This study aimed to investigate the etiology, clinical characteristics and treatment outcomes of choroidal neovascularization (CNV) in Chinese children and adolescents.

Cisplatin is an important chemotherapeutic agent is widely used to treat breast cancer and olaparib is the most studied PARP inhibitor to date. To explore the combinational anti-cancer potential and synergistic mechanism of Olaparib and cisplatin in breast cancer using network pharmacology. Drugs targets were drawn from PharmMapper, DrugBank, BATMAN-TCM, DrugCentral, STITCH, Swiss Institude of Bioinformatics and Comparative Toxigenomics Database (CTD). Breast cancer targets were extracted from OMIM, KEGG, GeneCards and DrugBank. The protein-protein interaction (PPI) network was created using the STRING database. Core targets were selected by incorporating PPI networks using Cytoscape 3.9.1. GO and KEGG analyses were performed to investigate common targets of Olaparib and cisplatin in breast cancer. The drug-disease-target network contained 82 nodes and 901 edges. The common targets obtained from Olaparib, cisplatin and breast cancer were identified, including ATK, p53, caspase-3, HSP90AA1, IL-6, IL-1β, ANXA5, SIRT1, caspase-9 and PARP. Core targets were primarily related to response to reactive oxygen species, regulation of apoptotic signaling pathway, regulation of DNA metabolic process, and regulation of cell activation. The KEGG pathway analysis revealed that Olaparib and cisplatin may affect breast cancer through platinum drug resistance and longevity regulating pathway. Furthermore, Olaparib combined with cisplatin downregulated the expression of caspase-3 and caspase-9 proteins and upregulated p53, PARP, and SIRT1 protein levels in MCF-7 cells. Functionally, the cooperative effect of Olaparib and cisplatin reduced the applied concentration of cisplatin and enhanced the anticancer effect, emphasizing the importance of combination therapy to overcome side effects and significantly improve the anticancer efficacy of cisplatin.

Treating colorectal cancer (CRC) poses challenges due to the lack of specific molecular targets. Although oxaliplatin (Ox) is commonly used to treat CRC, resistance frequently develops, necessitating the discovery of new therapeutics. This study explored the anticancer effects of Isoalantolactone (IAL) on human CRC cells HCT116 and Ox-resistant HCT116 (HCT116-OxR). Apoptosis, ROS generation, cell cycle distribution, mitochondrial membrane potential (MMP), and caspase activation were assessed through flow cytometry. Protein levels were determined by Western blot analysis. IAL reduced cell viability, measured by MTT assay, and inhibited anchorage-independent colony formation in CRC cells in a time- and concentration-dependent manner. The IC50 values for 48 h of incubation were below 10 µM. Annexin V/7-AAD double staining demonstrated that IAL induced apoptosis in HCT116 and HCT116-OxR cells, and Western blot analysis confirmed increased phosphorylation of JNK and p38 mitogen-activated protein kinase (MAPK). The inhibition of these kinases by SP600125 or SB203580 blocked the antiproliferative effects of IAL. Additionally, IAL triggered ROS generation and disrupted mitochondrial membranes, leading to caspase activation. Pretreatment with N-acetylcysteine (NAC) or Z-VAD-FMK inhibited the antiproliferative effects of IAL, highlighting the crucial roles of ROS generation and caspase activation in IAL-induced apoptosis in CRC cells. In summary, IAL exhibited anticancer effects in CRC cells by inducing apoptosis by elevating ROS level and activating JNK and p38 MAPK. These findings warrant further study to evaluate the therapeutic potential of IAL in treating CRC with various resistances.

Metastasis is one of the leading causes of cancer-related death worldwide. Fascin, a protein that bundles actin filaments to produce protrusions in cancer cells, plays a significant role in the enhancement of cell migration. This protein has been shown that the overexpression of this protein is related to the appearance of different types of cancer, such as colorectal cancer. In this study, we conducted in silico screening of the Enamine library, a compound library with a broad chemical space. Using a ligand-based virtual screening approach based on the pharmacophore model of G2, we identified the predicted inhibitors. First, these compounds were validated by physicochemical analysis. Differential scanning calorimetry (DSF) was used to study the binding between the predicted compounds and fascin protein, followed by an F-actin bundling assay to determine which compounds inhibited the bundling function of fascin. Z1362873773, which exhibited binding to fascin and inhibited F-actin bundling, was further tested in cell cultures to assess its effects on cancer cell viability and migration as well as in organoid models to evaluate potential cytotoxicity. Finally, we established a protocol that can be applied to discover anti-fascin agents from diverse compound libraries. A new molecule has been identified with considerable fascin inhibitory and migration-arresting capacity, which may lead to the development of new therapies to treat cancer.

