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Pulmonary hypertension in patients with multiple myeloma: A comprehensive review.

Multiple myeloma (MM) is a common hematological malignancy resulting from clonal proliferation of plasma cells and is defined by criteria set forth by the international myeloma working group. Pulmonary hypertension (PH) is defined by an elevated mean pulmonary artery pressure >20 mmHg measured during right heart catheterization. Echocardiography-diagnosed PH is relatively common in patients with MM and has been associated with increased mortality, morbidity, and poor stem cell transplant outcomes. PH in patients with MM (PH-MM) is usually multifactorial in origin. MM disease-specific factors,

Enhanced sialylation of bone marrow mesenchymal stromal cells contributes to immune remodeling through macrophage polarization in multiple myeloma patients.

INTRODUCTION: In multiple myeloma (MM), the immune system is disrupted, partly due to tumor-modified bone marrow mesenchymal stromal cells (BM-MSCs). These MSCs show altered glycosylation, including increased sialylation, which may promote immune evasion through Siglec interactions. METHODS: We quantified sialic acids and Siglec ligands on healthy donors-, MM-, T-MM-(treated multiple myeloma) and MGUS (monoclonal gammopathy of undetermined significance)-MSCs, and examined how different culture conditions (myeloma coculture, conditioned medium, hypoxia, inflammation, 3D culture) affect MSC gly

Application of Perinatal Derivatives on Oncological Preclinical Models: A Review of Animal Studies.

The increasing cancer incidence has certified oncological management as one of the most critical challenges for the coming decades. New anticancer strategies are still needed, despite the significant advances brought to the forefront in the last decades. The most recent, promising therapeutic approaches have benefitted from the application of human perinatal derivatives (PnD), biological mediators with proven benefits in several fields beyond oncology. To elucidate preclinical results and clinic outcomes achieved in the oncological field, we present a narrative review of the studies resorting

Revisiting Curcumin in Cancer Therapy: Recent Insights into Molecular Mechanisms, Nanoformulations, and Synergistic Combinations.

Curcumin has been extensively investigated as an anticancer agent, yet its clinical application remains constrained by low bioavailability, incomplete mechanistic understanding, and limited therapeutic optimization. In light of growing resistance to conventional chemotherapies and the demand for safer, multi-targeted agents, this review revisits curcumin with a contemporary lens. We critically evaluate the literature published since 2020, focusing on newly elucidated molecular mechanisms by which curcumin regulates tumor progression, including modulation of oncogenic signaling pathways (Wnt/β-

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… Curcumin promotes apoptosis, autophagy, and cellular senescence in cervical cancer SiHa cells [ 103 ]. Similarly, curcumin was found to impede cell growth in ovarian cancer SKOV 3 cells, causing cell cycle arrest [ 104 ]. …

Statins: a repurposed drug to fight cancer.

As competitive HMG-CoA reductase (HMGCR) inhibitors, statins not only reduce cholesterol and improve cardiovascular risk, but also exhibit pleiotropic effects that are independent of their lipid-lowering effects. Among them, the anti-cancer properties of statins have attracted much attention and indicated the potential of statins as repurposed drugs for the treatment of cancer. A large number of clinical and epidemiological studies have described the anticancer properties of statins, but the evidence for anticancer effectiveness of statins is inconsistent. It may be that certain molecular subt

Систематический обзор потенциального ускорения нееврокогнитивного старения пожилых лиц, переживших рак.

По мере роста показателей выживаемости больше внимания стало уделяться возможным когнитивным сиквелам у пожилых больных раком, что можно объяснить ускоренным старением мозга. В этом обзоре мы представляем полный обзор исследований, посвященных нейроимации, нейрокогнитивным и нейродегенеративным расстройствам у пожилых выживших жертв рака (см.>65 лет), на основе three базы данных (Pubmed, Web of Science and Medline). Ninety-six В него были включены исследования. Были обнаружены данные о функциональных и структурных изменениях в мозге (фронтальные области, базальная ганглиа, серые и белые вещест

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… The cellular mechanisms involved in this process include DNA damage and mutations, epigenetic aging, stem cell damage (oxidative stress), cellular senescence (telomere shortening), and inflammation. Each of these can contribute to neurocognitive aging and cognitive decline [ 16 ]. …

The crosstalk between non-coding RNAs and oxidative stress in cancer progression.

As living standards elevate, cancers are appearing in growing numbers among younger individuals globally and these risks escalate with advancing years. One of the reasons is that instability in the cancer genome reduces the effectiveness of conventional drug treatments and chemotherapy, compared with more targeted therapies. Previous research has discovered non-coding RNAs' crucial role in shaping genetic networks involved in cancer cell growth and invasion through their influence on messenger RNA production or protein binding. Additionally, the interaction between non-coding RNAs and oxidativ

Alternative Splicing: A Critical Regulator in Human Bone Biology and Tumor Progression.

