DER(16)T(1-16) IS A NONRANDOM SECONDARY CHROMOSOME ABERRATION IN MANYTYPES OF HUMAN NEOPLASIA, INCLUDING MYXOID LIPOSARCOMA, RHABDOMYOSARCOMA AND PHILADELPHIA-CHROMOSOME-POSITIVE ACUTE LYMPHOBLASTIC-LEUKEMIA

An unbalanced translocation between chromosomes 1 and 16, der(16)t(1;1 6), resulting in trisomy 1q and loss of genetic material from 16q, has been thus far suggested to constitute a nonrandom secondary abnormali ty in two types of closely related solid tumors - Ewing sarcoma and pe ripheral primitive neuroepithelial tumor (PNET). We report on three ca ses of soft tissue tumors, a myxoid liposarcoma, a PNET and a rhabdomy osarcoma, and four cases of hematologic disorders, two acute lymphobla stic leukemias (ALL), an acute mixed leukemia and a refractory anemia, that in addition to primary chromosome abnormalities displayed the pr esence of the der(16)t(1;16). All three cases of acute leukemia were P hiladelphia (Ph) chromosome-positive and all displayed both lymphoid a nd myeloid antigens. Our results and review of the literature indicate that the occurrence of der(16)t(1;16) is not limited to Ewing sarcoma and PNET, but that acquisition of this abnormality may represent a mo re general pathway of clonal evolution in several different tumor type s including Ph chromosome-positive ALL, myxoid liposarcoma, rhabdomyos arcoma, breast cancer, endometrial adenocarcinoma, myelodysplastic syn dromes, acute myeloid leukemia, retinoblastoma, and Wilms' tumor.