Coronavirus disease (COVID-19) infection increases the mortality of patients with hematological malignancies. The optimal treatment for de novo acute myeloid leukemia (AML) patients with severe pneumonia caused by COVID-19 is not clear.

Anaplastic lymphoma kinase (ALK)-positive non-small cell lung cancer (NSCLC) often shows incomplete responses and progression despite tyrosine kinase inhibitor (TKI) therapy. Preliminary data suggest that combining brigatinib, an ALK-selective TKI, with surgery or radiotherapy may improve outcomes. We retrospectively analyzed patients with advanced ALK-positive NSCLC who received brigatinib as first-line treatment combined with local therapy to assess safety and efficacy of this approach in a real-world setting. Among 9 patients, 6 (67%) had stage III and 3 (33%) had stage IV adenocarcinoma. Five patients received surgery, 3 received radiotherapy, and 1 received both. Brigatinib-related adverse events (AEs) occurred in 78% of patients, primarily mild (grade ≤ 2). Severe AEs (grade ≥ 3) were seen in 22% of patients and included dyspnea and hypertension. Brigatinib was discontinued in 22% of patients due to toxicity. Local therapy-related AEs were mostly grade 1. The objective response rate was 89%, with 2 complete and 6 partial responses. At data cutoff, brigatinib was ongoing in 55% of patients, with a median treatment duration of 14 months and a 2-year progression-free survival rate of 100%. Combining brigatinib with local therapy appears safe and potentially more effective for advanced ALK-positive NSCLC. Further studies are warranted.

In order to evaluate the short-term outcomes of switching to faricimab from other anti-vascular endothelial growth factor (VEGF) agents in Chinese patients with neovascular age-related macular degeneration (nAMD). This was a retrospective, observational study involving patients with nAMD who had insufficient response to previous anti-VEGF therapy and were switched to Faricimab. Best-corrected visual acuity, central macular thickness, and pigment epithelium detachment (PED) changes were recorded at baseline and after one month of treatment. Data were analyzed using paired t-tests to compare outcomes before and after the switch. This study included 35 eyes from 35 patients (mean age 69.74 ± 11.22 years) who were switched to Faricimab after an average of 6.27 ± 3.41 prior anti-VEGF injections for nAMD. While best-corrected visual acuity showed no significant improvement after one month (P = .06), significant reductions were observed in mean central macular thickness (P < .001), PED height (P < .001), PED volume (P < .001), presence of subretinal fluid (P = .03), and intraretinal fluid (P = .04). Additionally, the presence of PED decreased from 60% at baseline to 45.71% after one month (P = .02). No new safety concerns were identified during the study period. Switching to faricimab from other anti-VEGF agents resulted in significant short-term improvements in both visual and anatomical outcomes, including reduced central macular thickness, pigment epithelium detachment, and subretinal and intraretinal fluid. These findings suggest that Faricimab may offer a beneficial alternative for patients with an insufficient response to prior anti-VEGF therapies. Long-term follow-up studies are necessary to confirm the durability and long-term benefits of this treatment.

Allicin is a small-molecule natural product found in garlic (Allium sativum). We previously showed that allicin inhibits ornithine decarboxylase (ODC) in vitro and induces apoptotic cell death in pediatric neuroblastoma (NB) cancer cell cultures. However, its potency as an anticancer agent in vivo has not been sufficiently explored.

Eribulin is a microtubule inhibitor used in the treatment of various malignancies, including soft-tissue sarcoma. However, the development of eribulin resistance is a recalcitrant clinical problem. The present study demonstrates that super eribulin-resistant HT1080 human fibrosarcoma cells become highly malignant but can be eradicated synergistically by the combination of eribulin and methionine restriction in nude mice.

