiation, and capability to generate all types of terminally differentiated keratinocytes present in vivo, not only in the interfollicular epidermis but also in hair follicles. Thus, these findings have revealed a function of p21 as a suppressor of malignant but not Benign Skin-Tumor formation and a determinant of the growth/differentiation potential of keratinocyte subpopulations.

R Okuyama - One of the best experts on this subject based on the ideXlab platform.

  • p21waf1 cip1 functions as a suppressor of malignant Skin Tumor formation and a determinant of keratinocyte stem cell potential
    Proceedings of the National Academy of Sciences of the United States of America, 1999
    Co-Authors: G I Topley, R Okuyama, J G Gonzales, Claudio J Conti, G P Dotto
    Abstract:

    p21WAF1/Cip1 is one of the best characterized downstream targets of p53, and the growth suppressing function of this cyclin-dependent kinase inhibitor is well established. However, whether p21 exerts a Tumor-suppressing function of its own remains to be established. We report here that, similarly to loss of p53, disruption of the p21WAF1/Cip1 gene results in a markedly increased susceptibility to chemically induced Skin carcinoma formation, whereas the number of papillomas is reduced. Previous evidence indicates that malignant versus Benign keratinocyte Tumor formation is likely to involve distinct target-cell populations with a different commitment to differentiation. In parallel with the increased susceptibility to carcinoma formation, loss of p21WAF1/Cip1 was found to promote keratinocyte subpopulations with increased growth/differentiation potential, including clonal growth capability, reversible commitment to differentiation, and capability to generate all types of terminally differentiated keratinocytes present in vivo, not only in the interfollicular epidermis but also in hair follicles. Thus, these findings have revealed a function of p21 as a suppressor of malignant but not Benign Skin-Tumor formation and a determinant of the growth/differentiation potential of keratinocyte subpopulations.

  • p21 waf1 cip1 functions as a suppressor of malignant Skin Tumor formation and a determinant of keratinocyte stem cell potential
    Proceedings of the National Academy of Sciences of the United States of America, 1999
    Co-Authors: G I Topley, R Okuyama, J G Gonzales, C Conti, G P Dotto
    Abstract:

    p21WAF1/Cip1 is one of the best characterized downstream targets of p53, and the growth suppressing function of this cyclin-dependent kinase inhibitor is well established. However, whether p21 exerts a Tumor-suppressing function of its own remains to be established. We report here that, similarly to loss of p53, disruption of the p21WAF1/Cip1 gene results in a markedly increased susceptibility to chemically induced Skin carcinoma formation, whereas the number of papillomas is reduced. Previous evidence indicates that malignant versus Benign keratinocyte Tumor formation is likely to involve distinct target-cell populations with a different commitment to differentiation. In parallel with the increased susceptibility to carcinoma formation, loss of p21WAF1/Cip1 was found to promote keratinocyte subpopulations with increased growth/differentiation potential, including clonal growth capability, reversible commitment to differentiation, and capability to generate all types of terminally differentiated keratinocytes present in vivo, not only in the interfollicular epidermis but also in hair follicles. Thus, these findings have revealed a function of p21 as a suppressor of malignant but not Benign Skin-Tumor formation and a determinant of the growth/differentiation potential of keratinocyte subpopulations.

J G Gonzales - One of the best experts on this subject based on the ideXlab platform.

  • p21waf1 cip1 functions as a suppressor of malignant Skin Tumor formation and a determinant of keratinocyte stem cell potential
    Proceedings of the National Academy of Sciences of the United States of America, 1999
    Co-Authors: G I Topley, R Okuyama, J G Gonzales, Claudio J Conti, G P Dotto
    Abstract:

