Despite advances in breast cancer treatment, the number of lives lost each year remains high. One of the significant challenges in treating breast cancer is the highly complex and dynamic tumor microenvironment (TME), which often makes tumors resistant to various kinds of therapies. To overcome this, researchers are tuning and tweaking the body's immune cells, especially T cells and subsets, to clear cancerous cell residues more effectively from the patient's body. Recent research shows that long non-coding RNAs (lncRNAs), once considered "junk" DNA, play an essential role in shaping T cells' plasticity in healthy and cancerous tissues. In this review, we presented and discussed our perspectives on how specific lncRNAs control T-cell infiltration into tumors and how they contribute to immune escape. For example, LINC00472, MIAT, HITT, NKILA, and MALAT1 influence how T cells enter tumors, while SNHG1, TINCR, and GATA3-AS1 help cancer cells hide from immune attack. These lncRNAs can shift the balance between regulatory T cells (Tregs) and cytotoxic T cells (CTLs), either slowing tumor growth or helping cancer evade destruction by recruiting Tregs, M2 macrophages, and myeloid-derived suppressor cells (MDSCs). LncRNAs regulate key signalling pathways such as NF-κB, Wnt/β-catenin, PI3K/AKT, and JAK/STAT, often by acting as "sponges" for miRNAs that regulate immune checkpoints like PD-L1. Further, LncRNAs are found to remodel cytokine and chemokine networks, ultimately reshaping the TME. Overexpression of lncRNA, such as TINCR and MIAT, GATA3-AS1, leads to enhanced PD-L1 deubiquitination, thus aiding in tumor immune evasion. Moreover, our in silico analysis suggests that lncRNAs modulate various immune-related signaling pathways in T cells. Together, these insights reveal how lncRNAs could be harnessed to fine-tune T-cell plasticity, paving the way for more personalized immunotherapies and improving outcomes for breast cancer patients.

Background Synovial pathologies of the knee include a broad spectrum of inflammatory, infective, proliferative, and neoplastic disorders. Conventional Magnetic Resonance Imaging (MRI) is widely used for evaluation; however, it has limitations in differentiating lesions with overlapping morphological features. Diffusion-Weighted Imaging (DWI), a functional MRI technique, offers additional tissue characterization without the need for contrast administration. This study aimed to assess the added diagnostic value of DWI over conventional MRI in evaluating knee synovial pathologies. Methods This hospital-based, prospective, cross-sectional study was conducted from October 2022 to May 2024 and included 63 patients aged 18–70 years with clinically suspected knee synovial pathology. All patients underwent conventional MRI and DWI. Apparent diffusion coefficient (ADC) values were calculated by placing multiple regions of interest in areas of maximum synovial thickening. MRI findings were compared with histopathological diagnosis as the reference standard. Statistical analysis was performed using SPSS software, with kappa statistics used to assess diagnostic agreement and the Kruskal-Wallis test applied for intergroup ADC comparison. Results Inflammatory synovitis (61.9%) was the most common diagnosis, followed by tubercular synovitis (9.5%), pigmented villonodular synovitis (7.9%), synovial chondromatosis (7.9%), ganglion cysts (6.3%), hemangiomas (3.2%), and synovial sarcoma (3.2%). Diffusion restriction was observed in 81% of cases. Benign lesions such as ganglion cysts and hemangiomas showed high ADC values, while malignant lesions and pigmented villonodular synovitis demonstrated low ADC values. A statistically significant difference in ADC values among various synovial pathologies was observed (p < 0.05). The agreement between MRI and histopathology was excellent (κ = 0.836, p < 0.001). Conclusion The addition of DWI to conventional MRI significantly improves diagnostic confidence in the evaluation of knee synovial pathologies, especially in differentiating benign from malignant lesions and inflammatory from infective conditions. DWI serves as a valuable, non-contrast functional imaging tool that enhances diagnostic accuracy and supports better clinical decision-making. Trial Registration: Not applicable.

Multiple myeloma (MM) is a clonal plasma cell malignancy characterized by clinical heterogeneity, high relapse rates, and eventual drug resistance despite advances in therapy. Over the past two decades, phase 3 clinical trials have redefined MM management by integrating novel agents, monoclonal antibodies, and cellular therapies into frontline and relapsed/refractory settings. CD38-targeting antibodies, particularly daratumumab- and isatuximab-based regimens, have demonstrated superior depth of response, prolonged progression-free survival (PFS), and improved overall survival (OS) across transplant-eligible, transplant-ineligible, and relapsed populations. Proteasome inhibitor (PI) and immunomodulatory drug (IMiD)-based triplets and quadruplets, such as bortezomib, lenalidomide, and dexamethasone (VRd), carfilzomib, daratumumab, and dexamethasone (KdD), and pomalidomide and dexamethasone (Pd) combinations, have further enhanced treatment efficacy, while maintenance strategies primarily lenalidomide-based remain central to sustaining remission, with ongoing trials evaluating MRD-guided approaches. The emergence of B cell maturation antigen (BCMA)-targeted chimeric antigen receptor T (CAR-T) cell therapies, exemplified by idecabtagene vicleucel and ciltacabtagene autoleucel, has transformed outcomes in heavily pretreated, triple-class refractory patients, providing durable responses and quality of life benefits. Despite these advances, therapeutic decisions must consider patient frailty, cytogenetic risk, and prior treatment exposure. Future directions emphasize optimizing sequencing strategies, integrating bispecific antibodies, and validating MRD as a biomarker for treatment cessation. This review consolidates evidence from recent phase 3 trials to provide clinicians with an updated framework for personalized, risk-adapted management of MM.