Download Aggressive Breast Cancer by Regina H. DeFrina PDF

By Regina H. DeFrina

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Furthermore, PTEN-deficient cells are sensitive to an inhibitor of PI3K [104]. These results suggest that PTEN loss could serve as a predictor of The HER2 Oncogene in Breast Cancer 29 trastuzumab resistance and that PI3K inhibitors might overcome this type of resistance. On the other hand, PTEN expression was not correlated with relapsefree survival in the NSABP B-31 cohort [118]. HER2 OVEREXPRESSION AND CHEMOTHERAPY A possible link between HER2 overexpression and chemotherapeutic responsiveness was suggested by the observation of enhanced clinical activity with the addition of certain chemotherapeutic agents to trastuzumab in women with metastatic disease.

There appears to be no correlation between the presence of skin rash and antitumor efficacy, an association that has been seen with other drugs targeting the EGFR. Decreases in LVEF, interstitial lung disease, pneumonitis and hepatotoxicity have been observed in a small number of patients during therapy. A normal baseline LVEF should be confirmed pre-therapy, with periodic reevaluation during treatment. Circulating Serum HER2 Levels Several studies have addressed whether circulating HER2 protein extra cellular domain (ECD) levels can predict responsiveness to trastuzumab or lapatinib [123-126].

Theoretically, in addition to tumor heterogeneity, resistance to trastuzumab may be caused by altered receptor-antibody interaction, compensatory activation of the downstream pathways by increased signaling from either other members of the HER family or other receptors, or constitutive activation of downstream elements [108, 109]. Altered Receptor-Antibody Interaction The extracellular domain of HER2 may be cleaved by proteases, creating a truncated receptor to which trastuzumab is unable to bind [110].

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