    p21WAF1/Cip1 is one of the best characterized downstream targets of p53, and the growth suppressing function of this cyclin-dependent kinase inhibitor is well established. However, whether p21 exerts a Tumor-suppressing function of its own remains to be established. We report here that, similarly to loss of p53, disruption of the p21WAF1/Cip1 gene results in a markedly increased susceptibility to chemically induced Skin carcinoma formation, whereas the number of papillomas is reduced. Previous evidence indicates that malignant versus Benign keratinocyte Tumor formation is likely to involve distinct target-cell populations with a different commitment to differentiation. In parallel with the increased susceptibility to carcinoma formation, loss of p21WAF1/Cip1 was found to promote keratinocyte subpopulations with increased growth/differentiation potential, including clonal growth capability, reversible commitment to differentiation, and capability to generate all types of terminally differentiated keratinocytes present in vivo, not only in the interfollicular epidermis but also in hair follicles. Thus, these findings have revealed a function of p21 as a suppressor of malignant but not Benign Skin-Tumor formation and a determinant of the growth/differentiation potential of keratinocyte subpopulations.

  • p21 waf1 cip1 functions as a suppressor of malignant Skin Tumor formation and a determinant of keratinocyte stem cell potential
    Proceedings of the National Academy of Sciences of the United States of America, 1999
    Co-Authors: G I Topley, R Okuyama, J G Gonzales, C Conti, G P Dotto
    Abstract:

    p21WAF1/Cip1 is one of the best characterized downstream targets of p53, and the growth suppressing function of this cyclin-dependent kinase inhibitor is well established. However, whether p21 exerts a Tumor-suppressing function of its own remains to be established. We report here that, similarly to loss of p53, disruption of the p21WAF1/Cip1 gene results in a markedly increased susceptibility to chemically induced Skin carcinoma formation, whereas the number of papillomas is reduced. Previous evidence indicates that malignant versus Benign keratinocyte Tumor formation is likely to involve distinct target-cell populations with a different commitment to differentiation. In parallel with the increased susceptibility to carcinoma formation, loss of p21WAF1/Cip1 was found to promote keratinocyte subpopulations with increased growth/differentiation potential, including clonal growth capability, reversible commitment to differentiation, and capability to generate all types of terminally differentiated keratinocytes present in vivo, not only in the interfollicular epidermis but also in hair follicles. Thus, these findings have revealed a function of p21 as a suppressor of malignant but not Benign Skin-Tumor formation and a determinant of the growth/differentiation potential of keratinocyte subpopulations.

Xavier Sastregarau - One of the best experts on this subject based on the ideXlab platform.

  • activating mutations of the tyrosine kinase receptor fgfr3 are associated with Benign Skin Tumors in mice and humans
    Human Molecular Genetics, 2005
    Co-Authors: Armelle Logie, Claire Dunoislarde, Christophe Rosty, Olivier Levrel, Martine Blanche, Agnes Ribeiro, Jeanmarie Gasc, Jose L Jorcano, Sabine Werner, Xavier Sastregarau
    Abstract:

    Specific germline activating point mutations in the gene encoding the tyrosine kinase receptor FGFR3 (fibroblast growth factor receptor 3) result in autosomal dominant human skeletal dysplasias. The identification in multiple myeloma and in two epithelial cancers-bladder and cervical carcinomas-of somatic FGFR3 mutations identical to the germinal activating mutations found in skeletal dysplasias, together with functional studies, have suggested an oncogenic role for this receptor. Although acanthosis nigricans, a Benign Skin Tumor, has been found in some syndromes associated with germinal activating mutations of FGFR3, the role of activated FGFR3 in the epidermis has never been investigated. Here, we targeted an activated receptor mutant (S249C FGFR3) to the basal cells of the epidermis of transgenic mice. Mice expressing the transgene developed Benign epidermal Tumors with no sign of malignancy. These Skin lesions had features in common with acanthosis nigricans and other Benign human Skin Tumors, including seborrheic keratosis, one of the most common Benign epidermal Tumors in humans. We therefore screened a series of 62 cases of seborrheic keratosis for FGFR3 mutations. A large proportion of these Tumors (39%) harbored somatic activating FGFR3 mutations, identical to those associated with skeletal dysplasia syndromes and bladder and cervical neoplasms. Our findings directly implicate FGFR3 activation as a major cause of Benign epidermal Tumors in humans.