12. Matsumoto, N., Soeda, E., Ohashi, H., Fujimoto, M., Kato, R., Tsujita, T., Tomita, H., Kondo, S., Fukushima, Y., and Niikawa, N. (1997) A 1.2-megabase BAC/PAC contig spanning the 14q13 breakpoint of t(2;14) in a mirror-image polydactyly patient. Genomics 45: 11–16. 13. Ohta, T., Tohma, T., Soejima, H., Fukushima, Y., Nagai, T., Yoshiura, K., Jinno, Y., and Niikawa, N. (1993). The origin of cytologically unidentifiable chromosome abnormalities: Six cases ascertained by targeted chromosome-band painting. Hum. Genet. 92: 1–5. 14. Takagi, S., Fujikawa, K., Imai, T., Fukuhara, N., Fukudome, K., Minegishi, M., Tsuchiya, S., Konno, T., Hinuma, Y., and Yoshie, O. (1995). Identification of a highly specific surface marker of T-cell acute lymphoblastic leukemia and neuroblas- toma as a new member of the transmembrane 4 superfamily. Int. J. Cancer 61: 706 –715. Assignment of the Steroid Receptor Coactivator-1 (SRC-1) Gene to Human Chromosome Band 2p23 Melina Carapeti,* Ricardo C. T. Aguiar,² Andrew Chase,* John M. Goldman,* and Nicholas C. P. Cross* ,1 * Department of Haematology, Imperial College School of Medicine, Hammersmith Hospital, Du Cane Road, London W12 ONN, United Kingdom; and ² Division of Hematologic Malignancies, Dana Farber Cancer Institute, 44 Binney Street, Boston, Massachusetts 02115 Received March 16, 1998; accepted June 9, 1998 Nuclear receptor coactivators (NRCoAs) mediate the li- gand-dependent transcriptional activation of specific genes by nuclear receptors, for example, the receptors for steroid and thyroid hormones, retinoids, and vitamin D. Currently, three NRCoAs have been cloned: TIF2 (also known as GRIP1 or NCoA-2) (11), SRC-1 (also known as F-SRC-1 or NCoA-1) (8), and AIB1 (also known as RAC3, ACTR, or p/CIP) (2). These proteins are functionally and structurally homologous and are thought to stimulate gene expression by facilitating the assembly of basal transcription factors into a stable preinitiation complex. Recently NRCoAs have been shown to possess histone acetyl transferase (HAT) activity and also to interact directly with CBP, a general transcriptional co-inte- grator (10). It is likely, therefore, that NRCoAs mediate tran- scriptional activation by a mechanism that involves chroma- tin remodeling. Several lines of evidence have implicated abnormalities of NRCoAs in malignancy. The AIB1 gene at 20q12 is fre- quently amplified in breast and ovarian cancers (2), and we have recently cloned a novel fusion between the TIF2 and the MOZ genes at 8q13 and 8p11, respectively, in acute myeloid leukemia (AML) (1, 3). In addition, the ARA 70 gene was shown to be fused to RET in a case of human thyroid papil- lary carcinoma (9, 12), and TIF1 is fused to B-RAF in the mouse hepatoma-derived oncogene T18 (5). Although ARA 70 and TIF1 do not share sequence homology with the NRCoA family, they are also involved in the ligand-dependent acti- vation function of nuclear receptors. Here we have mapped the chromosomal localization of SRC-1 (GenBank Accession No. U40396) to determine whether this gene is also located at a region that has been implicated in malignancy. An SRC-1 probe, designed to a region of low homology between the NRCoA family mem- bers, was amplified from normal peripheral blood leukocyte cDNA with primers SRC1-A (5'-CTGAGCTAGCTGAACTA- GAC-3') and SRC1-B (5'-GGTGCTGTTGACTGTACAGT-3'). The probe was sequenced to confirm its identity and used to screen the gridded human library RPCI1. Four positive PAC clones (Nos. 100-G8, 115-I1, 125-H2, and 200-P18) were iso- lated and used as fluorescence in situ hybridization (FISH) probes on metaphases from phytohemagglutinin-stimulated pe- ripheral blood lymphocytes from a normal individual. PACs were labeled with digoxigenin by nick-translation and detected with sheep anti-digoxigenin (Boehringer-Mannheim, Germa- ny), rabbit anti-sheep fluorescein isothiocyanate (FITC; Vector, UK), and finally swine anti-rabbit FITC (Dako, UK). All four PACs specifically hybridized to chromosome band 2p23 and to no other region (Fig. 1A). A gridded CEPH mega-YAC library was also screened with the SRC-1 probe. Several positive clones were identified, including Nos. 744h7, 765d3, 916f8, and 953d6. Comparison with the existing map of chro- mosome 2 (4) indicates that SRC-1 maps to the short arm in the vicinity of markers D2S144 and D2S171 (Fig. 1B). These markers have been mapped to 48 cM and 149 cR of the genetic and radiation hybrid maps, respectively, and are contained in the contig WC2.2 (http://www.genome.wi.mit. edu:80/cgi-bin/contig/lookup_contig). Translocations involving chromosome 2p23 or neighboring bands have been reported in a variety of hematological ma- lignancies (6). The ALK gene at 2p23 is disrupted by t(2; 5)(p23;q35) in anaplastic large-cell lymphoma (7), but the molecular etiology of other translocations, for example, the t(2;3)(p23;q26) in AML, is unknown. The mapping of SRC-1 to 2p23 provides a further candidate gene for disruption by these translocations. ACKNOWLEDGMENTS We thank the Medical Research Council Human Genome Mapping Project (MRC HGMP) Resource Centre (Hinxton, UK) for providing the PAC clones and CEPH megaYAC clones. REFERENCES 1. Aguiar, R. C. T., Chase, A., Coulthard, S., Macdonald, D. H. C., Carapeti, M., Reiter, A., Sohal, J., Lennard, A., Goldman, J. M., and Cross, N. C. P. (1997). Abnormalities of chromosome band 1 To whom correspondence should be addressed. Telephone: + 44 181 383 3302. Fax: + 44 181 740 9679. E-mail: ncross@rpms.ac.uk. 242 BRIEF REPORTS GENOMICS 52, 242–244 (1998) ARTICLE NO. GE985446 0888-7543/98 $25.00 Copyright © 1998 by Academic Press All rights of reproduction in any form reserved.