Cancer is a grave disease that arises because of abnormal cell growth and can invade or spread to other body parts (1). The rate of occurrence of cancer worldwide is increasing at an alarming rate, 12.7 million cases in 2008 (2). The p53 is a key protein for tumour suppression and found to be mutated in over half of all human cancers (3). Individuals with Li–Fraumeni Syndrome, a classic cancer predisposition disorder, inherit mutant p53 allele and are highly cancer-prone (4). The null mutation of p53 does not display embryonic lethality but have decreased survival as compared to wild-type mice; the majority of p53 mice succumbed to tumours between 2–9 months of age (5, 6).
Earlier studies on WDR13 suggest its involvement in cell cycle regulation in different tissues like pancreas (7–9), liver (10) adipose (11), colon (12) and uterus (13). Wdr13 expression has also been reported in many human cancers like breast cancer, glioma, Ewing’s sarcoma, lung cancer, melanoma, testes cancer, ovary teratocarcinoma, and urothelial cancer (Human protein atlas http://www.proteinatlas.org/ENSG00000101940-WDR13/cancer). High expression of WDR13 in above mentioned cancers further strengthens the postulate that WDR13 has a vital role in regulating cell cycle. Therefore, it was interesting to study the cancerous phenotype after the introgression of Wdr13-null mutation in a cancer mouse model. To test above proposition, Wdr13−/0 mice were mated with p53−/ − mice and Wdr13−/0|p53−/ − double knockout mouse was generated.