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AIM: To retrospectively assess the acute and long-term toxicity using aromatase inhibitors (AI) therapy concurrently with hypofractionated radiotherapy (HFRT) in breast cancer patients. METHODS: From November 1999 to October 2007, 66 patients were treated with breast HFRT and concurrent AI. In 63 patients (95.5%), HFRT delivered a total dose of 32.5 Gy to the whole breast within 5 wk (five fractions, one fraction per week). Other fractionations were chosen in three patients for the patients’ personal convenience. A subsequent boost to the tumor bed was delivered in 35 patients (53.0%). Acute toxicities were scored according to the Common Toxicity Criteria for Adverse Events v3. Late toxicity was defined as any toxicity occurring more than 6 mo after completion of HFRT and was scored according to the Late Effects Normal Tissue Task Force-Subjective, Objective, Management and Analytic scale. RESULTS: At the end of the HFRT course, 19 patients (28.8%) had no irradiation-related toxicity. Acute grade 1-2 epithelitis was observed in 46 patients (69.7%). One grade 3 toxicity (1.5%) was observed. With a median follow-up of 34 mo (range: 12-94 mo), 31 patients (47%) had no toxicity, and 35 patients (53%) presented with grade 1-2 fibrosis. No grade 3 or greater delayed toxicity was observed. CONCLUSION: We found that AI was well tolerated when given concurrently with HFRT. All toxicities were mild to moderate, and no treatment disruption was necessary. Further prospective assessment is warranted.

The treatment of nude mice bearing tumors of transplanted human leukemic cells with drugs known to induce differentiation of the same leukemic cells in vitro does not always affect tumor yield, tumor cell differentiation or nude mice survival. We have transplanted human monoblastic leukemic cells of the U-937 cell line into newborn Swiss nu/nu mice. Priming with cyclophosphamide, followed by subcutaneous injections of at least 10 x 10(6) cells allowed us to obtain solid tumors. The cytology, HLA phenotype and in vitro proliferation characteristics of the U-937 tumor cells were conserved. However, these tumor cells were more tumorigenic when reinjected into nude mice and showed a modified response to differentiation induction. A decreased capacity to differentiate with retinoic acid (RA) and a resistance to 1-beta-D arabinofuranosyl cytosine (Ara-C) and 1-25 dihydroxy vitamin D3 (1-25 (OH)2 D3) were noted in three tumor cell lines tested. With regard to the latter, the resistance was not due to a modification of the number of cell receptors. The study shows that though in vivo transplantation of human leukemic cells in nude mice may lead to a selection of resistant cells, systematic checking of in vitro differentiation characteristics of the tumor cells permits the nude mouse model to be maintained for the in vivo screening of new differentiating agents.

Background: Ocular adnexal lymphomas may be antigen-driven disorders; however, the source of the putative antigen or antigens is still unknown. Hence, we assessed whether Chlamydiae infection is associated with the development of ocular adnexal lymphomas. Methods: The presence of Chlamydia psittaci, trachomatis, and pneumoniae DNA was investigated by polymerase chain reaction in 40 ocular adnexal lymphoma samples, 20 nonneoplastic orbital biopsies, 26 reactive lymphadenopathy samples, and peripheral blood mononuclear cells (PBMCs) from 21 lymphoma patients and 38 healthy individuals. Seven patients with chlamydia-positive PBMCs were treated with the antibiotic doxycycline, and objective response was assessed in four patients with measurable lymphoma lesions. Differences in Chlamydiae DNA detection between the case patients and the control subjects were analyzed using the Fisher exact test. All statistical tests were two-sided. Results: Thirty-two of the 40 (80%) ocular adnexal lymphoma samples carried C . psittaci DNA, whereas all lymphoma samples were negative for C. trachomatis and C. pneumoniae. In contrast, none of the 20 nonneoplastic orbital biopsies (0% versus 80%; P