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[Cancer Research 48, 5557-5564, October 1, 1988]
© 1988 American Association for Cancer Research

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Frequent Nonrandom Chromosome Abnormalities in 27 Patients with Untreated Large Cell Lymphoma and Immunoblastic Lymphoma1

Fernando Cabanillas2, Sen Pathak, Jose Trujillo, John Manning, Ruth Katz, Peter McLaughlin, William S. Velasquez, Fredrick B. Hagemeister, Angela Goodacre, Ann Cork, James J. Butler and Emil J Freireich

Departments of Hematology [F. C., P. M., W. S. V., F. B. H., E. J F.], Genetics [S. P., A. G.], Laboratory Medicine [J. T., A. C.], and Pathology [J. M., J. J. B.], The University of Texas-M. D. Anderson Hospital and Tumor Institute at Houston, Houston, Texas 77030

Fresh tumor samples from 27 patients with large cell lymphoma, either previously untreated (26 patients) or minimally treated (one patient), were processed for cytogenetic studies. Cytogenetic abnormalities were observed in all patients, most commonly in chromosomes 1, 3, 7, 12, 14, 17, and 18. Nine chromosomal breakpoints appeared frequently: 14q32 in 14 instances; 18q21 in seven; 9p13-21, 17p11-13, and 3q21-23 in six each; 1p11-21 in five instances; 1p36 in four; and 2p21-23 in three. The most common structural abnormalities were t(14;18)(q32;q21) in seven patients (26%) and 17p- in six (22%). The presence of 17p- was associated with a significantly higher proliferative capacity as manifested by the percentage of S phase = 22% versus 11% for cases without 17p- (P < 0.05). Trisomy 12, typical of small lymphocytic lymphoma, was seen in five patients in this series, all of whom had diffuse large cell lymphoma; frequently, it appeared simultaneously with t(14;18). The two patients with immunoblastic lymphoma of B-cell type had an abnormality involving chromosome 2p21-23. Deletions in the long arm of chromosome 6, previously described as typical of diffuse large cell lymphoma and B-cell immunoblastic lymphoma were observed infrequently in this series. However, this abnormality has been present in 50% of patients with large cell lymphoma previously exposed to therapy, suggesting that it may be related to effects of chemotherapy or to clonal evolution.

1 Supported in part by the Hudson Ard Memorial Fund and CA 39809 from the National Cancer Institute, NIH, Bethesda, MD 20205.

2 To whom requests for reprints should be addressed, at the University of Texas-M. D. Anderson Hospital, 1515 Holcombe Boulevard, Houston, TX 77030.

Received 11/ 3/87. Revised 4/22/88. Accepted 6/28/88.




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Copyright © 1988 by the American Association for Cancer Research.