Cancer Genetics and Cytogenetics 123 (2000) 55–60 0165-4608/00/$ – see front matter © 2000 Elsevier Science Inc. All rights reserved. PII: S0165-4608(00)00305-8 No evidence of increased chromosomal aberrations and micronuclei in lymphocytes from nonfamilial thyroid cancer patients prior to radiotherapy Octávia Monteiro Gil a,d , Nuno G. Oliveira a,e , António S. Rodrigues a,f , António Laires a,c , Teresa C. Ferreira b , Edward Limbert b , José Rueff a, * a Department of Genetics, Faculty of Medical Sciences, New University of Lisbon, Rua da Junqueira 96, P-1349-008, Lisbon, Portugal b Portuguese Oncology Institute of Lisbon, Lisbon, Portugal c Faculty of Sciences and Technology, New University of Lisbon, Lisbon, Portugal d Nuclear and Technological Institute, Department of Radiological Protection and Nuclear Safety, Lisbon, Portugal e Faculty of Pharmacy, University of Lisbon, Lisbon, Portugal f University Lusófona, Lisbon, Portugal Received 21 March 2000; accepted 21 June 2000 Abstract The relationship between the presence of high frequencies of chromosomal aberrations in periph- eral lymphocytes and predisposition to cancer has been suggested for some cancer diseases. In nonfamilial thyroid cancer, the few reports available are equivocal. The aim of this study was to assess the possible chromosomal instability in peripheral blood lymphocytes from 22 patients suf- fering from nonfamilial thyroid cancer. For this purpose, 2 classic cytogenetic assays, the chromo- somal aberrations assay and cytokinesis-blocked micronucleus assay, were chosen. The frequency of chromosomal aberrations excluding gaps (%) was 1.68  1.39 (mean value  SD) for the pa- tients group versus 2.20  1.87 for the control group. The frequency of binucleated lymphocytes with micronuclei (‰) was 5.41  3.51 (mean value  SD) for the patients group versus 5.37  3.21 for the control group. The results obtained revealed no significant differences between both groups. The present study reinforces the idea that constitutional chromosomal instability in pe- ripheral blood lymphocytes is not visible in nonfamilial thyroid carcinomas. © 2000 Elsevier Sci- ence Inc. All rights reserved. 1. Introduction Thyroid cancer represents less than 1% of all human can- cers; however, it is the most frequent endocrine neoplasia [1]. The nonfamilial papillary and follicular thyroid carcino- mas are the most frequent histological varieties, with a long- term (10-year) survival rate of more than 90% [2]. The annual incidence rate for thyroid carcinomas ob- served in various regions of the world ranges from 0.5 to 10 cases per 100,000 population. These diseases are unusual in children and adolescents, and its incidence increases with age in adults (reviewed in Schlumberger [1]). The majority of cases occur between 25 and 65 years of age [3]. The pap- illary and follicular carcinomas are 2–4 times more frequent in women than in men [1, 4]. Exposure to ionizing radiation is the only verified cause of thyroid carcinogenesis in humans, especially when re- ceived at a young age, although dietary iodine deficiency has been linked to this pathology [5]. Alterations in gene ex- pression have been found in thyroid tumors, leading to the view that oncogene activation and tumor suppressor gene inactivation may be factors in its development [6]. The presence of high frequencies of chromosomal aberra- tions in peripheral lymphocytes of individuals predisposed to cancer has been well established in some DNA repair defi- ciency syndromes, such as Bloom syndrome, Fanconi ane- mia, and ataxia-telangiectasia (reviewed in Friedberg et al. [7]). The same evidence was found in patients suffering from prostate cancer [8]. Other types of cancer, such as testicular cancer [9], Hodgkin disease [10], lung cancer [11], and carci- noma of the cervix uteri [12] have been reported as diseases associated with some type of chromosomal instability. How- ever, other reports point to negative evidence of chromosome instability in peripheral lymphocytes in other cancers, namely * Corresponding author. Tel.: +351-21-361-0290; fax: +351-21-362- 2018. E-mail address: rueff.gene@fcm.unl.pt or jose.rueff@gene.unl. mailpac.pt (J. Rueff).