Chromosome abnormalities in poorly differentiated lymphocytic lymphoma.

Abstract Thirteen patients with malignant lymphoma, poorly differentiated lymphocytic type, were studied with cytogenetic and/or immunological techniques. When the involved tissues were grouped according to more current classifications, cells from 11 patients were found to be predominantly of the small cleaved type, and those from two patients were predominantly of the small noncleaved type. Banding studies of chromosomes were performed on cells from tissues primarily involved by poorly differentiated lymphocytic malignant lymphoma in nine cases and from a phytohemagglutinin-stimulated peripheral blood culture in one case. Chromosomally abnormal cells were observed in every case. In each patient from whom an adequate sample was obtained, a consistent clonal abnormality could be detected. The modal chromosome number of the aneuploid clone was in the diploid range for nine of the patients; the tenth patient had a mixture of diploid and triploid clones. The karyotype in most patients was very abnormal, with as many as 17 structural rearrangements seen in the malignant cells of an individual patient. One chromosome, however, was consistently abnormal in some cells from every patient, namely, 14. In nine patients, this abnormality involved the translocation of material from another chromosome to the end of No. 14 (14q+). The donor chromosome in the translocation was No. 8 in one, No. 11 in one, and No. 18 in four and possibly in two others. Thus, although not previously recognized, a t(14;18) may be a relatively common event in poorly differentiated lymphocytic malignant lymphoma. Six patients showed an abnormality of No. 1, including translocations to either the long or short arm in five. A loss of one No. 9 and a gain of one No. 12 were each seen in three patients. Nine of the ten patients studied with banding had from one to four incompletely identified marker chromosomes per cell. Immunological studies were done on seven patients who were in the leukemic phase; five patients had surface immunoglobin, which was shown to be Mκ in three and Mλ in one. Two patients had neither bone marrow-derived nor thymusderived cell surface markers and were classified as “null.” No clear correlation between cytogenetic and immunological markers was seen in the four patients in whom both studies were performed. In some patients, failure to express surface markers ( i.e. , “null” cell type) may be related to increasing aneuploidy.