Treatment of cervical cancer stage IB2 and higher according to FIGO consists of chemo-radiotherapy with brachytherapy [87]. In the treatment of advanced cancers, radiotherapy in combination with cisplatin is used after surgery [88].Radiotherapy can be distinguished by high-dose rate (HDR) brachytherapy [89]. Brachytherapy allows a high dose of radiation to be delivered to the tumor with limited radiation reaching normal tissues that are close to the tumor [90]. In the case of gynecological tumors, this will mainly be the bladder and rectum [89]. The main radioisotopes used in radiotherapy of cervical cancers are Ir-192 and Co-60, with iridium being the more commonly used isotope [91]. A compilation of results showing the toxicity and impact on patient survival depending on the radioisotope used is an important subject of research. Some sources show that Ir-192 and Co-60 do not differ in terms of survival or toxicity when used in brachytherapy [91,92]. A study importing the effects of iridium and cobalt radiation on the bladder and rectum showed no differences between the two isotopes [93]. Other work presents iridium as a radioisotope with better physical properties, allowing for more satisfactory brachytherapy effects [94]. It is likely that Ir-192 may contribute to greater tumor regression and will also damage nearby tissues to a lesser extent [95]. It is possible that cobalt-60 is most effective in low-grade tumors and those less than 2 cm in diameter [96]. An important consideration in the choice of radioisotope for the treatment of gynecological cancers is the cost of therapy. The cobalt isotope compares more favourably in economic terms [92]. This is related to the longer half-life of the cobalt isotope than that of iridium, 5.26 years, 73.8 days respectively, which contributes to the need to replace the iridium source 3–4 times per year [97]. Even the need for larger shielding when using cobalt than when using iridium brachytherapy does not outweigh the cost of using Ir-192 [98]. Therefore, brachytherapy with Co-60 is proving to be an important alternative for hospitals with lower financial resources [99]. Furthermore, according to the examples in the literature, it can be noted that cobalt compounds differ in their biochemical and biophysical properties. These characteristics and the lower toxicity of cobalt compared to other transition metals have sparked interest in cobalt as a new potential anticancer drug that could yield clinically relevant results [100]. Pasukonien created cobalt ferrite nanoparticles (Co-SPIONs) to study uptake, toxicity and effects on stem-like properties in the human ovarian cancer cell line A2780 and pancreatic cancer cell line MiaPaCa2. It was observed that both cell lines accumulated Co-SPIONs, but that A2780 cells (ovarian cancer cell line) were more sensitive to cobalt ferrite exposure. The nanoparticle could be used for diagnostics and targeted cancer therapy, but the safe concentration should be carefully assessed depending on the type of cancer cells [101]. Furthermore, it has been shown that three cobalt (II) complexes [Co(MQL)2Cl2] (CoCl), [Co(MQL)2Br2] (CoBr) and [Co(MQL)2I2] (CoI), containing 8-methoxyquinoline (MQL), can probably exhibit greater antiproliferative activity than cisplatin for the treatment of cisplatin-resistant ovarian cancers [102]. The work by Law et al. tested whether six different cobalt tris(bipyridine) complexes, depending on a given concentration, could inhibit the proliferation of cancer cells in various tissues, which would occur by arresting cell cycle progression. In the case of cervical cancer cells (HeLa) to which complex 2 [CoIII(4,4′-Me2-bpy)3](PF6)3 was applied, only a high concentration stopped the HeLa cancer cell in S phase. To confirm this, the levels of cell cycle regulatory proteins from G1 to S phase were examined. An accumulation of cyclin A and E2F was observed, which could suggest that complex 2 prevents the proliferation of the cancer cell by arresting it in S phase. This study demonstrates the possible efficacy of alternative metal compounds in cancer cells in vivo in arresting their proliferation, which is important data, especially considering the limitations of cisplatin, carboplatin in cancer therapy due to the production of resistance against these compounds after the initial treatment [103].