In the breast cancer cells, it has been found that enhanced resistance to cisplatin under hypoxic conditions was mediated through HIF-1α [42], whereas in osteosarcoma cells hypoxia-induced resistance to cisplatin, doxorubicin and etoposide has been found to be HIF-independent and to occur via hypoxia-driven attenuation of p53 activation [43]. This evidence concerns the gene HIF1A and breast carcinoma.