Skip to main content
Figure 2 | Breast Cancer Research

Figure 2

From: Low expression levels of ATM may substitute for CHEK2 /TP53 mutations predicting resistance towards anthracycline and mitomycin chemotherapy in breast cancer

Figure 2

Alterations in the p53 functional pathway predicts chemoresistance. (A) Schematic illustration of the three central players (ATM, Chk2 and p53), activated in response to chemotherapy induced double stranded DNA breaks. All patients in this study with tumors displaying lack of response to neoadjuvant treatment with doxorubicin or 5-fluorouracil/mitomycin (left) or epirubicin (right) harbor alterations affecting at least one of these factors, leaving the functional pathway disrupted and thus, cells resistant to therapy. (B) Graphs displaying P-values for the correlations between defects in the p53 functional pathway, defined as low expression of ATM or mutations affecting either TP53-L2/L3 domains or CHEK2, and lack of response to neoadjuvant treatment with doxorubicin or 5-fluorouracil/mitomycin (blue line) or epirubicin (red line). Percentage on the X-axis indicates the portion of the patients cohorts defined as "low ATM expressors".

Back to article page