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Vasculogenic mimicry (VM) is a brand‐new tumour vascular paradigm independent of angiogenesis that describes the specific capacity of aggressive cancer cells to form vessel‐like networks that provide adequate blood supply for tumour growth. A variety of molecule mechanisms and signal pathways participate in VM induction. Additionally, cancer stem cell and epithelial‐mesenchymal transitions are also shown to be implicated in VM formation. As a unique perfusion way, VM is associated with tumour invasion, metastasis and poor cancer patient prognosis. Due to VM's important effects on tumour progression, more VM‐related strategies are being utilized for anticancer treatment. Here, with regard to the above aspects, we make a review of advanced research on VM in cancer.

Background During these last years, new agents have dramatically improved the survival of the metastatic patients. Oligometastases represent a continuous field of interest in which the integration of metastases-directed therapy and drugs could further improve the oncologic outcomes. Herein a narrative review is performed regarding the main rationale in combining immunotherapy and target therapies with SBRT looking at the available clinical data in case of oligometastatic NSCLC, Melanoma and Kidney cancer. Material and method Narrative Review regarding retrospective and prospective studies published between January 2009 to November 2019 with at least 20 patients analyzed. Results Concerning the combination between SBRT and Immunotherapy, the correct sequence of remains uncertain, and seems to be drug-dependent. The optimal patients’ selection is crucial to expect substantial benefits to SBRT/Immunotherapy combination and, among several factors. A potential field of interest is represented by the so-called oligoprogressed disease, in which SBRT could improve the long-term efficacy of the existing target therapy. Conclusions A low tumor burden seems to be the most relevant, thus making the oligometastatic disease represent the ideal setting for the use of combination therapies with immunological drugs.

Alzheimer's disease (AD) is a complex and multifactorial neurodegenerative disorder, recognized as the most prevalent form of dementia. It is characterized by multiple pathological processes, including amyloid‐beta accumulation, neurofibrillary tangles, and neuroinflammation. The therapeutic efficacy of traditional single‐target drugs has been limited, failing to cure, halt, or reverse disease progression. Therefore, this complex disease warrants comprehensive therapeutic strategies like multi‐target drug design (MTDD). MTDD represents a promising strategy to target multiple pathological pathways concurrently. The integration of advanced technologies, including artificial intelligence, machine learning, and nanomedicine, can further enhance the precision and effectiveness of MTDD. This review explores various MTDD approaches, including multi‐target‐directed ligands, multi‐target compound combinations, and polypharmacology. These strategies aim to address the multifaceted nature of AD pathology more effectively than single‐target approaches. MTDD offers key advantages, including pathway‐level synergy, broader therapeutic scope, and potential for improved efficacy. However, MTDD faces various challenges and limitations, such as the complexity of drug design, difficulty of crossing the blood–brain barrier, and regulatory hurdles. Despite these challenges, recent advancements in computational methods and drug delivery systems show promise in overcoming these barriers. Future research should focus on optimizing delivery systems, improving in silico modeling, and translating multi‐target strategies into clinically viable therapies for AD. This review addresses these needs by critically analyzing recent technologies, advantages, challenges, limitations, and future directions of MTDD, underscoring its potential to transform AD treatment.

Wuweizisu B (WSB), a bioactive lignan derived from Schisandra chinensis, has shown promise as a multi-target anticancer agent with unique therapeutic advantages over conventional therapies. The present review systematically examined the molecular mechanisms underlying the anticancer effects of WSB, including induction of cell cycle arrest, promotion of apoptosis through mitochondrial and death receptor pathways, inhibition of epithelial-mesenchymal transition and remodeling of the tumor immune microenvironment. WSB exhibits synergistic potential with chemotherapy and immunotherapy and can reverse multidrug resistance (MDR) by modulating key pathways such as STAT3, P-glycoprotein (P-gp), and survivin. To address pharmacokinetic limitations, particularly low oral bioavailability, the present review discussed innovative delivery strategies such as nanotechnology-based formulations to enhance tumor targeting. Thus, with its pleiotropic mechanisms, low toxicity profile, and broad-spectrum efficacy across multiple cancers, the WSB merits further investigation as a complementary oncology therapeutic. However, its clinical translation faces challenges, including potential hepatotoxicity and lack of clinical validation. The present review consolidated current knowledge of WSB's anticancer potential while providing a roadmap for clinical development, emphasizing the need for biomarker-driven trials and precision delivery systems to fully realize its therapeutic value in personalized medicine.

