Mesenchymal stem cells (MSCs) can maintain immune homeostasis and many preclinical trials with MSCs have been carried out around the world. In vitro culture of MSCs has been found to result in the decline of immunomodulatory capacity, migration and proliferation. To address these problems, simulating the extracellular environment for preconditioning of MSCs is a promising and inexpensive method. Biophysical cues in the external environment that MSCs are exposed to have been shown to affect MSC migration, residency, differentiation, secretion, etc. We review the main ways in which MSCs exert their immunomodulatory ability, and summarize recent advances in mechanical preconditioning of MSCs to enhance immunomodulatory capacity and related mechanical signal sensing and transduction mechanisms.

The evolution of lymphoma is a multifactorial process that leads to unavoidable lymphoma heterogeneity in the form of genetic mutations, chromosomal translocations and other variations. Multi‑omics analyses based on single‑cell assays can reveal and characterize tumor components, enabling us to determine the timing of mutations and to profile disease progression. Increasing numbers of studies are using single‑cell transcriptomics to unravel the mechanisms of lymphoma evolution, drug resistance and therapeutic approaches. Various single‑cell multi‑omics measurements involving genomics, transcriptomics and epigenomics have improved knowledge of the complex lymphatic system and made it possible to obtain individualized and precise tumor biological characteristics, which cannot be accessed from bulk cell analysis, and this can facilitate individualized treatment. In the present review, the advances in multi‑omics analysis based on single‑cell assays of lymphoma specimens were systematically discussed, including the sequencing of the single‑cell from genomic and transcriptomic perspectives, the landscape of the lymphoma microenvironment, the development of single‑cell histology biomarkers, the identification of lymphoma origin and evolution, as well as the current challenges and future prospects of single‑cell multi‑omics. The authors' insights may contribute to the exploration of novel lymphoma biomarkers and the discovery of efficient treatment combinations that target immunological checkpoints and underlying molecular mechanisms.

Male accessory breast cancer is an extremely rare tumor. Several risk factors have been identified, including genetic and hormonal abnormalities. Accessory breast carcinoma usually occurs under the axilla or in the inguinal region. Clinical diagnosis is frequently delayed due to the general lack of awareness among physicians and patients. In the present study, the case of a 63-year-old male patient who was diagnosed with accessory breast cancer at a local advanced stage was reported. However, the patient was successfully treated with endocrine therapy.

Multiple myeloma (MM) is a clonal malignancy characterized by the proliferation of malignant plasma cells in the bone marrow and the production of monoclonal immunoglobulin. In addition to genetic changes, gene hypermethylation is an alternative mechanism of tumor suppressor gene inactivation in MM. The cyclin-dependent kinase inhibitor 1 (CDKN2B or p15^INK4B) gene lies adjacent to the tumor suppressor gene, cyclin-dependent kinase inhibitor 2 (CDKN2A), and is frequently mutated and deleted in a wide variety of tumors, including MM. However, there is a lack of systematic analysis of p15 epigenetic modification such as methylation in MM from different studies that can provide more powerful estimation of an effect. In this study, we have systematically reviewed the studies of p15^INK4B promoter methylation in MM and quantified the association between p15^INK4B promoter methylation and MM using meta-analysis methods. We observed that the frequency of p15^INK4B methylation is significantly higher in MM patients than in normal healthy controls. The pooled odds ratio (OR) from ten studies including 394 MM and 99 normal individuals is 0.08, while confidence interval (CI) is 0.03–0.21 (P<0.00001). This indicates that p15^INK4B inactivation through methylation plays an important role in the pathogenesis of MM. In addition, the frequency of p15^INK4B methylation was significantly higher in patients with MM than in those with asymptomatic monoclonal gammopathy of undetermined significance. The pooled OR from four studies is 0.40, 95% CI =0.21–0.78 (P=0.007). These results suggest that silencing of p15^INK4B gene expression by epigenetic modification such as promoter hypermethylation plays a role not only in the initiation of MM but also in plasma cell malignant transformation, disease progression, and development.

Mechanical stimulation is the key physical factor in cell environment. Mechanotransduction acts as a fundamental regulator of cell behavior, regulating cell proliferation, differentiation, apoptosis, and exhibiting specific signature alterations during the pathological process. As research continues, the role of epigenetic science in mechanotransduction is attracting attention. However, the molecular mechanism of the synergistic effect between mechanotransduction and epigenetics in physiological and pathological processes has not been clarified. We focus on how histone modifications, as important components of epigenetics, are coordinated with multiple signaling pathways to control cell fate and disease progression. Specifically, we propose that histone modifications can form regulatory feedback loops with signaling pathways, that is, histone modifications can not only serve as downstream regulators of signaling pathways for target gene transcription but also provide feedback to regulate signaling pathways. Mechanotransduction and epigenetic changes could be potential markers and therapeutic targets in clinical practice.