Sadaf Sarfraz


Cell cycle checkpointkinase2, influences the chemotherapeutic response in breast cancer patients



ABSTRACT

Checkpoint kinase2 (CHEK2, chk2) is a multifunctional kinase gene which controls the cell cycle in response to DNA damage by phosphorylation of other genes. During DNA damage repair it has ability to control and prevent tumorigenesis either by maintaining normal cell growth or putting cell to apoptosis or senescence. CHEK2 protein inhibits the entry of CDC25C phosphatase into mitosis and tend to stabilize the tumor suppressor protein p53, causing the arrest of cell cycle in G1 phase. Its protein also interacts with breast cancer gene 1 BRCA1, which tends to maintain the normal cell cycle repair mechanism. CHEK2 considered to have significance in therapeutic approach and positive influence on radiotherapy in breast cancer patients. In different types of breast tumors, activated CHK2 linked directly with phenotype of tumor it can also be responsible for causing resistance in DNA damage during treatment. Similarly, the loss of CHEK2 in breast cancer patients could be lethal as it directly interacts with the proteins necessary for DNA damage repair. In this research we will find the expression levels of CHEK2 of breast cancer patients at different stages to analyze how they vary during chemotherapy. 

CHEK2 Gene

FINDINGS

The study found that the genes, ATM, CHEK2, and RAD51 involved in DNA damage sensors, effectors, and repair mechanisms are independent but associated with the response of chemotherapeutics. Molecular analysis of these three candidate genes, ATM, CHEK2 and RAD51 revealed that their expression in breast cancer patients alters due to different chemotherapeutic drugs and affects the survival probability of patients. The expression of these genes can  be considered important biomarkers to indicate the efficiency of different chemotherapeutic regimes and prognostic outcome 

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