title: Growth hormone supplementation increased latency to tumourigenesis in Atm-deficient mice.
abstract: Growth hormone (GH) is important for cell growth and differentiation, has multiple effects on lymphoid tissue and may promote blast cell proliferation and cancer development. We studied the effect of GH on longevity and tumour formation in Atm-deficient mice, an established model of the human cancer prone syndrome ataxia telangiectasia (AT). AT is a devastating recessive disorder that is characterized by progressive cerebellar ataxia, immunodeficiency, chromosomal instability and cancer susceptibility. Since AT patients also show endocrinological abnormalities the question has been raised as to whether GH therapy could be beneficial and/or increase the cancer risk in AT. We found that treatment with GH significantly increased longevity of Atm-deficient mice. In addition, GH ameliorated locomotoric behaviour and improved T-cell immunity. Thus, our data demonstrated that GH treatment is not necessarily accompanied by increased cancer development in diseases with chromosomal instability and cancer susceptibility and might be beneficial for AT patients.
authors.affiliation: Pediatric Children's Hospital, Johann Wolfgang Goethe-University, Frankfurt/Main, Germany. ralf.schubert@kgu.de
authors.forename: Ralf
authors.initials: R
authors.lastname: Schubert
authors.forename: Nathalie
authors.initials: N
authors.lastname: Schmitz
authors.forename: Julia
authors.initials: J
authors.lastname: Pietzner
authors.forename: Christa
authors.initials: C
authors.lastname: Tandi
authors.forename: Alf
authors.initials: A
authors.lastname: Theisen
authors.forename: Ruth
authors.initials: R
authors.lastname: Dresel
authors.forename: Martin
authors.initials: M
authors.lastname: Christmann
authors.forename: Stefan
authors.initials: S
authors.lastname: Zielen
mesh_terms: D000818:Animals; D001260:Ataxia Telangiectasia / Q000150:complications / Q000188:drug therapy*; D064007:Ataxia Telangiectasia Mutated Proteins; D018797:Cell Cycle Proteins / Q000235:genetics; D004268:DNA-Binding Proteins / Q000172:deficiency / Q000235:genetics; D004195:Disease Models, Animal; D005260:Female; D013006:Growth Hormone / Q000008:administration & dosage / Q000235:genetics / Q000627:therapeutic use*; D006801:Humans; D008223:Lymphoma / Q000209:etiology / Q000235:genetics / Q000503:physiopathology / Q000517:prevention & control; D008297:Male; D051379:Mice; D017346:Protein Serine-Threonine Kinases / Q000172:deficiency / Q000235:genetics; D051381:Rats; D011994:Recombinant Proteins / Q000008:administration & dosage / Q000235:genetics / Q000627:therapeutic use*; D013601:T-Lymphocytes / Q000276:immunology; D013953:Thymus Neoplasms / Q000209:etiology / Q000235:genetics / Q000503:physiopathology / Q000517:prevention & control; D016896:Treatment Outcome; D025521:Tumor Suppressor Proteins / Q000172:deficiency / Q000235:genetics
chemical_list: D018797:Cell Cycle Proteins; D004268:DNA-Binding Proteins; D011994:Recombinant Proteins; D025521:Tumor Suppressor Proteins; D013006:Growth Hormone; C576324:ATM protein, human; D064007:Ataxia Telangiectasia Mutated Proteins; C576325:Atm protein, mouse; D017346:Protein Serine-Threonine Kinases