Briz et al 1 described a method to detect maternal cell contamination of cord blood. They used PCR amplification of genomic hypervariable regions followed by run on agarose gels stained with ethidium bromide and visualised under UV transillumination. In our opinion, the method used by Briz et al, although simple and inexpensive, has a low sensitivity to identify maternal cells in cord blood samples. The sensitivity reported was between 0.5 and 1% with a contamination incidence of 1.25% (one contaminated of 80 cord blood samples). Sociè et al 2 reported the same sensitivity levels using minisatellite PCR amplification followed by Southern blotting and radioactive detection. In this way the authors identified one contaminated cord blood sample out of 47. Later on, the same group reported a more sensitive technique to identify maternal DNA contamination. 3 They described a PCR amplification of the polymorphic TPO sequence followed by Southern blotting and radioactive detection with a sensitivity of 0.01%.A sensitivity as high as this can also be obtained through techniques which do not need radioactivity. 4 In our experience, we achieved a sensitivity of 0.04% with a contamination incidence of 18% (11 contaminated of 60 cord blood samples). 5 We used a PCR amplification of genomic hypervariable regions, followed by chemiluminescent detection.Many other papers dealing with this subject 2-8 have been published with a variable contamination incidence depending on the technique used.In our opinion it would be more important to establish at what level the maternal cell contamination may exert a clinically relevant effect, if the maternal contamination is due to metabolically active cells, which kind of cells are involved, what is the number of maternal cells acceptable in a cord blood transplantation and what is the possible correlation between GVHD and maternal contamination. We underline the importance of correlating the contamination data with clinical results. This could be achieved with retrospective studies on cord blood transplanted patients who experienced GVHD and with an analysis of the maternal contamination entity using a standard method with a defined sensitivity. Otherwise, the conclusions drawn on the contamination rate can be misleading. Anaphylactoid reaction to granulocyte colonystimulating factor used in mobilization of peripheral blood stem cellWith wider use of the hematopoietic growth factors in both allogeneic and autologous stem cell transplantation, several unusual complications such as splenic rupture and anaphylWe suggest that a workshop should be set up to analyse the problem of maternal cell contamination in cord blood samples and to establish an appropriate standard method to detect maternal contamination. F PoliCentro actic reaction have been reported. [1][2][3][4][5][6][7] We report a case of severe anaphylactoid reaction after intravenous administration of rhG-CSF and the successful use of rhGM-CSF.A 52-year-old Caucasian female presented with a right axillary mass. Biopsy confirmed the ...

We describe a patient presenting with postmenopausal vaginal bleeding and a uterine mass subjected to endometrial biopsy that showed a high-grade non-Hodgkin's lymphoma, consistent with a diffuse large B-cell lymphoma. Staging computed tomography (CT) scans of the chest, abdomen, and pelvis revealed three lung nodules in addition to the uterine mass. Fine needle aspirate of one lung lesion showed lymphomatous involvement. She was treated with intensive chemotherapy alone and has remained in complete remission 21 months after diagnosis. The literature on primary lymphoma of the uterine corpus is reviewed.

Arsenic trioxide has been shown to be effective and approved by the US Food and Drug Administration in treating patients with relapsed acute promyelocytic leukemia (APL). 1,2 The dermatologic side effects of arsenic trioxide such as pruritus and dermatitis are usually mild and self-limiting. We report a case of severe radiation recall dermatitis in a patient with APL treated with arsenic trioxide.This patient was a 49-year-old African-American female when she was diagnosed with stage IIb left breast cancer in 1999 treated with modified radial mastectomy. After surgery, she received adjuvant chemotherapy with four cycles of adriamycin/cyclophosphamide and four cycles of paclitaxel, followed by adjuvant radiation to the left chest wall, left supraclavicular and left internal mammary nodes, 5000 cGy in 25 daily fractions, and tamoxifen. She had done extremely well until September 2001 when her white blood cell (WBC) decreased to 3700/ml, Hgb to 9.9 g/dl with MCV being 100.6 fl, and platelet count 220 000/ml. When she was referred to this institution in February 2002, the WBC was 1500/ml. Serum haptoglobin was 182 mg/dl, serum iron 140 mg/dl, TIBC 236 mg/dl, vitamin B 12 level 489 pg/ml (normal 210-705), RBC folate level 760 ng/ml (normal 4164). Bone marrow examination revealed 80% cellularity and 68% promyelocytes and blasts with prominent Auer rods consistent with APL. The diagnosis was confirmed by cytogenetic study and florescence in situ hybridization of the bone marrow showing 46,XX,t(15;17)(q22;q21) [20]. She was treated with all-trans-retinoic acid (ATRA) 45 mg/m 2 /day, daunorubicin 50 mg/m 2 /day days 3-6, and cytarabine 200 mg/m 2 /day continuous infusion days 3-9 with complete morphologic and molecular remission achieved in 5 weeks. Intravenous dexrazoxane 500 mg/m 2 was also added because her left ventricular ejection fraction was only 44% probably secondary to prior Adriamycin and chest wall radiation. She then received consolidation therapy consisting of arsenic trioxide 0.15 mg/kg/day for 5 days each week for 5 weeks, repeat once after 2 weeks of rest. By day 2 at week 3 of the second cycle of arsenic trioxide, she started noticing skin peeling off her feet and hands. In addition, she also noticed hyperpigmentation, vesicular formation and superficial desquamation of the left chest wall, well demarcated to her previous radiation field (Figure 1). In view of a possible radiation recall reaction, arsenic trioxide was discontinued. No systemic antibiotic was prescribed because cellulitis was unlikely with such a well-defined margin. The skin lesions were treated with topical triamcinolone/ silver sulfadiazine cream with good response. She proceeded with further consolidation of ATRA and daunorubicin/dexrazoxane without further problem. She is currently on maintenance ATRA and in continuous remission 1 year after diagnosis.Radiation recall is an inflammatory reaction at a previously irradiated fields usually associated but not limited to cytotoxic drugs. The common inciting agents (complete list of refer...

results indicate that the absolute degradation rate is approximately 50% per day (ie an increase of the Ct value with one cycle) in PB MNC.Although our data are based on a limited and heterogeneous set of samples, they clearly indicate that transcripts are rapidly degraded ex vivo and that the rate of degradation can differ between different types of transcripts, between PB and BM, and between patients. As such differential degradation will results in an over-or underestimation of MRD levels, samples should preferably be processed on the day of sampling; this processing should include at least the Ficoll density centrifugation-based separation of MNC and the cell lysis step of the RNA extraction. Even better, because changes in transcript levels can already occur within the initial 4 h, 5 samples should be collected in tubes with immediate stabilization of intracellular RNA, thereby preventing any degradation of control gene and/or fusion gene transcripts. Such reagents for stabilization of RNA have recently successfully been applied in a multi-center study (Mueller et al, Blood 2003; 102: 64a abstract We read with interest the paper by Ruchatz et al 1 on the effect of imatinib on hematopoietic recovery following idarubicin exposure in murine model. We describe an elderly patient with chronic myeloid leukemia (CML) and transformed large B-cell lymphoma treated with imatinib mesylate and combination chemotherapy.This is an 87-year-old male with a history of follicular lymphoma involving left cervical nodes in 1996, and he refused further therapy. He presented again in July 2000 with a markedly elevated WBC of 223 000/ml. A bone marrow examination confirmed the diagnosis of CML in chronic phase with cytogenetic study showing 45X,-Y,t(9; 22)(q34; q11) [25].

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