Alternative splicing (AS) is the central mechanism of transcriptional regulation and generates diverse splice variants that influence protein structure, function, and intracellular activity. AS plays critical roles in tissue differentiation, organ development, and disease progression. This review focuses on the pivotal roles of AS in bone biology, highlighting its regulatory effects on osteoblasts, osteoclasts, chondrocytes, bone matrix remodeling, and bone remodeling, as well as the involvement of AS-related RNA-binding proteins in these processes. We also emphasize bone-specific AS events an

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… Δ133p53α is a p53 AS variant lacking the N-terminal transactivation domain, which resists cellular senescence by antagonizing full-length p53 [ 94 – 96 ]. …

The Health-Promoting Effects and the Mechanism of Intermittent Fasting.

Intermittent fasting (IF) is an eating pattern in which individuals go extended periods with little or no energy intake after consuming regular food in intervening periods. IF has several health-promoting effects. It can effectively reduce weight, fasting insulin levels, and blood glucose levels. It can also increase the antitumor activity of medicines and cause improvement in the case of neurological diseases, such as memory deficit, to achieve enhanced metabolic function and prolonged longevity. Additionally, IF activates several biological pathways to induce autophagy, encourages cell renew

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… Cellular senescence in aging and age-related diseases: implications for neurodegenerative diseases. International Review of Neurobiology . 2020;155:203–234. doi: 10.1016/bs.irn.2020.03.019. 57. Wang F. X., Xu C. L., Su C., Li J., Lin J. …

Ketosis Suppression and Ageing (KetoSAge): The Effects of Suppressing Ketosis in Long Term Keto-Adapted Non-Athletic Females.

Most studies on ketosis have focused on short-term effects, male athletes, or weight loss. Hereby, we studied the effects of short-term ketosis suppression in healthy women on long-standing ketosis. Ten lean (BMI 20.5 ± 1.4), metabolically healthy, pre-menopausal women (age 32.3 ± 8.9) maintaining nutritional ketosis (NK) for > 1 year (3.9 years ± 2.3) underwent three 21-day phases: nutritional ketosis (NK; P1), suppressed ketosis (SuK; P2), and returned to NK (P3). Adherence to each phase was confirmed with daily capillary D-beta-hydroxybutyrate (BHB) tests (P1 = 1.9 ± 0.7; P2 = 0.1 ± 0.1; an

Cancer-Associated Fibroblasts: Heterogeneity, Cancer Pathogenesis, and Therapeutic Targets.

Cancer-associated fibroblasts (CAFs) are functionally diverse stromal regulators that orchestrate tumor progression, metastasis, and therapy resistance through dynamic crosstalk within the tumor microenvironment (TME). Recent advances in single-cell multiomics and spatial transcriptomics have identified conserved CAF subtypes with distinct molecular signatures, spatial distributions, and context-dependent roles, highlighting their dual capacity to promote immunosuppression or restrain tumor growth. However, therapeutic strategies struggle to reconcile this functional duality, hindering clinica

Keyword Index for Volume 95

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Protein Quality Control in Glioblastoma: A Review of the Current Literature with New Perspectives on Therapeutic Targets.

Protein quality control allows eukaryotes to maintain proteostasis under the stress of constantly changing conditions. In this review, we discuss the current literature on PQC, highlighting flaws that must exist for malignancy to occur. At the nidus of PQC, the expression of BAG1-6 reflects the cell environment; each isoform directs proteins toward different, parallel branches of the quality control cascade. The sum of these branches creates a net shift toward either homeostasis or apoptosis. With an established role in ALP, Bag3 is necessary for cell survival in stress conditions including th

Тела эндогенных кетонов связаны с метаболической уязвимостью и инвалидностью при множественном склерозе.

Цель: Тела кетона могут быть полезными биомаркерами в множестве склероза (МС), поскольку патофизиологические процессы, лежащие в основе развития заболеваний MS, вызывают метаболический стресс. Цель заключалась в оценке связей кетоновых тел с биомаркерами метаболического, подстрекательского и окислительного стресса в MS. Методы: Образцы крови и неврологические оценки были получены от 153 здоровых контрольных приборов (HC), 187 релапсирующих излучающих веществ (RRMS) и 91 пациента с прогрессивным MS (PMS). AcAc, BHB и ацетон измерялись с помощью спектроскопии протонного ядерного магнитного резон

Immunodeficiencies and CFTR dysfunction: results from a systematic screening in a cohort of adults with cystic fibrosis and CFTR-related disorders.

