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Molecular pathogenesis of the chromosome 16 inversion in the M4Eo subtype of acute myeloid leukemia [see comments]
Blood (1995) 85 (9): 2289–2302.
Molecular characterization of 16p deletions associated with inversion 16 defines the critical fusion for leukemogenesis
P Marlton, DF Claxton, P Liu, EH Estey, M Beran, M LeBeau, JR Testa, FS Collins, JD Rowley, MJ Siciliano
Blood (1995) 85 (3): 772–779.
Identification of yeast artificial chromosomes containing the inversion 16 p-arm breakpoint associated with acute myelomonocytic leukemia
P Liu, DF Claxton, P Marlton, A Hajra, J Siciliano, M Freedman, SC Chandrasekharappa, K Yanagisawa, RL Stallings, FS Collins
Blood (1993) 82 (3): 716–721.
Interaction of Sp1 with the human gamma globin promoter: binding and transactivation of normal and mutant promoters
Blood (1991) 78 (7): 1853–1863.
The -175T----C mutation increases promoter strength in erythroid cells: correlation with evolutionary conservation of binding sites for two trans-acting factors
DL Gumucio, WK Lockwood, JL Weber, AM Saulino, K Delgrosso, S Surrey, E Schwartz, M Goodman, FS Collins
Blood (1990) 75 (3): 756–761.
Sizing of the human T cell receptor alpha locus and detection of a large deletion in the Molt-4 cell line
Blood (1988) 71 (6): 1744–1747.
The deletion in both common types of hereditary persistence of fetal hemoglobin is approximately 105 kilobases
Blood (1987) 70 (6): 1797–1803.
Concordance of a point mutation 5' to the A gamma-globin gene with A gamma beta + hereditary persistence of fetal hemoglobin in Greeks
PG Waber, MA Bender, RE Gelinas, C Kattamis, A Karaklis, K Sofroniadou, G Stamatoyannopoulos, FS Collins, BG Forget, HH Jr Kazazian
Blood (1986) 67 (2): 551–554.
Concordance of a point mutation 5' to the G gamma globin gene with G gamma beta +. Hereditary persistence of fetal hemoglobin in the black population
Blood (1984) 64 (6): 1292–1296.