Anna Sikorska

Karyotype changes during long-term targeted therapy of chronic myeloid leukemia with imatinib.

The main risk factors during imatinib therapy of chronic myeloid leukemia are still subject to discussion. A group of 39 patients was cytogenetically examined and monitored before and during long-term treatment with imatinib. The cytogenetic response was investigated using karyotype analysis and fluorescence in situ hybridisation method. Different therapy effects were shown for three subgroups distinguished before the start of treatment: patients with the sole translocation t(9;22) with a typical pattern of BCR/ABL fusion vs. patients with submicroscopic deletion in the fusion region ABL/BCR of the sole t(9;22) vs. patients with aberrations additional to t(9;22) and without submicroscopic deletion. Of the two group with sole t(9;22) the group with deletion in the ABL/BCL region suffered a poorer treatment outcome than the group without deletion. The risk of progression of cytogenetic changes in group with deletion was more than nine times higher than in patients with sole t(9;22) without deletion (statistically significant).

Localized gastric diffuse large B-cell lymphoma and Hodgkin's lymphoma as secondary neoplasms in two patients with chronic lymphocytic leukemia

Gastrointestinal tract may be involved in the course of chronic lymphocytic leukemia (CLL) and other lymphomas, as well as in cases of Richter’s syndrome [1 – 3]. While transformation of CLL into localized gastric diffuse large B-cell lymphoma (DLBCL) has been reported [4 – 6], an isolated Hodgkin’s lymphoma (HL) developing in the stomach in patients with CLL has not yet been described in the available literature. In most patients with localized gastric DLBCL associated with CLL, molecular studies reveal a different clonal origin of lymphoma cells representing a new neoplasm [4 – 6]. Less frequently, the same immunoglobulin (Ig) gene rearrangement has been found by polymerase chain reaction (PCR) and sequencing analyses [5]. In such cases DLBCL arises through transformation of a pre-existing CLL clone and represents a true molecular lymphoma transformation [7]. We describe transformation into DLBCL and HL, both localized in the stomach, in two patients with CLL. The first patient, a 67-year-old man was referred to the clinic with WBC-1476 10/l and lymphocytosis (94% lymphocytes). He had slightly enlarged peripheral lymph nodes (diameter 1 – 2 cm) and splenomegaly (19 cm). The morphology and immunophenotype (CD19, CD20, CD5, CD23 and Ig kappa positive) of cervical lymph node and bone marrow were consistent with the diagnosis of CLL according to the WHO classification [8]. CLL – Rai stage II was diagnosed. One month later progressive epigastric pain appeared. On endoscopic examination a large (56 46 3.5 cm) ulcerating tumor was found in the gastric antrum. Histopathological evaluation of gastric biopsy and surgically removed stomach showed infiltration by large lymphoma cells (DLBCL) with phenotype CD45þ, CD20þ, bcl6þ, Ig lambdaþ, EBV-LMP1þ, CD57, CD237 and MIB1 in 85% cells. DLBCL cells were intermingled with foci of small CLL cells expressing CD20, CD5 and CD23 (Figure 1A). The uninvolved mucosa showed the features of chronic gastritis with no evidence of Helicobacter pylori (Hp) infection. Lymph nodes of the small curvature, spleen and liver were involved by CLL without the presence of large transformed cells. The patient was treated with six courses of CHOP program and is still in complete remission 22 months after chemotherapy. The second patient, a 76-year-old man presented with mild peripheral lymph nodes enlargement, WBC-24,66 10/l, lymphocytosis-86% and 80% small lymphocytes on the bone marrow smear. Histopathological and immunohistochemical studies of cervical lymph node were consistent with CLL diagnosis (CD20þ, CD5þ, CD23þ, CD43þ, Ig lambdaþ, MIB1 in 15% cells). CLL – Rai stage I was diagnosed. The patient had recurrent severe infections and the treatment with six courses of cyclophosphamide and cladribine (2-CdA) was initiated. Following the treatment partial remission was achieved. Two years later the patient was

Nabyta choroba von Willebranda (AVWS) przyczyną skazy krwotocznej u chorej z wywiadem niedoczynności tarczycy i niewydolnością nerek

B. Baran *, E. Odnoczko , E. Stefanska-Windyga , K. Bykowska , J. Oldenburg , J. Windyga 1 Zaklad Hemostazy i Chorob Metabolicznych, Instytut Hematologii i Transfuzjologii, Warszawa, Polska Poradnia Zaburzen Hemostazy, Instytut Hematologii i Transfuzjologii, Warszawa, Polska 3 Instytut Hematologii Eksperymentalnej i Transfuzjologii, Bonn, Niemcy *Autor prezentujący i do korespondencji. Adres email: bbaran@ihit.waw.pl