Indeed, the concept of self-esteem is approached since then in humanistic psychology as an inalienable right for every person, summarized in the following sentence:

Every human being, with no exception, for the mere fact to be it, is worthy of unconditional respect of everybody else; he deserves to esteem himself and to be esteemed. Measurement
Self-esteem is typically assessed using self-report inventories. One of the most widely used instruments, the Rosenberg self-esteem scale (RSES) is a 10-item self-esteem scale score that requires participants to indicate their level of agreement with a series of statements about themselves. An alternative measure, the Coopersmith Inventory uses a 50-question battery over a variety of topics and asks subjects whether they rate someone as similar or dissimilar to themselves. If a subjects answers demonstrate solid self-regard, the scale regards them as well adjusted. If those answers reveal some inner shame, it considers them to be prone to social deviance.Implicit measures of self-esteem began to be used in the 1980s. These rely on indirect measures of cognitive processing thought to be linked to implicit self-esteem, including the name letter task (or initial preference task) and the Implicit Association Task.Such indirect measures are designed to reduce awareness of the process of assessment. When using them to assess implicit self-esteem, psychologists apply self-relevant stimuli to the participant and then measure how quickly a person identifies positive or negative stimuli.
CDR formation requires activation of both the protein regulator of actin polymerization N-WASP, mediated by ERK1/2, and of the actin-depolymerizing protein cofilin, mediated by EGFR/ERBB1. Furthermore, this latter event may be inhibited by the negative cell motility regulator p140Cap, as we found that p140Cap overexpression led to cofilin deactivation and inhibition of CDR formation. Normal cell division—mitosis—has checkpoints that keep cell division under control. Some of the proteins that control this cycle are called cdk2 (CDKs). Overexpression of HER2 sidesteps these checkpoints, causing cells to proliferate in an uncontrolled fashion. This is caused by phosphorylation by Akt.Trastuzumab binds to domain IV of the extracellular segment of the HER2/neu receptor. Monoclonal antibodies that bind to this region have been shown to reverse the phenotype of HER2/neu expressing tumor cells. Cells treated with trastuzumab undergo arrest during the G1 phase of the cell cycle so there is reduced proliferation. It has been suggested that trastuzumab does not alter HER-2 expression, but downregulates activation of AKT. In addition, trastuzumab suppresses angiogenesis both by induction of antiangiogenic factors and repression of proangiogenic factors. It is thought that a contribution to the unregulated growth observed in cancer could be due to proteolytic cleavage of HER2/neu that results in the release of the extracellular domain. One of the most relevant proteins that trastuzumab activates is the tumor suppressor p27 (kip1), also known as CDKN1B.