BackgroundImmunodeficiencies (IDs) are conditions caused by immune system dysfunctions which predispose to chronic infections. Cystic fibrosis (CF) patients are characterized by the presence of bronchiectasis filled with hyper-viscous secretions that constitute the ideal environment for infections. Although CF and IDs might share similarities in the pathophysiological mechanism of bronchiectasis development, they each offer different treatment options. We hypothesize that the introduction of a bundle of tests would increase the number of ID diagnoses among adults with Cystic Fibrosis Transmemb

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… Is cellular senescence involved in cystic fibrosis? Respir Res 2019 ; 20 : 32 . 30764828 10.1186/s12931-019-0993-2 PMC6376730 27 Lara-Reyna S Holbrook J Jarosz-Griffiths HH , et al . Dysregulated signalling pathways in innate immune cells with cystic fibrosis mutations . …

SETD2 and EZH2: Two epigenetic drivers of prostate cancer.

Prostate cancer is a prevalent malignancy among men, characterized by complex mechanisms underlying metastasis and treatment resistance. Epigenetic modifications play a crucial role in regulating prostate cancer progression, particularly involving histone methyltransferases such as SET-domain containing 2 (SETD2) and Enhancer of Zeste homolog 2 (EZH2). SETD2 contributes to chromatin stability by catalyzing the trimethylation of histone H3 lysine 36 (H3K36me3), and its downregulation is strongly correlated with increased invasiveness and epithelial-mesenchymal transition in prostate cancer. Con

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… As a major regulator in cell-cycle progression, autophagy, and apoptosis, EZH2 promotes DNA damage repair and inhibits cellular senescence 44 - 46 . … Regulation of Cellular Senescence by Polycomb Chromatin Modifiers through Distinct DNA Damage- and Histone Methylation-Dependent Pathways. Cell Rep. 2018;22(13):3480–3492. doi: 10.1016/j.celrep.2018.03.002. 47. Xu J, Wang Z, Lu W, Jiang H, Lu J, Qiu J. et al. …

NF-κB in Cell Deaths, Therapeutic Resistance and Nanotherapy of Tumors: Recent Advances.

The transcription factor nuclear factor-κB (NF-κB) plays a complicated role in multiple tumors. Mounting evidence demonstrates that NF-κB activation supports tumorigenesis and development by enhancing cell proliferation, invasion, and metastasis, preventing cell death, facilitating angiogenesis, regulating tumor immune microenvironment and metabolism, and inducing therapeutic resistance. Notably, NF-κB functions as a double-edged sword exerting positive or negative influences on cancers. In this review, we summarize and discuss recent research on the regulation of NF-κB in cancer cell deaths,

Dysregulated Dermal Mesenchymal Stem Cell Proliferation and Differentiation Interfered by Glucose Metabolism in Psoriasis.

BACKGROUND AND OBJECTIVES: Psoriasis is a chronic inflammatory skin disease, which the mechanisms behind its initiation and development are related to many factors. DMSCs (dermal mesenchymal stem cells) represent an important member of the skin microenvironment and play an important role in the surrounding environment and in neighbouring cells, but they are also affected by the microenvironment. We studied the glucose metabolism of DMSCs in psoriasis patients and a control group to reveal the relationship among glucose metabolism, cell proliferation activity，and VEC (vascular endothelial cell)

Cytotoxic CD4+ T cells: origin, biological functions, diseases and therapeutic targets.

Cytotoxic CD4+ T lymphocytes are a unique subset of CD4+ T cells characterized by their cytokine secretion and cytolytic activity. Unlike traditional CD4+ helper T cells, cytotoxic CD4+ T lymphocytes exhibit similar cytotoxicity to that of CD8+ T cells, revealing unexpected plasticity in CD4+ T-cell functions. This flexibility suggests that CD4+ T cells can transform and acquire effector functions beyond their conventional functions, emphasizing their importance in various immune responses. Despite the identification of cytotoxic CD4+ T lymphocytes decades ago, recent advancements have broaden

Sex Differences in Cancer and Cardiotoxicity: Mechanisms, Outcomes, and Clinical Implications Across Solid and Hematological Malignancies.

Sex differences influence cancer incidence, treatment response, and susceptibility to cardiovascular toxicity. Males exhibit higher rates and poorer outcomes in most non-sex-specific cancers, while females more frequently experience treatment-related adverse events, including cancer therapy-related cardiac dysfunction. Biological factors such as hormonal status, genetic polymorphisms, immune responses, and pharmacokinetics contribute to these disparities. In cardio-oncology, women-particularly premenopausal or with specific genotypes-may be at increased risk for cardiotoxicity after treatment

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… Cancer Risk Factors Sex differences in cancer incidence may be attributed to differences in the prevalence of established cancer risk factors, sex hormones, genetics, epigenetics, cellular senescence, metabolism and immune responses [ 12 ]. … With advancing age, cancer incidence and prevalence rates increase more sharply in males compared to females, which may be partially explained by sex-based variations in cellular senescence. …