Among various cancers, primary liver cancer is the seventh most diagnosed malignancy and is the second most prevalent contributor to cancer-causing deaths. During conventional treatment, the recurrence of disease, low drug inefficacy, and severe side effects are the main limitations. Recently, natural anticancer medicines from the Middle East, Korea, China, Europe, North America, and India have attracted a lot of interest due to their low side effects and better remedial properties. The current study investigated the antioxidative and anticancer effects of ethanolic (BME) and n-hexane (BMH) extracts of B. monnieri (L.) Wettst.

Acute lymphoblastic leukemia (ALL) is a significant concern in both pediatric and adult demographics. Despite 156 approved cancer therapies based on small molecules, a mere five apply to all types of leukemia. Unfortunately, adherence to these treatments is low due to adverse side effects. Consequently, there is an urgent need to identify more effective treatment options for ALL. This study presents a potential solution. We have designed over fifty analogs of carbamazepine, utilizing a combination of ligand-based and structure-based drug design methodologies. Among these analogs, we identified the CR80 analog, which demonstrated predicted binding values of -8.66 kcal/mol against beta-tubulin, a favorable LogP, and IC50 values suitable for in vitro evaluation. The CR80 compound was synthesized with a yield of 50% and subsequently assessed in vitro against the U-937 cell line. It obtained an IC50 value of 0.8 micromolar to 1 micromolar and a selectivity index of two, thus marking it as a promising candidate for in vivo studies.

This study presents a novel approach that integrates LLMs with real-time biomedical literature to uncover drug-gene relationships, transforming how cancer researchers identify therapeutic targets, repurpose drugs, and interpret complex molecular interactions. GeneRxGPT, our user-friendly tool, enables researchers to leverage this approach without requiring computational expertise.

To examine the feasibility of high-frequency sampling of symptoms and gather preliminary data on whether daily exercise behavior is related to daily symptom fluctuations.

There is a gap in knowledge about the efficacy of exercise in managing cancer-related fatigue (CRF) in adolescents and young adults (AYAs) during and after chemotherapy.

Polymeric drug delivery systems (DDSs) have gained significant attention in cancer therapy. However, these systems often respond to a single biological stimulus in tumor tissues or cells, limiting their effectiveness. While multi-sensitive DDSs improve therapeutic precision, their complex synthesis involving multi-step modifications remains challenging. Developing functionally integrated and simplified multiple stimuli-responsive DDSs is crucial to addressing tumor diversity and enhancing treatment efficacy.

Gestational trophoblastic neoplasia (GTN) is a rare but aggressive malignancy that follows normal or aberrant pregnancies. Until the advent of immunotherapy in 2017, surgery and chemotherapy were the standard treatment modalities, with chemotherapy remaining the cornerstone. However, chemoresistance and high-risk disease present significant challenges in managing GTN. Recent advancements in immunotherapy, particularly immune checkpoint inhibitors (ICIs), have offered new hope for managing these difficult cases. This review provides the comprehensive overview of the mechanisms underlying ICIs in GTN, and explores the potential synergy of combining ICIs with targeted therapies, such as vascular endothelial growth factor and epidermal growth factor receptor inhibitors. We also provide an overview of the latest evidence on the use of ICIs in treating GTN, focusing on their effectiveness in both low- and high-risk cases, as well as in chemorefractory settings. In addition, we discuss ongoing clinical trials, immune-related adverse events associated with ICIs, biomarker-driven approaches, immunosuppressive tumor microenvironments, and the challenges posed with ICIs resistance. The review also explores future directions, including the integration of ICIs into standard regimens, the potential for personalized treatment based on tumor biology, and the importance of fertility preservation in young patients with GTN. In conclusion, while challenges remain, immunotherapy represents a promising frontier in GTN treatment, with the potential to improve outcomes and provide a more personalized approach to care.

