Adenomatosis - Explore the Science & Experts | ideXlab

Scan Science and Technology

Contact Leading Edge Experts & Companies

Adenomatosis

The Experts below are selected from a list of 4473 Experts worldwide ranked by ideXlab platform

J. M. Sharp – One of the best experts on this subject based on the ideXlab platform.

  • epithelial tumour cells in the lungs of sheep with pulmonary Adenomatosis are major sites of replication for jaagsiekte retrovirus
    Journal of General Virology, 1995
    Co-Authors: Massimo Palmarini, Patricia Dewar, M De Las Heras, N F Inglis, Robert G Dalziel, J. M. Sharp

    Abstract:

    Sheep pulmonary Adenomatosis (SPA) is a naturally occurring contagious lung tumour of sheep which has been associated aetiologically with a type D- and B- related retrovirus (Jaagsiekte retrovirus; JSRV). To improve understanding of the aetio-pathogenesis of SPA, the distribution and the sites of JSRV replication in sheep with naturally or experimentally induced SPA or in unaffected controls were identified. New immunological reagents were produced and a blocking enzymelinked immunosorbent assay (B-ELISA) and an immunohistochemical technique for the detection of JSRV major capsid protein at the tissue and cellular levels were developed. JSRV was detected only in the respiratory tract of sheep affected by pulmonary Adenomatosis and specifically in the transformed epithelial cells of the alveoli of SPA-affected sheep.

  • Sheep Pulmonary Adenomatosis: Studies on Its Aetiology
    Maedi-Visna and Related Diseases, 1990
    Co-Authors: J. M. Sharp, K. W. Angus

    Abstract:

    Sheep pulmonary Adenomatosis (SPA) is a contagious lung tumour that can be transmitted experimentally. Two viruses have been associated with the disease, a herpesvirus and a retrovirus.

Armelle Fatome – One of the best experts on this subject based on the ideXlab platform.

  • hepatocyte nuclear factor 1α gene inactivation cosegregation between liver Adenomatosis and diabetes phenotypes in two maturity onset diabetes of the young mody 3 families
    The Journal of Clinical Endocrinology and Metabolism, 2004
    Co-Authors: Yves Reznik, Emmanuelle Jeannot, Thong Dao, Regis Coutant, Laurence Chiche, Severine Clauin, Pierre Rousselot, Monique Fabre, Frederic Oberti, Armelle Fatome

    Abstract:

    Heterozygous germline mutations of the hepatocyte nuclear factor (HNF)-1 alpha are associated with maturity-onset diabetes of the young (MODY)3. Recently, the biallelic inactivation of the HNF-1 alpha gene was reported in liver adenomas. We show the occurrence of liver Adenomatosis in six MODY3-affected patients from two unrelated and large families. Liver Adenomatosis was characterized by the presence of numerous adenomas within a normal hepatic parenchyma. The HNF-1 alpha hot-spot germline mutation P291fs was identified in the two probands and in 16 relatives from the two families. The six patients affected by liver Adenomatosis and diabetes exhibited the mutation. The analysis of liver-cell tumors from two affected patients evidenced the biallelic inactivation of HNF-1 alpha. The familial screening confirmed the clinical heterogeneity of the liver phenotype, from silent liver Adenomatosis to fatal hemorrhage. These observations warrant the systematic screening for liver Adenomatosis in MODY3 families to prevent its potentially deadly complications. Moreover, such screening may help to determine if a particular mutational spectrum of HNF-1 alpha is associated with liver Adenomatosis and to establish its prevalence in this frequent form of diabetes in the young adult.

