RESUMO
This review paper analyzes the ethical implications of billing patients for electronic communication with physicians through electronic health records, a practice already adopted by medical institutions such as the Cleveland Clinic. The analysis assesses how billing aligns with pillars of medical ethics which include beneficence, respect for persons, and justice. Although billing may enhance communication, improve patient care, and alleviate physician burnout, concerns arise over potential consequences on patient autonomy, trust, and health care disparities. The review delves into the intricate balance of these ethical principles by first considering the potential benefits of incentivizing concise questions and improving physician workload management through billing. By reducing messages, this approach can potentially mitigate burnout and enhance care. It also acknowledges potential drawbacks such as deterring patients because of financial constraints and eroding trust in physicians and the medical team. It emphasizes the necessity of thoroughly examining all aspects of this intricate ethical dilemma to formulate a nuanced solution that protects patient well-being while respecting physicians. We propose a middle-ground approach involving nominal and transparent billing on the basis of the question's complexity, urgency, and level of expertise required in the response. Transparent billing policies, up-front communication of costs, and potential fee waivers on the basis of socioeconomic status can address equity concerns and maintain patient trust. Striking a balance between the potential benefits and drawbacks of billing for patient questions is crucial in maintaining ethical patient-physician interactions and equitable health care provision. The analysis underscores the importance of aligning online patient-physician communication with ethical principles within the evolving digital health care landscape.
RESUMO
Non-small cell lung cancer (NSCLC) is characterized by genomic alterations, yet a targetable mutation has not been discovered in nearly half of all patients. Recent studies have identified amplification of RICTOR, an mTORC2-specific cofactor, as a novel actionable target in NSCLC. mTORC2 is one of two distinct mTOR complexes to sense environmental cues and regulate a variety of cellular processes, including cell growth, proliferation, and metabolism, all of which promote tumorigenesis when aberrantly regulated. Interestingly, other components of mTORC2 are not coamplified with RICTOR in human lung cancer, raising the question as to whether RICTOR amplification-induced changes are dependent on mTORC2 function. To model RICTOR amplification, we overexpressed Rictor using the Cas9 Synergistic Activation Mediator system. Overexpression of Rictor increased mTORC2 integrity and signaling, but at the expense of mTORC1, suggesting that overexpressed Rictor recruits common components away from mTORC1. Additionally, Rictor overexpression increases the proliferation and growth of NSCLC 3D cultures and tumors in vivo. Conversely, knockout of RICTOR leads to decreased mTORC2 formation and activity, but increased mTORC1 function. Because Rictor has mTOR-dependent and -independent functions, we also knocked out mLST8, a shared mTOR cofactor but is specifically required for mTORC2 function. Inducible loss of mLST8 in RICTOR-amplified NSCLC cells inhibited mTORC2 integrity and signaling, tumor cell proliferation, and tumor growth. Collectively, these data identify a mechanism for Rictor-driven tumor progression and provide further rationale for the development of an mTORC2-specific inhibitor. IMPLICATIONS: RICTOR amplification drives NSCLC proliferation through formation of mTORC2, suggesting mTORC2-specific inhibition could be a beneficial therapeutic option.