Erratum: New approaches to progeria (Pediatrics (2007) 120, (834-841) DOI: 10.1542/peds.2007-1356);New approaches to Progeria

Pediatrics

Volumn 120, Issue 4, 2007, Pages 834-841

  Kieran, Mark W ^a,b   Gordon, Leslie ^c   Kleinman, Monica ^b  

^a DANA FARBER CANCER INSTITUTE   (United States)

^b BOSTON CHILDREN S HOSPITAL   (United States)

^c BROWN UNIVERSITY   (United States)

Author keywords

Farnesyltransferase inhibitor; FTI; Lamin A; Premature aging; Progeria; Review article

Indexed keywords

PROTEIN FARNESYLTRANSFERASE INHIBITOR;

BODY COMPOSITION; BONE DENSITY; CELL CULTURE; DISEASE COURSE; DNA MODIFICATION; DUAL ENERGY X RAY ABSORPTIOMETRY; ENERGY EXPENDITURE; FIBROBLAST; GENE; GENE IDENTIFICATION; GENE MUTATION; HUMAN; LAMIN A GENE; PHENOTYPE; PRIORITY JOURNAL; PROGERIA; REVIEW;

EID: 35148898709     PISSN: 00314005     EISSN: 02105721     Source Type: Journal    
DOI: 10.1542/peds.2007-3049     Document Type: Erratum

References (40)

