{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,5]],"date-time":"2026-10-05T19:08:36Z","timestamp":1791227316252,"version":"4.1.0"},"reference-count":44,"publisher":"National Academy of Sciences","issue":"11","content-domain":{"domain":["www.pnas.org"],"crossmark-restriction":true},"short-container-title":["Proc. Natl. Acad. Sci. U.S.A."],"published-print":{"date-parts":[[1998,5,26]]},"abstract":"<jats:p>\n                    We examined the\n                    <jats:italic>MLL<\/jats:italic>\n                    genomic translocation breakpoint in acute myeloid leukemia of infant twins. Southern blot analysis in both cases showed two identical\n                    <jats:italic>MLL<\/jats:italic>\n                    gene rearrangements indicating chromosomal translocation. The rearrangements were detectable in the second twin before signs of clinical disease and the intensity relative to the normal fragment indicated that the translocation was not constitutional. Fluorescence\n                    <jats:italic>in situ<\/jats:italic>\n                    hybridization with an\n                    <jats:italic>MLL<\/jats:italic>\n                    -specific probe and karyotype analyses suggested t(11;22)(q23;q11.2) disrupting\n                    <jats:italic>MLL<\/jats:italic>\n                    . Known 5\u2032 sequence from\n                    <jats:italic>MLL<\/jats:italic>\n                    but unknown 3\u2032 sequence from chromosome band 22q11.2 formed the breakpoint junction on the der(11) chromosome. We used panhandle variant PCR to clone the translocation breakpoint. By ligating a single-stranded oligonucleotide that was homologous to known 5\u2032\n                    <jats:italic>MLL<\/jats:italic>\n                    genomic sequence to the 5\u2032 ends of\n                    <jats:italic>Bam<\/jats:italic>\n                    HI-digested DNA through a bridging oligonucleotide, we formed the stem\u2013loop template for panhandle variant PCR which yielded products of 3.9 kb. The\n                    <jats:italic>MLL<\/jats:italic>\n                    genomic breakpoint was in intron 7. The sequence of the partner DNA from band 22q11.2 was identical to the hCDC\n                    <jats:italic>rel<\/jats:italic>\n                    (human cell division cycle related) gene that maps to the region commonly deleted in DiGeorge and velocardiofacial syndromes. Both\n                    <jats:italic>MLL<\/jats:italic>\n                    and hCDC\n                    <jats:italic>rel<\/jats:italic>\n                    contained homologous CT, TTTGTG, and GAA sequences within a few base pairs of their respective breakpoints, which may have been important in uniting these two genes by translocation. Reverse transcriptase-PCR amplified an in-frame fusion of\n                    <jats:italic>MLL<\/jats:italic>\n                    exon 7 to hCDC\n                    <jats:italic>rel<\/jats:italic>\n                    exon 3, indicating that an\n                    <jats:italic>MLL<\/jats:italic>\n                    -hCDC\n                    <jats:italic>rel<\/jats:italic>\n                    chimeric mRNA had been transcribed. Panhandle variant PCR is a powerful strategy for cloning translocation breakpoints where the partner gene is undetermined. This application of the method identified a region of chromosome band 22q11.2 involved in both leukemia and a constitutional disorder.\n                  <\/jats:p>","DOI":"10.1073\/pnas.95.11.6413","type":"journal-article","created":{"date-parts":[[2002,7,26]],"date-time":"2002-07-26T10:40:11Z","timestamp":1027680011000},"page":"6413-6418","update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":145,"title":["t(11;22)(q23;q11.2) in acute myeloid leukemia of infant twins fuses\n                    <i>MLL<\/i>\n                    with hCDC\n                    <i>rel<\/i>\n                    , a cell division cycle gene in the genomic region of deletion in DiGeorge and velocardiofacial syndromes"],"prefix":"10.1073","volume":"95","author":[{"given":"Maureen D.","family":"Megonigal","sequence":"first","affiliation":[{"name":"Divisions of Oncology and Human Genetics and Molecular Biology, Joseph Stokes, Jr., Research Institute, Children\u2019s Hospital of Philadelphia, Department of Pediatrics, University of Pennsylvania School of Medicine, Philadelphia, PA 19104; Department of Pediatrics, University of Iowa, Iowa City, IA 52242; Division of Pediatric Oncology, Department of Pediatrics, Columbia University College of Physicians and Surgeons, New York, NY 10032; Jefferson Medical College, Philadelphia, PA 19106"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Eric F.","family":"Rappaport","sequence":"additional","affiliation":[{"name":"Divisions of Oncology and Human Genetics and Molecular Biology, Joseph Stokes, Jr., Research Institute, Children\u2019s Hospital of Philadelphia, Department of Pediatrics, University of Pennsylvania School of Medicine, Philadelphia, PA 19104; Department of Pediatrics, University of Iowa, Iowa City, IA 52242; Division of Pediatric Oncology, Department of Pediatrics, Columbia University College of Physicians and Surgeons, New York, NY 10032; Jefferson Medical 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