  • hepatocyte nuclear factor 1α gene inactivation cosegregation between liver Adenomatosis and diabetes phenotypes in two maturity onset diabetes of the young mody 3 families
    The Journal of Clinical Endocrinology and Metabolism, 2004
    Co-Authors: Yves Reznik, Emmanuelle Jeannot, Armelle Fatome, Regis Coutant, Laurence Chiche, Severine Clauin, Pierre Rousselot, Monique Fabre, Frederic Oberti, Jessica Zucmanrossi

    Abstract:

    Heterozygous germline mutations of the hepatocyte nuclear factor (HNF)-1α are associated with maturity-onset diabetes of the young (MODY)3. Recently, the biallelic inactivation of the HNF-1α gene was reported in liver adenomas. We show the occurrence of liver Adenomatosis in six MODY3-affected patients from two unrelated and large families. Liver Adenomatosis was characterized by the presence of numerous adenomas within a normal hepatic parenchyma. The HNF-1α hot-spot germline mutation P291fs was identified in the two probands and in 16 relatives from the two families. The six patients affected by liver Adenomatosis and diabetes exhibited the mutation. The analysis of liver-cell tumors from two affected patients evidenced the biallelic inactivation of HNF-1α. The familial screening confirmed the clinical heterogeneity of the liver phenotype, from silent liver Adenomatosis to fatal hemorrhage. These observations warrant the systematic screening for liver Adenomatosis in MODY3 families to prevent its potent…

Yves Reznik – One of the best experts on this subject based on the ideXlab platform.

  • hepatocyte nuclear factor 1α gene inactivation cosegregation between liver Adenomatosis and diabetes phenotypes in two maturity onset diabetes of the young mody 3 families
    The Journal of Clinical Endocrinology and Metabolism, 2004
    Co-Authors: Yves Reznik, Emmanuelle Jeannot, Thong Dao, Regis Coutant, Laurence Chiche, Severine Clauin, Pierre Rousselot, Monique Fabre, Frederic Oberti, Armelle Fatome

    Abstract:

    Heterozygous germline mutations of the hepatocyte nuclear factor (HNF)-1 alpha are associated with maturity-onset diabetes of the young (MODY)3. Recently, the biallelic inactivation of the HNF-1 alpha gene was reported in liver adenomas. We show the occurrence of liver Adenomatosis in six MODY3-affected patients from two unrelated and large families. Liver Adenomatosis was characterized by the presence of numerous adenomas within a normal hepatic parenchyma. The HNF-1 alpha hot-spot germline mutation P291fs was identified in the two probands and in 16 relatives from the two families. The six patients affected by liver Adenomatosis and diabetes exhibited the mutation. The analysis of liver-cell tumors from two affected patients evidenced the biallelic inactivation of HNF-1 alpha. The familial screening confirmed the clinical heterogeneity of the liver phenotype, from silent liver Adenomatosis to fatal hemorrhage. These observations warrant the systematic screening for liver Adenomatosis in MODY3 families to prevent its potentially deadly complications. Moreover, such screening may help to determine if a particular mutational spectrum of HNF-1 alpha is associated with liver Adenomatosis and to establish its prevalence in this frequent form of diabetes in the young adult.

  • hepatocyte nuclear factor 1α gene inactivation cosegregation between liver Adenomatosis and diabetes phenotypes in two maturity onset diabetes of the young mody 3 families
    The Journal of Clinical Endocrinology and Metabolism, 2004
    Co-Authors: Yves Reznik, Emmanuelle Jeannot, Armelle Fatome, Regis Coutant, Laurence Chiche, Severine Clauin, Pierre Rousselot, Monique Fabre, Frederic Oberti, Jessica Zucmanrossi

    Abstract:

    Heterozygous germline mutations of the hepatocyte nuclear factor (HNF)-1α are associated with maturity-onset diabetes of the young (MODY)3. Recently, the biallelic inactivation of the HNF-1α gene was reported in liver adenomas. We show the occurrence of liver Adenomatosis in six MODY3-affected patients from two unrelated and large families. Liver Adenomatosis was characterized by the presence of numerous adenomas within a normal hepatic parenchyma. The HNF-1α hot-spot germline mutation P291fs was identified in the two probands and in 16 relatives from the two families. The six patients affected by liver Adenomatosis and diabetes exhibited the mutation. The analysis of liver-cell tumors from two affected patients evidenced the biallelic inactivation of HNF-1α. The familial screening confirmed the clinical heterogeneity of the liver phenotype, from silent liver Adenomatosis to fatal hemorrhage. These observations warrant the systematic screening for liver Adenomatosis in MODY3 families to prevent its potent…