title: t(11;14)-positive mantle cell lymphomas exhibit complex karyotypes and share similarities with B-cell chronic lymphocytic leukemia.
abstract: Until now, few data on additional chromosomal aberrations in t(11;14)-positive mantle cell lymphomas (MCLs) have been published. We analyzed 39 t(11;14)-positive MCLs by either comparative genomic hybridization (CGH; n = 8), fluorescence in situ hybridization (FISH) with a set of DNA probes detecting the most frequent aberrations in B-cell neoplasms (n = 12), or both techniques (n = 19). The t(11;14) was present in all cases. In 37 of 39 cases, chromosomal imbalances were found. In 27 cases, complex karyotypes, i.e., >/= 3 aberrations, were identified. The most frequent aberrations were losses of 13q14-21 or 13q32-34 (27 cases), 9p21 (16 cases), and 11q22-23 (12 cases) and gains of 3q26-29 (19 cases), 8q22-24 (11 cases), and 18q21-22 (9 cases). In 26% of cases (7 of 27) analyzed by CGH, a total of 10 high-level DNA amplifications were identified. Although in comparison with B-cell chronic lymphopcytic leukemia (B-CLL) MCL is characterized by a much higher complexity of chromosomal aberrations, there are striking similarities: 13q14 deletions were identified in more than 50% of both MCL and B-CLL cases. In contrast, in our CGH database containing 293 B-cell lymphomas, this aberration was found in only 11% of other nodal lymphomas. Even more strikingly, 11q deletions, which are present in 20%-30 % of MCL and B-CLL, were found very rarely in other nodal B-cell lymphomas (CGH: 1 of 208 cases; FISH: 1 of 69 cases). These data show that MCL is characterized by specific secondary aberrations and that there may be similarities in the pathogenesis of MCL and B-CLL. Genes Chromosomes Cancer 27:285-294, 2000.
authors.affiliation: Abt. Innere Medizin III der Universität Ulm, Ulm, Germany.
authors.forename: M
authors.initials: M
authors.lastname: Bentz
authors.forename: A
authors.initials: A
authors.lastname: Plesch
authors.forename: L
authors.initials: L
authors.lastname: Bullinger
authors.forename: S
authors.initials: S
authors.lastname: Stilgenbauer
authors.forename: G
authors.initials: G
authors.lastname: Ott
authors.forename: H K
authors.initials: HK
authors.lastname: Müller-Hermelink
authors.forename: M
authors.initials: M
authors.lastname: Baudis
authors.forename: T F
authors.initials: TF
authors.lastname: Barth
authors.forename: P
authors.initials: P
authors.lastname: Möller
authors.forename: P
authors.initials: P
authors.lastname: Lichter
authors.forename: H
authors.initials: H
authors.lastname: Döhner
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D002872:Chromosome Deletion; D002880:Chromosomes, Human, Pair 11 / Q000235:genetics*; D002883:Chromosomes, Human, Pair 14 / Q000235:genetics*; D005260:Female; D005784:Gene Amplification; D019254:Genes, bcl-2 / Q000235:genetics; D006801:Humans; D017404:In Situ Hybridization, Fluorescence; D007399:Interphase / Q000235:genetics; D007621:Karyotyping; D015451:Leukemia, Lymphocytic, Chronic, B-Cell / Q000235:genetics* / Q000473:pathology; D020522:Lymphoma, Mantle-Cell / Q000235:genetics* / Q000473:pathology; D008297:Male; D008875:Middle Aged; D009693:Nucleic Acid Hybridization; D014178:Translocation, Genetic / Q000235:genetics*