Tumors pose a serious threat to global public health and are usually treated from two aspects: tumor cells and tumor microenvironment. Compared with traditional chemotherapy drugs, traditional Chinese medicine (TCM) monomers have advantages in tumor treatment, such as multiple targets, multiple levels and synergistic intervention. However, most TCM active ingredients have disadvantages such as poor water solubility and stability, which restrict their clinical application. Nano drug delivery systems have the functions of improving the bioavailability of TCM anti-tumor active ingredients, enhancing tissue targeting, achieving controlled drug release, and inhibiting tumor multidrug resistance. Compared with free monomers, they have higher therapeutic effects and fewer side effects. This article summarizes five commonly used anti-tumor TCM monomer nanocarriers, including lipid nanomaterials, exosomes, polymer micelles, carbon nanotubes, and dendrimers, and explains their anti-tumor mechanisms after combining with TCM, such as inhibiting tumor cell proliferation and metastasis, regulating tumor microenvironment, etc. At the same time, the potential of nano drug delivery systems combined with radiotherapy and immunotherapy is discussed, as well as the current problems of potential toxicity, long-term stability, and complex amplification process, as well as future development directions, aiming to provide a reference for promoting the clinical application of nano drug delivery systems for TCM anti-tumor active ingredients.

Phyllanthus reticulatus is a plant species belonging to the family Euphorbiaceae. The plant is native to tropical areas of India, Bangladesh, China, and the Malay Islands. The plant is known for its medicinal properties and has been traditionally used as a diuretic, cooling medicine, and remedy for spongy and bleeding gums. Literature revealed the plant's hepatoprotective, hypolipidemic, antinociceptive, analgesic, anti-inflammatory, antimalarial, cytotoxic, and antimicrobial, anticancer properties. A plant species with significant medicinal potential and its leaves have been studied for their potential therapeutic applications in managing diabetes and diarrhea. This study highlights the chemical profile of P. reticulatus methanolic leaf extract by phytochemical and GC-MS analysis, revealing nine major peaks with active chemical components. FTIR analysis showed the presence of six biologically active functional groups. The methanolic leaf extract showed the existence of 93.44 mg/g, a significant amount of phenolic content, and 55.35 mg/g of flavonoid content. The elemental concentration of plant leaf revealed the presence of 12 elements. The DPPH and PM assay showed the antioxidant properties of the leaf extract, as evidenced by its anticancer property of the leaf extract with 28.56 % cell growth inhibition on the HCT-116 colon cancer cell line at 24 h in a dose-dependent manner. This is the first report on Phyllanthus reticulatus, which reports the spectroscopic and anticancer properties of the leaf extract on colon cancer. The study opens avenues for further investigation into the bioactive constituents of Phyllanthus reticulatus leaves and their mechanisms of action, paving the way for future studies and potential drug development.

The use of complementary integrative medicine (CIM) by cancer patients is currently very common. The main reasons why patients turn to CIM are to improve quality of life (QoL) and support the immune system. Unfortunately, many patients rely on CIM self-prescription, neglecting the risk of interactions with anticancer treatments (ACTs). The primary objective is to demonstrate the feasibility of combining CIM and ACT in a multidisciplinary approach to improve the QoL of cancer patients and to reduce ACT's adverse events.

In recent years, molecular target drugs have become integral in treating malignant tumours. Multikinase inhibitors (MKIs) have been associated with serious skin disorders, including hand-foot skin reaction (HFSR), which impair patient quality of life, often disrupting activities of daily living necessitating dose reduction or discontinuation. As the pathogenic mechanisms of these skin disorders are unknown, no effective treatments have been established. Previously, by drug repurposing using an in vitro culture system, certain azole antifungal drugs (AFDs) were identified that prevented sorafenib-induced cell death of normal human epidermal keratinocytes. In this study, topical ketoconazole demonstrated clinical improvement in hyperkeratosis and pain associated with sorafenib-induced HFSR. Investigation of the mechanism using the in vitro culture system revealed sorafenib to be particularly cytotoxic among MKIs. Annexin V and TUNEL staining revealed apoptosis was mainly involved in this cytotoxicity. Antibody arrays and western blot showed increased levels of secretion of interleukin-1 receptor antagonist and macrophage migration inhibitory factor in culture supernatants. AFDs suppressed the secretion of these cytokines and reduced apoptosis in keratinocytes. This study reveals one aspect of the pathogenesis of sorafenib-induced HFSR and demonstrates that AFDs may be an effective treatment.