Human Chk2 protein kinase is involved in DNA damage checkpoint pathway. After DNA damage Chk2 is phosphorylated at multiple sites in N-terminal SCD (SQ/TQ cluster domain) and activated.

In the last progress report, I described our progress on the isolation of Chk2 mutant cells and their characterization. That aim is essentially completed.

Chk2 is a critical regulator of DNA damage repair checkpoint controls. Mutations in Chk2 confer an increased risk of breast cancer. However, the regulation of Chk2-mediated pathways is still not clear.

Overall. Our data suggest that mutations in CHEK2 may contribute to prostate cancer risk and that the DNA-damage-signaling pathway may play an important role in the development prostate cancer.

Familial breast cancer accounts for 15 to 35% of all breast cancers. Mutations in a number of genes are now known to cause susceptibility to breast cancer; the most notorious are the BRCA1 and BRCA2 genes.

We have shown that 53BP1, a tumor suppressor p53 binding proteins, is a key transducer in the DNA damage response signaling.

53BP1 binds to the tumor suppressor protein p53 and has a potential role in DNA damage responses.

Breast cancer is a very heterogeneous disease. Many pathological alterations contribute to breast cancer development. Some initiate the cancer formation or accelerate its progression.