Correspondence to: Julius Brtko, Laboratory of Molecular Endocrinology, Institute of Experimental Endocrinology, Centre of Excellence Acknowledged by the European Commission, Slovak Academy of Sciences, Vlarska 3, 833 06 Bratislava, Slovakia E-mail: julius.brtko@savba.sk Thyroid non-Hodgkin’s lymphoma (TNHL) is an uncommon tumour, representing 2–8% of thyroid malignancies and approximately 1–2% of extranodal lymphomas. TNHL is a relative rare, and it occurs most frequently in elderly women and has been linked to Hashimoto’s thyroiditis. The female preponderance is due to its origin from chronic lymphocytic thyroiditis, which tends to occur in elderly women (Evans et al. 1995; Harrington et al. 2005). A number of controversies exist regarding the roles of surgery, radiotherapy and chemotherapy in the management of this disease (Ha et al. 2001). Surgery occupied a pre-eminent place in management of TNHL, in recent years, the appreciation that TNHL is sensitive to radiotherapy and chemotherapy has resulted in a move towards limited number of surgical interventions (Harrington et al. 2005). Retinoids, rexinoids and their biologically active derivatives are involved in a complex arrangement of physiological and developmental responses in many tissues of higher vertebrates. Both retinoids and rexinoids are either natural or synthetic compounds related to retinoic acids that act through interaction with two basic types of nuclear receptors belonging to the nuclear receptor superfamily: all-trans retinoic acid receptors, known as nuclear retinoid receptors (RARα, RARβ, and RARγ) and retinoid X receptors (RXRα, RXRβ and RXRγ) play a crucial role in both physiological and pathophysiological conditions as retinoid-inducible transcription factors (Brtko et al. 2009). Retinoids inhibit carcinogenesis, suppress premalignant epithelial lesions and tumour growth and invasion in a variety of tissues. Natural and synthetic retinoids exert important biological effects due to their antiproliferative and apoptosis-inducing effects. They are also known to cause redifferentiation or to prevent further dedifferentiation of various tumour tissues (Brtko and Thalhamer 2003; Brtko 2007). Acute promyelocytic leukemia (APL), characterized by its distinctive FAB-M3 morphology and its association with a bleeding coagulopathy, is known to be associated with at least four types of non-random reciprocal chromosomal translocation, but always involving the retinoic acid receptor α gene (RARα) on chromosome 17. The majority of APL patients with the promyelocytic gene-RARα fusion 21 and the rare cases of the nucleophosmin gene-RARα fusion 22 respond to retinoic acid-induced differentiation therapy; however, APL patients with the promyelocytic leukemia zinc finger gene-RARα fusion are unresponsive (So et al. 2000). Here, we report the case of a 67-year-old woman in Slovakia who was admited to the Saint Elizabeth Institute of Oncology in Bratislava with a neck stiffness. Magnetic resonance demonstrated thyroid neoplasia with the size of 52 × 63 × 90 mm. The pathological examination after surgery confirmed TNHL of unspecified origin. The patient after tyreoidectomy underwent radiation therapy with the total dose of 60.0 Gy. TNHL tissue from this patient has been analyzed in order to get information about expression of all known subtypes of nuclear retinoid and nuclear retinoid X receptors mediating the effects of retinoic acids at the nuclear/cellular level. Determination of mRNA levels encoding all isoforms of nuclear retinoid receptors (RARα, RARβ, RARγ) and nuclear retinoid X receptors (RXRα, RXRβ, RXRγ) has been performed by the reverse transcription and subsequent PCR analyses by previously established protocols in this laboratory (Szabova et al. 2003). The band intensities were measured using the STS 6220I Documentation System (Ultralum, USA) and normalized to the band intensity of PCR product corresponding to the house keeper gene GAPDH (Fig. 1). As shown in Fig. 1, the TNHL tissue excised from the patient thyroid expressed all isoforms of RARs or RXRs. Gen. Physiol. Biophys. (2010), 29, 411–413