Aflatoxin B1 aldehyde reductase (AFAR) genes cluster at 1p35-1p36.1 in a region frequently altered in human tumour cells. 
Alterations of the distal portion of the short arm of chromosome 1 (1p) are among the earliest abnormalities of human colorectal tumours.  Recently, we have cloned the Aflatoxin B1 aldehyde reductase (AFAR) gene from a smallest region of overlapping deletion that is frequently (48%) hemizygously deleted in sporadic colorectal cancer.  AFAR is expressed in a broad range of tissues.  Its closely related rat protein is the major factor conferring resistance of rats towards aflatoxin B1-induced liver carcinogenesis.  Here, we have identified cDNAs covering two additional human AFAR-related genes localized in close proximity to the previously described AFAR at 1p35-36.  We have analysed their structure and tissue-related expression.  One of them, AFAR3, carries a Selenocysteine-Insertion Element (SECIS)-like structure that during translation may recode an in-frame TGA-stop codon to a selenocysteine.  Two additional AFAR-pseudogenes are localized at Xq25 and 1p12, respectively.  AFAR exon sequences share an identity of DNA and amino acids of more than 78%.  Also large blocks of intronic sequences can be up to 98.6% identical.  Knowledge of the AFAR genes and their structure will be essential in genetic and functional studies, where discrimination of the genes and proteins is a prerequisite for evaluating their individual functions.