Search

During the past two decades, a number of two-terminal switching devices have been demonstrated in the literature. They typically exhibit hysteric behavior in the current-to-voltage characteristics. These devices have often been also referred to as memristive devices. Their capacity to switch and exhibit electrical hysteresis has made them well-suited for applications such as data storage, in-memory computing, and in-sensor computing or in-memory sensing. The aim of this perspective paper is to is twofold. Firstly, it seeks to provide a comprehensive examination of the existing research findings in the field and engage in a critical discussion regarding the potential for the development of new non-Von-Neumann computing machines that can seamlessly integrate sensing and computing within memory units. Secondly, this paper aims to demonstrate the practical application of such an innovative approach in the realm of cancer medicine. Specifically, it explores the modern concept of employing multiple cancer markers simultaneously to enhance the efficiency of diagnostic processes in cancer medicine.

Human cancers are products of multistep processes resulting in abnormal cell growth and differentiation, along with a loss of apoptotic function, leading to the uncontrolled expansion of neoplastic cells and their spread to surrounding tissues and, ultimately, distant parts of the body [...].

Liquid biopsies have caused a significant revolution in cancer diagnosis, and the use of point of care (PoC) platforms has the potential to bring liquid biopsy-based cancer detection closer to patients. These platforms provide rapid and on-site analysis by reducing the time between sample collection and results output. The aim of this tutorial content is to provide readers an in-depth understanding regarding the choice of the ideal sensing platform suitable for specific cancer-related biomarkers.

Most metastatic cancers remain incurable due to the emergence of apoptosis-resistant clones, fuelled by intratumour heterogeneity and tumour evolution. To improve treatment, therapies should not only kill cancer cells but also activate the immune system against the tumour to eliminate any residual cancer cells that survive treatment. While current cancer therapies rely heavily on apoptosis - a largely immunologically silent form of cell death - there is growing interest in harnessing immunogenic forms of cell death such as necroptosis. Unlike apoptosis, necroptosis generates second messengers that act on immune cells in the tumour microenvironment, alerting them of danger. This lytic form of cell death optimizes the provision of antigens and adjuvanticity for immune cells, potentially boosting anticancer treatment approaches by combining cellular suicide and immune response approaches. In this Review, we discuss the mechanisms of necroptosis and how it activates antigen-presenting cells, drives cross-priming of CD8 + T cells and induces antitumour immune responses. We also examine the opportunities and potential drawbacks of such strategies for exposing cancer cells to immunological attacks., (© 2024. Springer Nature Limited.)

The control of biological cell death is essential for the body's appropriate growth. The resistance of cells to the apoptotic process presents a new difficulty in the treatment of cancer. To combat cancer cells, researchers are working to find new apoptotic pathways and components to activate. One of the processes of regulated cell death (RCD) is referred to as ferroptosis marked by a decline in the activity of lipid glutathione peroxidase 4 (GPX4) after the buildup of reactive oxygen species (ROS). Since lipid peroxidation is a crucial component of ferroptosis and is required for its start, numerous medicines have been studied, particularly for the treatment of cancer. In this context, autophagy is an additional form of RCD that can govern ferroptosis through shared signaling pathways/factors involved in both mechanisms. In this review, we will explore the molecular mechanisms underlying ferroptosis and its association with autophagy, to gain fresh insights into their interplay in cancer advancement, and the potential of natural products for its treatment., (© 2023. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.)

Protein lipidation describes a diverse class of post-translational modifications (PTMs) that is regulated by over 40 enzymes, targeting more than 1,000 substrates at over 3,000 sites. Lipidated proteins include more than 150 oncoproteins, including mediators of cancer initiation, progression and immunity, receptor kinases, transcription factors, G protein-coupled receptors and extracellular signalling proteins. Lipidation regulates the physical interactions of its protein substrates with cell membranes, regulating protein signalling and trafficking, and has a key role in metabolism and immunity. Targeting protein lipidation, therefore, offers a unique approach to modulate otherwise undruggable oncoproteins; however, the full spectrum of opportunities to target the dysregulation of these PTMs in cancer remains to be explored. This is attributable in part to the technological challenges of identifying the targets and the roles of protein lipidation. The early stage of drug discovery for many enzymes in the pathway contrasts with efforts for drugging similarly common PTMs such as phosphorylation and acetylation, which are routinely studied and targeted in relevant cancer contexts. Here, we review recent advances in identifying targetable protein lipidation pathways in cancer, the current state-of-the-art in drug discovery, and the status of ongoing clinical trials, which have the potential to deliver novel oncology therapeutics targeting protein lipidation., (© 2024. Springer Nature Limited.)