Colorectal cancer (CRC) is one of the most common malignant cancers worldwide and seriously threatens human health. The clustered regulatory interspaced short palindromic repeat/CRISPR-associate nuclease 9 (CRISPR/Cas9) system is an adaptive immune system of bacteria or archaea. Since its introduction, research into various aspects of treatment approaches for CRC has been accelerated, including investigation of the oncogenes, tumor suppressor genes (TSGs), drug resistance genes, target genes, mouse model construction, and especially in genome-wide library screening. Furthermore, the CRISPR/Cas9 system can be utilized for gene therapy for CRC, specifically involving in the molecular targeted drug delivery or targeted knockout in vivo. In this review, we elucidate the mechanism of the CRISPR/Cas9 system and its comprehensive applications in CRC. Additionally, we discussed the issue of off-target effects associated with CRISPR/Cas9, which serves to restrict its practical application. Future research on CRC should in-depth and systematically utilize the CRISPR/Cas9 system thereby achieving clinical practice.

Bronchopulmonary dysplasia (BPD), also known as neonatal chronic lung disease, is an important cause of respiratory illness in preterm newborns that results in significant morbidity and mortality. Long noncoding RNAs (lncRNAs) have been discovered with many biological functions. However, the role of lncRNAs in the pathogenesis of BPD remains poorly understood. Here, we established a mouse lung injury model that mimicked human BPD. Subsequently, we found the lncRNA H19 expression level was significantly increased in BPD compared with normal lung tissues using quantitative real-time polymerase chain reaction. Next, we observed that overexpression of lncRNA H19 enhanced mitogen-activated protein kinase (MAPK) signaling pathway. In addition, we also found that dysfunction of lncRNA H19 altered the expression of inflammatory factors. Thus, our study validates that lncRNA H19 contributes to the progression of BPD by regulating MAPK signaling pathway, which could be used as a potential target for treating BPD.

Despite excellent results in frontline therapy, particularly in pediatric age, refractory Burkitt lymphoma still remains a therapeutic challenge, with dismal outcome. The prognosis is very poor, ranging from less than 10% to 30-40%, with longer survival only in transplanted patients. On account of the paucity of data, mostly reporting on small series of patients, with heterogeneous characteristics and salvage treatments, at present it is impossible to draw definitive conclusions on the treatment of choice for this difficult to treat subset of patients. New insights into Burkitt lymphoma/leukemia cell biology have led to the development of new drugs, currently being tested, directed at different specific targets. Herein, we describe the results so far reported in refractory Burkitt lymphoma/leukemia, with standard treatments and hematopoietic stem cell transplant, and we review the new targeted drugs currently under evaluation.

Head and neck squamous cell carcinoma (HNSCC) is highly variable by tumor site, histologic type, molecular characteristics, and clinical outcome. During recent years, emerging targeted therapies have been focused on driver genes. HNSCC involves several genetic alterations, such as co-occurrence, multiple feedback loops, and cross-talk communications. These different kinds of genetic alterations interact with each other and mediate targeted therapy response. In the current review, it is emphasized that future treatment strategy in HNSCC will not solely be based on \"synthetic lethality\" approaches directed against overactivated genes. More importantly, biologic, genetic, and epigenetic alterations of HNSCC will be taken into consideration to guide the therapy. The emerging genetic alterations in HNSCC and its effect on targeted therapy response are discussed in detail. Hopefully, novel combination regimens for the treatment of HNSCC can be developed.

Despite recent advances in chronic heart failure management (either pharmacological or non-pharmacological), the prognosis of heart failure (HF) patients remains poor. This poor prognosis emphasizes the need for developing novel pathways for testing new HF drugs, beyond neurohumoral and hemodynamic modulation approaches. The development of new drugs for HF therapy must thus necessarily focus on novel approaches such as the direct effect on cardiomyocytes, coronary microcirculation, and myocardial interstitium. This review summarizes principal evidence on new possible pharmacological targets for the treatment of HF patients, mainly focusing on microcirculation, cardiomyocyte, and anti-inflammatory therapy.