Clinical Cancer Research Joint Metastasis Research Society-AACR Conference on Metastasis Translational Cancer Medicine 2008: Cancer Clinical Trials and Personalized Medicine
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Clinical Cancer Research Vol. 10, 6535-6543, October 1, 2004
© 2004 American Association for Cancer Research


Clinical Trials

No Long-Term Increase in Sperm Aneuploidy Rates after Anticancer Therapy

Sperm Fluorescence In situ Hybridization Analysis in 26 Patients Treated for Testicular Cancer or Lymphoma

Claire Thomas1, Christine Cans2, Roberte Pelletier3, Christine De Robertis3, Mira Hazzouri4, Bernard Sele1,2,3, Sophie Rousseaux3 and Sylviane Hennebicq1,2,3

1 Centre d’étude et de Conservation des Oeufs et du Sperme humain, Service de génétique, CHU Grenoble, Grenoble Cedex 9, France; 2 Service d’Information et d’Informatique Medicale, Centre Hospitalo-Universitaire Grenoble, Grenoble Cedex 9, France; 3 INSERM U309, Institut Albert Bonniot, UJF Grenoble I, La Tronche Cedex, France; and 4 Lebanese University, Department of Biology, Fanar, Lebanon

Purpose: Lymphomas and testicular cancers are the most frequent malignancies among young men. With recent improvement of survival rates, for many patients, the question is raised of the consequences of the anticancer treatments on their fertility and more specifically of a potential genetic risk for the offspring. This article presents the study of sperm aneuploidy rates in the largest population of cancer-treated patients studied thus far.

Experimental Design: In the present study, 38 patients were initially included 7 months to 5 years after a cancer treatment by chemotherapy and/or radiotherapy for testicular cancer (n = 19) or lymphoma (n = 19). Twelve of them were azoospermic. Sperm aneuploidy rates of chromosomes X, Y, 13, 18, and 21 were analyzed by multicolor fluorescent in situ hybridization in the 26 other patients.

Results: In most cases, the disomy/diploidy rates after cancer therapy did not significantly differ from those observed in the group of control healthy donors. Only five patients (one lymphoma and four testicular cancer) showed significant but still moderate increases in disomic and/or diploid sperm. For the lymphoma patient, the short posttherapeutic delay after the treatment could explain the elevated aneuploidy rates, whereas no risk factor in the clinical, biological, or therapeutic records could be identified in any of the four testicular cancer patients with elevated sperm aneuploidy rates.

Conclusions: These data suggest an absence of long-term effect of anticancer therapy on sperm aneuploidy rates, and therefore, no long-term increased risk of aneuploidy for the offspring obtained either spontaneously or after assisted reproductive techniques.




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Cancer Research Clinical Cancer Research
Cancer Epidemiology Biomarkers & Prevention Molecular Cancer Therapeutics
Molecular Cancer Research Cancer Prevention Research
Cancer Prevention Journals Portal Cancer Reviews Online
Annual Meeting Education Book Cell Growth & Differentiation
Copyright © 2004 by the American Association for Cancer Research.