The overproduction of reactive oxygen species (ROS) has been associated with various human diseases. ROS exert a multitude of biological effects with both physiological and pathological consequences. Monosodium glutamate (MSG), a sodium salt of the natural amino acid glutamate, is a flavor-enhancing food additive, which is widely used in Asian cuisine and is an ingredient that brings out the “umami” meat flavor. MSG consumption in rats is associated with ROS generation. Owing to its consumption as part of the fast-food culture and concerns about its possible effects on pregnancy, we aimed to study the impact of MSG on placental trophoblast cells. MSG exposure influenced trophoblast invasion and differentiation, two of the most critical functions during placentation through enhanced production of ROS. Similar findings were also observed on MSG-treated placental explants, as confirmed by elevated Nrf2 levels. Ultrastructural studies revealed signs of subcellular injury by MSG exposure. Mechanistically, MSG-induced oxidative stress with endoplasmic reticulum stress pathways involving Xbp1s and IRE1α was observed. The effect of MSG through an increased ROS production indicates that its long-term exposure might have adverse health effect by compromising key trophoblast functions.

Breast cancer is among the most common cancer in women worldwide. It is accompanied by significant psychosocial, cultural, and spiritual challenges that have a substantial impact on treatment adherence, care-seeking behavior, and perceptions of the disease. These psychosocial aspects of cancer are still largely unexplored in Tajikistan, where stigma, cultural norms, and the dearth of organized psycho-oncology services all contribute to increased distress, delayed diagnosis, and low patient engagement. In order to direct the methodical integration of psychosocial care into breast cancer control, this perspective paper suggests a hybrid psycho-oncology framework for Tajikistan based on transferable and contextually relevant models from Africa and India. Instead of serving as a supplemental mental health intervention, it seeks to understand how culturally sensitive psycho-oncology can serve as a fundamental part of oncology services in a setting with limited resources and high stigma. The study explores culturally mediated barriers that influence screening behaviour, diagnostic engagement, and treatment adherence among Tajik women, including fear of social exposure, body image disruption, gendered distress, and privacy-related anxieties. It does this by combining clinical insights and established psycho-oncology practices from similar low- and middle-income contexts. The analysis demonstrates how structured interventions can enhance early detection, continuity of care, and quality of life. These interventions include regular distress screening, counselling, community engagement, family-inclusive care, and palliative psychosocial support. Instead of offering empirical results, this viewpoint promotes a translational framework for cooperatively integrating psycho-oncology into Tajikistan's cancer care system. As a scalable approach for workforce development, capacity building, and long-term integration of psycho-oncology into cancer care systems throughout Central Asia, it suggests a tripartite collaborative model involving Tajikistan, India, and Uganda.

Within the context of larger studies examining how dynamic membrane behaviour can directly influence cell fate, immunity and cellular identity.Trogocytosis at the cancer-immune interface: Guha and Banerjee (2025) provide the conceptual framework for the collection by reviewing the mechanisms, biological consequences, and therapeutic implications of trogocytosis in cancer. They emphasise that the principle of trogocytosis is context-dependent. How the cellular transfer contributes to tumour development depends on the donor and recipient cell type, the mode of transfer, the identity of the transferred cargo, and the biological consequence (phenotype) established by trogocytosis. As a result, trogocytosis cannot be categorised as either tumor enhancing nor tumour-suppressing.Membrane exchange as such can impact antigen expression level, surface availability of receptors, checkpoint status, and immune cell function inside the TME. Tumour cells can gain anti-immune molecules, whereas immune cells may acquire tumour-associated moieties or modify the targets via receptor ripping and other contact-mediated mechanisms. The bidirectional nature of this crosstalk can be especially important in cellular immunotherapy. In a CAR-T or CAR-NK cell, antigen transfer from tumour cells may serve to reduce target antigen levels on tumour cells while presenting these targets on immune cells, settings which can potentially enhance tumour antigen escape, inducing changes in effector cell phenotype, stimulating exhaustion and/or fratricide. However, immune cell trogocytosis may also serve to suppress tumour activity, and hence the real interest here lies in determining who is doing the transferring of what to whom, under which circumstances, and at what functional impact. As such, the resulting model-attenuated STAT1-CH25H signaling, altered cholesterolassociated membrane regulation, increased membrane fluidity, and enhanced trogocytosisproviding a mechanistic bridge between cell state, lipid biology, membrane biophysics, and intercellular exchange. This observation matters because CSCs are well known for their tendency towards persistence, plasticity, resistance to therapies, and reemergence. A heightened trogocytic ability would then give these kinds of cells another, genetic-free avenue for promptly changing their surface identity in response to being attacked. As the result does, it moved the field's efforts beyond the basic question: Do tumor cells indeed pursue trogocytosis, toward that of: Which tumor-cell states specifically afford that capability, and what programs at the biophysical and molecular level permit it?From membrane exchange to acquired cellular identity: Together, the cancer-focused contributions suggest a useful conceptual distinction between intrinsic cellular identity and acquired membrane identity. Intrinsic identity reflects molecules produced through a cell's own transcriptional, translational, and metabolic programs. Acquired membrane identity reflects proteins, receptors, lipids, or other membrane components obtained through physical interaction with neighboring cells. In a trogocytosis-active environment, the functional cellular state may therefore emerge from both. This distinction has experimental implications. Detection of a surface molecule does not necessarily establish that the cell displaying it synthesized it. In tumors, inflammatory tissues, and engineered cellular therapies, investigators may increasingly need to distinguish endogenous expression from trogocytic acquisition. The CSC study adds a further dimension by suggesting that the ability to acquire such an identity is itself regulated by membrane state. Collectively, these contributions encourage a view of the plasma membrane not simply as a boundary, but as an adaptive interface through which cellular phenotype can be modified (Miyake & Karasuyama.,2021). In cancer, tumor and immune cells should therefore not always be regarded as fixed participants entering an interaction with immutable identities. Through trogocytosis, the interaction itself can alter the molecular phenotype and subsequent behavior of the participants (Li et al.,2021). The next phase of the field may be defined by four deceptively simple questions: Who gives? Who receives? What is transferred? And what does the recipient become? Answering them may transform trogocytosis from an intriguing cellular phenomenon into a mechanistically defined and therapeutically actionable dimension of cancer immunity.