 Systemic chemotherapy for operable breast cancer significantly decreases the risk of relapse and death. However, it is not possible to identify those patients at the outset who are likely to respond to adjuvant treatment and which type of treatment should be used. Adjuvant treatment given before surgery neoadjuvant therapy has a number of theoretical advantages in breast cancer, including a reduction in the requirement for mastectomy. Access to the primary tumor during early treatment allows for in vivo testing for change in molecular markers by repeat biopsies that may occur with successful treatment. Established prognostic factors like tumor size and nodal involvement are important indicators for breast cancer relapse and survival but have not been shown to be predictive of sensitivity to treatment. Estrogen receptor ER and progesterone receptor PgR expression predict for response to tamoxifen and endocrine treatment. However, predictive markers for chemotherapy are not established. Overexpression of c-erbB-2 has been associated with decreased response to CMF chemotherapy cyclophosphamide, methotrexate, and 5-fluorouracil in most studies. Accumulation of aberrant protein expressed by the mutated tumor suppressor gene p53 product may be associated with relative resistance to cytotoxic therapy. Tissue growth kinetics are determined by the balance between programmed cell death apoptosis and cell proliferation, and any alteration between the two may be regarded as a key element for the uncontrolled growth of malignant tumors. In vitro experiments suggest that many anti-cancer agents achieve their effect by inducing apoptosis. Mechanisms that suppress this process may, therefore, be important in the development of intrinsic and acquired chemotherapy resistance. A clinical study has reported an increase in labeled apoptotic leukemic cells during treatment. In breast cancer biopsy specimens, chemotherapy was found to induce apoptosis within the first 24 hours of treatment. 