Many in vitro studies demonstrated the cancer-inducing effects of thyroid hormones (Bergh et al., 2005, Davis et al., 2004, Lin et al., 1999, Lin et al., 2013). Thyroid hormones bind to membrane as well as nuclear receptors and activate various oncogenic paths within the cell, which in turn triggers cell growth and angiogenesis, while at the same time inhibiting cell apoptosis. Therefore, thyroid hormones have an established role in cancer development, but also prognosis and outcome. Based on in vitro studies, clinical studies were conducted indicating a link between higher serum thyroid hormone levels and lower TSH levels with a higher risk of solid and hematologic malignancies (Dalamaga et al., 2008, Hellevik et al., 2009, Khan et al., 2016). Furthermore, higher thyroid hormone levels have also positively correlated with worse prognosis (Tosovic, Bondeson, Bondeson, Ericsson, & Manjer, 2014) and higher mortality rates (Journy et al., 2017) in cancer patients. Additionally, hypothyroidism has been positively correlated with a decreased risk of cancer (Schmidinger et al., 2011, Søgaard et al., 2016), better treatment outcome, better prognosis (Berghoff et al., 2020, Riesenbeck et al., 2011), and prolonged survival (Buda-Nowak et al., 2017) in cancer patients, which is particularly demonstrated in renal malignancies (Baldazzi et al., 2012).

Still, this association is not unambiguous (Ellerhorst et al., 2001, Fabian et al., 2015, Sohn et al., 2020). However, even if an association between clinical and subclinical hyperthyroidism and the risk of cancer development is debated (Ittermann et al., 2010, Vadiveloo et al., 2011, Zhang et al., 2014), the relationship between higher thyroid hormone levels and worse prognosis is demonstrated in different cancers. Accordingly, the rapid restoration of the euthyroid state is crucial not only for prognostic purposes but also to eliminate the interference of hyperthyroidism on cancer therapies.