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Summary. In 140 patients with de novo acute myeloid leukaemia (AML) standard cytogenetics were compared with RT-PCR for the detection of t(8;21), t(15;17) and inv(16) and fluorescence in situ hybridization (FISH) for numerical aberrations of chromosomes 7, 8, X and Y. RT-PCR detected 18 cases with t(8;21), 12 with t(15;17) and seven with inv(16). In two cases with t(8;21), two with t(15;17) and four with inv(16) these aberrations had not been detected by standard cytogenetics. There were no false negative PCR results. In 12 patients with these chromosomal changes, standard cytogenetics revealed additional chromosomal aberrations. In 16 patients sole numerical aberrations of the chromosomes 7, 8, X or Y were found by FISH. In these patients the sensitivity of FISH and standard cytogenetics was comparable. In 87 patients no aberrations could be found by PCR and FISH whereas in 24 of these patients standard cytogenetics revealed an abnormal karyotype. These data recommend the combination of standard cytogenetics and molecular techniques to improve the sensitivity for the detection of genetic lesions in AML. Once chromosomal markers have been identified by combined analysis these markers could be used to monitor residual disease during/after chemotherapy, by RT-PCR and/or FISH.

Summary:therapy and stem cell support appears possible. Peters et al 2,3 reported a 78% overall survival (OS) in this high-risk breast cancer subgroup after high-dose chemotherapy folTwenty-one high-risk patients with primary stage II/III breast cancer were treated with high-dose chemolowed by stem cell support (median follow-up 4.5 years).Gianni et al 4 showed a OS of 78% after 5 years in these therapy comprising etoposide, ifosfamide, carboplatin and epirubicin (VIC-E). Tumor cells of epithelial origin patients. Several authors have suggested that tumour cells present in stem cell transplants may contribute to relapse were analyzed using the monoclonal antibodies CK2 (IgG 1 ) and A45-B/B3 (IgG 1 ) against cytokeratin (CK) in patients treated with high-dose chemotherapy and stem cell support. [5][6][7][8][9] To determine the significance of tumor cell For the present study 21 female patients with high-risk patient number only a trend towards a superior relapsebreast cancer and involvement of seven to nine (three free survival in the patient group with CK negative patients) and 10 or more (18 patients) axillary lymph nodes transplants can be shown by Kaplan-Meier analysis.were used. Informed consent was obtained from all Keywords: tumor cells; peripheral blood stem cell transpatients. All patients had histologically proven resectable plantation; bone marrow; breast cancer breast cancer (19 invasive ductal, two invasive lobular).After an extensive diagnostic program, patients were staged according to the UICC breast cancer classification as folBreast cancer accounts for approximately 30% of all canlows: UICC stage IIA n = 4 (19%), IIB n = 8 (38%), IIIA cers in women. It is one of the most common malignancies n = 5 (24%), IIIB n = 4 (19%). Median age of the patients and the second leading cause of death in women. 1 The 10-at time of primary surgery was 50.8 years . No year relapse rate, increasing with the number of lymph patient had received previous chemotherapy, radiotherapy nodes involved, is about 20% for negative lymph node or immunotherapy. Patient characteristics are shown in stages and greater than 60% in women with one to three Table 1. lymph nodes involved. Patients with stage II/III breast cancer and 10 or more involved axillary lymph nodes can curTreatment rently expect only a 15-20% 10-year disease-free survival. Improvement of treatment outcome with standard-dose Patients were treated with two cycles of induction chemoinduction chemotherapy followed by high-dose chemotherapy with the standard-dose VIP-E regimen, which consisted of etoposide 500 mg/m 2 , ifosfamide 4000 mg/m 2 , cisplatin 50 mg/m 2 and epirubicin 50 mg/m 2 . 13 Mesna uro-

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We analyzed 447 patients with de novo AML using alpha-satellite probes for the chromosomes 7, 8, X, and Y and RT-PCR for t(8;21), t(15;17) and inv(16). In 130/447 patients (29%) chromosomal aberrations were found. Thirty-three patients (7%) had a t(8;21); 11 of these had the additional loss of a sex chromosome (p<0.001) and two a trisomy 8. Twenty-nine patients (6%) had a t(15;17); four of these had a trisomy 8. Sixteen patients (4%) displayed an inv(16); four of these had a trisomy 8. Twenty-two patients (5%) had a sole trisomy 8 and one patient the combination of trisomy 8 and trisomy X. Five patients (1%) displayed the loss of a Y-chromosome as the sole abnormality and two patients had a sole trisomy X. In 22 patients (5%) a monosomy 7 was found, and in none of these patients were additional chromosomal aberrations detected by RT-PCR (p < 0.05). In conclusion, trisomy 8 and the loss of a gonosome are frequently associated with structural chromosomal aberrations with a significant association of -X/Y and t(8;21). The absence of these genomic lesions in AMLs with monosomy 7 suggests that the monosomy 7 has a specific role in the development of these leukemias and their clinical course.