Break in the BCL1 locus is closely associated with intermediate lymphocytic lymphoma subtype
✍ Scribed by Dr. Ruth Rimokh; Françoise Berger; Pascale Cornillet; Kamal Wahbi; Jean-Pierre Rouault; Martine Ffrench; Paul-André Bryon; Myfène Gadoux; Odile Gentilhomme; Daniel Germain; Jean-Pierre Magaud
- Book ID
- 102220781
- Publisher
- John Wiley and Sons
- Year
- 1990
- Tongue
- English
- Weight
- 405 KB
- Volume
- 2
- Category
- Article
- ISSN
- 1045-2257
No coin nor oath required. For personal study only.
✦ Synopsis
The t( I I ; 14)(q I3;q32) is a recurring translocation associated with some chronic B-cell lymphocytic malignancies; the putative protooncogene BCLI, located at the chromosome band I I q I 3, can be involved during the translocation process. In order t o determine if BCLI rearrangement is associated with a particular subtype of lymphoma, we analysed I 3 I B-cell non-Hodgkin's lymphoma samples by Southern blot analysis, using a BCLI probe. The BCLI locus was rearranged in 9 out of 25 (36%) cases of intermediate lymphocytic cell lymphomas (ILL), in I out of 8 cases of diffuse small cleaved cell lymphoma, in I out of I 2 cases of diffuse mixed cell lymphoma and in I out of 21 cases of diffuse large cell lymphoma. In contrast, BCLl was never found rearranged in any of the 46 follicular lymphomas analysed. The BCL2 gene was in germ-line configuration in all ILL. Sequential hybridization of Southern blots with JH, Cp, and BCLI probes identified comigrating fragments in only one case of ILL, which suggests that, in all the other cases, either the rearrangement of BCLI did not result from a t( I I ; 14) translocation or the break on chromosome 14 occurred outside the JH or Cp regions. These results indicate that rearrangement of the BCLI locus may be closely associated with ILL and could be considered as a genotypic marker of this lymphoma subtype.
MATERIALS AND METHODS Tissue Samples
Fresh tissues were obtained from diagnostic specimens from 148 patients at the
📜 SIMILAR VOLUMES
Cell kinetics, is a predictive parameter of breast-cancer aggressiveness, and mutations occurring in mammary tumorigenesis may favor iuncontrolled cell proliferation. In this study, cell kinetics, clinico-pathological characteristics and genetic alterations at the irrt-2, bcl-I, c-myc, c-erbB-2, and