1. Ramírez CL, Cadiñanos J, Varela I, Freije JM, López-Otín C. Human progeroid syndromes, aging and cancer: new genetic and epigenetic insights into old questions. Cell Mol Life Sci. 2007;64:155-170
2. Meta M, Yang SH, Bergo MO, Fong LG, Young SG. Protein farnesyltransferase inhibitors and progeria. Trends Mol Med. 2006;12:480-487
3. Young SG, Meta M, Yang SH, Fong LG. Prelamin A farnesylation and progeroid syndromes. J Biol Chem. 2006;281:39741-39745
4. Rusiñol AE, Sinensky MS. Farnesylated lamins, progeroid syndromes and farnesyl transferase inhibitors. J Cell Sci. 2006;119:3265-3272
5. Navarro CL, Cau P, Lévy N. Molecular bases of progeroid syndromes. Hum Mol Genet. 2006;15:R151-R161
6. Scaffidi P, Gordon L, Misteli T. The cell nucleus and aging: tantalizing clues and hopeful promises. PLoS Biol. 2005;3:e395
7. Pollex RL, Hegele RA. Hutchinson-Gilford progeria syndrome. Clin Genet. 2004;66:375-381
8. Hutchinson J. Case of congenital absence of hair, with atrophic condition of the skin and its appendages, in a boy whose mother had been almost wholly bald from alopecia areata from the age of six. Lancet. 1886;I:923
9. Gilford H. Ateleiosis and progeria: continuous youth and premature old age. Br Med J. 1904;2:914-918
10. Hennekam RC. Hutchinson-Gilford progeria syndrome: review of the phenotype. Am J Med Genet A. 2006;140:2603-2624
11. McClintock D, Gordon LB, Djabali K. Hutchinson-Gilford progeria mutant lamin A primarily targets human vascular cells as detected by an anti-Lamin A G608G antibody. Proc Natl Acad Sci U S A. 2006;103:2154-2159
12. Lans H, Hoeijmakers JH. Cell biology: ageing nucleus gets out of shape. Nature. 2006;440:32-34
13. Csoka A, English S, Simkevich C, et al. Genome-scale expression profiling of Hutchinson-Gilford progeria syndrome reveals widespread transcriptional misregulation leading to mesodermal/mesenchymal defects and accelerated atherosclerosis. Aging Cell. 2004;3:235-243
14. Maciel AT. Evidence for autosomal recessive inheritance of progeria (Hutchinson Gilford). Am J Med Genet. 1988;31:483-487
15. Khalifa MM. Hutchinson-Gilford progeria syndrome: report of a Libyan family and evidence of autosomal recessive inheritance. Clin Genet. 1989;35:125-132
16. Cao H, Hegele RA. LMNA is mutated in Hutchinson-Gilford progeria (MIM 176670) but not in Wiedemann-Rautenstrauch progeroid syndrome (MIM 264090). J Hum Genet. 2003;48:271-274
17. De Sandre-Giovannoli A, Bernard R, Cau P, et al. Lamin A truncation in Hutchinson-Gilford progeria. Science. 2003;300:2055
18. Eriksson M, Brown WT, Gordon LB, et al. Recurrent de novo point mutations in lamin A cause Hutchinson-Gilford progeria syndrome. Nature. 2003;423:293-298
19. Lammerding J, Fong LG, Ji JY, et al. Lamins A and C but not lamin B1 regulate nuclear mechanics. J Biol Chem. 2006;281:25768-25780
20. Fong LG, Ng JK, Meta M, et al. Heterozygosity for Lmna deficiency eliminates the progeria-like phenotypes in Zmp-ste24-deficient mice. Proc Natl Acad Sci U S A. 2004;101:18111-18116
21. Young SG, Fong LG, Michaelis S. Prelamin A, Zmpste24, misshapen cell nuclei, and progeria: new evidence suggesting that protein farnesylation could be important for disease pathogenesis. J Lipid Res. 2005;46:2531-2558
22. Shackleton S, Smallwood DT, Clayton P, et al. Compound heterozygous ZMPSTE24 mutations reduce prelamin A processing and result in a severe progeroid phenotype. J Med Genet. 2005;42:e36
23. Goldman R, Shumaker DK, Erdos MR, et al. Accumulation of mutant lamin A causes progressive changes in nuclear architecture in Hutchinson-Gilford progeria syndrome. Proc Natl Acad Sci U S A. 2004;101:8963-8968
24. Shaw RJ, Cantley LC. Ras, PI(3)K and mTOR signalling controls tumour cell growth. Nature. 2006;441:424-430
25. Adjei AA. Farnesyltransferase inhibitors. Cancer Chemother Biol Response Modif. 2005;22:123-133
26. Yang SH, Bergo MO, Toth JI, et al. Blocking protein farnesyltransferase improves nuclear blebbing in mouse fibroblasts with a targeted Hutchinson-Gilford progeria syndrome mutation. Proc Natl Acad Sci U S A. 2005;102:10291-10296
27. Toth JI, Yang SH, Qiao X, et al. Blocking protein farnesyltransferase improves nuclear shape in fibroblasts from humans with progeroid syndromes. Proc Natl Acad Sci U S A. 2005;102:12873-12878
28. Capell BC, Erdos MR, Madigan JP, et al. Inhibiting farnesylation of progerin prevents the characteristic nuclear blebbing of Hutchinson-Gilford progeria syndrome. Proc Natl Acad Sci U S A. 2005;102:12879-12884
29. Liu Y, Rusinol A, Sinensky M, Wang Y, Zou Y. DNA damage responses in progeroid syndromes arise from defective maturation of prelamin A. J Cell Sci. 2006;119:4644-4649
30. Shumaker DK, Dechat T, Kohlmaier A, et al. Mutant nuclear lamin A leads to progressive alterations of epigenetic control in premature aging. Proc Natl Acad Sci U S A. 2006;103:8703-8708
31. Mounkes LC, Kozlov S, Hernandez L, Sullivan T, Stewart CL. A progeroid syndrome in mice is caused by defects in A-type lamins. Nature. 2003;423:298-301
32. Fong L, Ng J, Lammerding J, et al. Prelamin A and lamin A appear to be dispensable in the nuclear lamina. J Clin Invest. 2006;116:743-752
33. Varga R, Eriksson M, Erdos MR, et al. Progressive vascular smooth muscle cell defects in a mouse model of Hutchinson-Gilford progeria syndrome. Proc Natl Acad Sci U S A. 2006;103:3250-3255
34. Yang SH, Meta M, Qiao X, et al. A farnesyltransferase inhibitor improves disease phenotypes in mice with a Hutchinson-Gilford progeria syndrome mutation. J Clin Invest. 2006;116:2115-2121
35. Capell BC, Erdos MR, Eriksson M, et al. In vitro and in vivo effects of farnesyltransferase inhibitors for Hutchinson-Gilford progeria syndrome [abstract]. Presented at: American Society of Human Genetics; October 9-13, 2006; New Orleans, LA
36. Kieran MW, Packer RJ, Onar A, et al. Phase I and pharmacokinetic study of the oral farnesyltransferase inhibitor lonafarnib administered twice daily to pediatric patients with advanced central nervous system tumors using a modified continuous reassessment method: a Pediatric Brain Tumor Consortium study. J Clin Oncol. 2007;25:3137-3143
37. Campbell SE, Laliberte L, Wolf-Jensen N, et al. A medical and research database for Hutchinson-Gilford progeria syndrome [abstract]. Presented at: Progeria Research Foundation International Workshop on Progeria; November 3-5, 2005; Boston, MA
38. Scaffidi P, Misteli T. Reversal of the cellular phenotype in the premature aging disease Hutchinson-Gilford progeria syndrome. Nat Med. 2005;11:440-445
39. Huang S, Chen L, Libina N, et al. Correction of cellular phenotypes of Hutchinson-Gilford progeria cells by RNA interference. Hum Genet. 2005;118:444-450
40. Scaffidi P, Misteli T. Lamin A-dependent nuclear defects in human aging. Science. 2006;312:1059-1063