5-(Hydroxymethyl)uracil may be formed during the course of the two processes: oxidation/hydroxylation of thymine with resultant formation of 5-hydroxymethyluracil paired with adenine (produced by reactive oxygen species) and reacting of reactive oxygen species with 5-methylcytosine forming 5-hydroxymethylcytosine, followed by its deamination to 5-hydroxymethyluracil mispaired with guanine. Determination and quantification of hydroxymethyl uracil in urine serve as a potential biomarker of oxidative DNA damage. It was discovered, that urinary 5-hydroxymethyluracil might reflect the oxidative stress/chronic inflammation in colorectal cancer although the diagnostic performance for early-detection is moderate.

Estradiol mustard (developmental code name NSC-112259), also known as chlorphenacyl estradiol diester, as well as estradiol 3,17β-bis(4-(bis(2-chloroethyl)amino)phenyl)acetate, is a synthetic, steroidal estrogen and alkylating antineoplastic agent and a nitrogen mustard-coupled estrogen ester that was never marketed.[1] It is selectively distributed into estrogen receptor (ER)-positive tissues such as ER-expressing tumors like those seen in breast and prostate cancers. For this reason, estradiol mustard and other cytostatic-linked estrogens like estramustine phosphate have reduced toxicity relative to non-linked nitrogen mustard alkylating antineoplastic agents. However, they may stimulate breast tumor growth due to their inherent estrogenic activity and are said to be devoid of major therapeutic efficacy in breast cancer,[3] although estramustine phosphate has been approved for and is used (almost exclusively) in the treatment of prostate cancer.