Final answer:
Tamoxifen prevents breast cancer by acting as a selective estrogen receptor modulator, blocking estrogen from binding to its receptors in breast tissue, and thus inhibiting the growth of ER-positive tumors. Lapatinib, on the other hand, inhibits the autophosphorylation of the HER2/neu tyrosine kinase receptor, which is overexpressed in some breast cancers, thereby reducing tumor growth.
Step-by-step explanation:
Tamoxifen is a medication broadly used in the treatment and prevention of breast cancer. It functions as a selective estrogen receptor modulator (SERM), which means it has both agonist and antagonist effects on estrogen receptors depending on the target tissue. In the context of breast tissue, where estrogen can promote cancer growth, Tamoxifen acts primarily as an antagonist. It binds to estrogen receptors on breast cells, thereby preventing the actual estrogen hormone from binding to these receptors. As a consequence, it reduces the estrogen-stimulated growth of breast cancer cells, particularly in tumors that are estrogen receptor positive (ER-positive).
Lapatinib, another medication used to treat breast cancer, targets a different mechanism. It is an inhibitor of the HER2/neu tyrosine kinase receptor, which is overexpressed in about 30 percent of human breast cancers. This overexpression can cause unregulated cell division and tumor growth. By inhibiting the phosphorylation process of this receptor, Lapatinib prevents subsequent signaling pathways that lead to cell division. Thus, Lapatinib would inhibit the autophosphorylation of HER2, an essential step for these tumor cells to proliferate.