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

• Published in: Clinical cancer research 2004-10, Vol.10 (19), p.6535-6543
• Main Authors: THOMAS, Claire, CANS, Christine, PELLETIER, Roberte, DE ROBERTIS, Christine, HAZZOURI, Mira, SELE, Bernard, ROUSSEAUX, Sophie, HENNEBICQ, Sylviane
• Format: Article
• Language: English
• Subjects: Adolescent; Adult; Aneuploidy; Antineoplastic agents; Biological and medical sciences; Chromosome Aberrations - drug effects; Chromosome Aberrations - radiation effects; Humans; In Situ Hybridization, Fluorescence; Lymphoma - drug therapy; Lymphoma - genetics; Lymphoma - radiotherapy; Male; Medical sciences; Middle Aged; Pharmacology. Drug treatments; Sperm Motility - drug effects; Sperm Motility - radiation effects; Spermatozoa - drug effects; Spermatozoa - metabolism; Spermatozoa - radiation effects; Testicular Neoplasms - drug therapy; Testicular Neoplasms - genetics; Testicular Neoplasms - radiotherapy; Time Factors; Treatment Outcome; Tumors
• ISSN: 1078-0432; 1557-3265
• DOI: 10.1158/1078-0432.CCR-04-0582

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. 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. 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. 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.