This review aimed to evaluate the effects of exercise-based interventions on cancer therapy-related cardiovascular toxicity (CTR-CVT) in individuals with cancer.

Febrile neutropenia (FN) is a life-threatening complication of chemotherapy. Although practice guidelines suggest the use of existing prediction models when making decisions to prevent and treat FN, recent evidence suggests that these models are limited in their discriminative ability. This study aims to systematically review and critically evaluate the recent literature to assess the question: what evidence-based clinical prediction models can be used to predict FN or its outcomes?

The patient was a 54-year-old woman with chronic myeloid leukemia. Ten months after treatment with dasatinib, she developed a cough. Imaging studies showed ground-glass patterns in the lower lung fields of both lungs, which led to suspicion of drug-induced lung injury and prompted discontinuation of dasatinib. A transbronchial lung biopsy showed epithelioid granuloma without necrosis in the alveolar region. There were no other systemic symptoms or signs to support a diagnosis of sarcoidosis. Fifteen days after withdrawal of dasatinib, both the cough and X-ray findings improved. Granulomatous tissue was detected on lung biopsy, which indicates that drug-induced sarcoidosis-like reaction (DISR) may cause interstitial lung injury as a respiratory complication of dasatinib treatment. Case reports of DISR following administration of immune checkpoint inhibitors and immunomodulatory drugs have recently become more frequent. Here we report a case of dasatinib-induced DISR with a review of the literature.

Zolbetuximab, a first-in-class monoclonal antibody targeting Claudin 18.2 (CLDN 18.2), has demonstrated significant survival benefit when combined with chemotherapy in HER2-negative, CLDN 18.2-positive advanced gastric/gastroesophageal junction (G/GEJ) adenocarcinoma. However, its integration into clinical practice presents two major challenges: the best treatment selection between zolbetuximab or immune checkpoint inhibitor (ICI)-based regimens in patients co-expressing programmed death-ligand 1 (PD-L1), and the management of zolbetuximab-related nausea and vomiting (N/V). We critically reviewed evidence from randomized controlled trials, regulatory approvals, and recent expert consensus on zolbetuximab management. In CLDN 18.2-positive/PD-L1-positive patients, ICIs may offer greater long-term survival benefit especially in case of high PD-L1 CPS, while zolbetuximab may be preferred in patients with negative-to-low CPS or ICIs contraindications. N/V, reported in more than three-quarter of patients, is more frequent and severe during the first infusion, due to zolbetuximab loading dose and faster infusion rate. Proper management includes accurate adherence to high-risk antiemetic protocols (including NK-1/5-HT3 antagonists and corticosteroids) and careful control of infusion rates with a stop and go strategy. In case of CLDN 18.2 and PD-L1 CPS co-positivity, we advocate the use of PD-L1 CPS ≥ 10 as a practical decision-making threshold for favoring ICI-based regimens. However, the treatment selection should be tailored on comorbidities, comprehensive molecular characterization and available subsequent options. To ensure the optimal use of zolbetuximab, special attention is required during the first cycle, due to higher risk of infusion-related N/V. We suggest that the optimization of both prophylactic and on-treatment antiemetic strategies is essential to enhance zolbetuximab adherence and maximize clinical outcomes.

The unique characteristics of cancer are crucial for comprehending the processes underlying cancer initiation, development, and maintenance. These hallmarks guide the development of novel therapeutic strategies aimed at fundamental traits of cancer, resulting in more targeted therapies with the possibility for sustained effectiveness and minimized adverse effects. Drug repurposing, a novel approach that leverages the known safety and pharmacological properties of existing drugs, has surfaced as a viable alternative to traditional drug development. This method expedites the timescale for introducing novel medicines into clinical practice, often demonstrating reduced failure rates in clinical trials. Recent data substantiates the therapeutic efficacy of many repurposed medications in the management of oral squamous cell carcinomas (OSCC), a highly aggressive and treatment-resistant malignancy. Prominent instances include metformin, phenformin, propranolol, acetylsalicylic acid, celecoxib, itraconazole, statins, dihydroartemisinin, and methotrexate. These pharmaceuticals demonstrated diverse anticancer actions, rendering them valuable tools in the therapy of OSCC. This review provides a comprehensive overview of molecular signaling in the reprocessing of drugs for OSCC.

The chick embryo chorioallantoic membrane (CAM) model is gaining increasing attention from cancer researchers worldwide. Its affordability, short experimental duration, robustness, and ease of tumor xenograft visualization make it a valuable tool in cancer research. This review explores recent advancements and potential applications of the avian CAM model, including the following: (1) studying tumor growth and metastasis, (2) investigating mechanisms of tumor chemoresistance, (3) optimizing drug delivery methods, (4) improving bioimaging techniques, (5) evaluating immuno-oncology drug efficacy, (6) examining tumor-extracellular matrix interactions, (7) analyzing tumor angiogenesis, and (8) exploring the roles of microRNAs in cancer. Additionally, we compare the in ovo CAM model with other in vivo animal models and in vitro cell culture systems. Positioned between in vitro and in vivo models in terms of cost-effectiveness and accuracy in cancer recapitulation, the CAM model enhances both preclinical and translational research. Its expanding use in cancer studies and therapy development is expected to continue growing.

Murine double minute 2 (MDM2) is an oncogene that plays a crucial role in regulating the activity of the tumor suppressor protein p53. By binding to p53, MDM2 promotes its degradation, thus promoting the malignant proliferation. The MDM2-p53 interaction has thus generated interest as a therapeutic target, particularly in some sarcomas characterized by the amplification of the MDM2 gene. In this manuscript, we provide an overview of the current and emerging targeted therapies for MDM2-amplified sarcomas.

Aclarubicin (also called aclacinomycin A) is an antineoplastic from the anthracycline class that is used in China and Japan but not in Europe nor in the USA. Aclarubicin induces much less DNA damage than the classical anthracyclines doxorubicin, daunorubicin, epirubicin, idarubicin, and the anthracene mitoxantrone, but is equally effective in inhibiting DNA-to-RNA transcription and in eliciting immunogenic stress in malignant cells. Accordingly, aclarubicin lacks the DNA damage-associated cardiotoxicity that is dose-limiting for classical anthracyclines. Conversely, aclarubicin is at least as potent as other anthracyclines in inducing immunogenic cell death (ICD), which is key for the mode of action of efficient chemotherapeutics. This combination of reduced toxicity and equivalent ICD-stimulatory activity may explain why, as compared to other anthracyclines, aclarubicin is particularly efficient against acute myeloid leukemia. As a result, we advocate for clinical studies seeking to replace the anthracyclines used in Western medicine by aclarubicin-like compounds. Such clinical studies should not only embrace hematological malignancies but should also concern solid cancers, including those in which ICD-inducing chemotherapies are followed by immunotherapies targeting the PD-1/PD-L1 interaction.

Endocrine therapy is an essential treatment to improve disease-free and overall survival in patients with hormone receptor-positive breast cancer. However, symptoms associated with endocrine therapy severely affect patients' quality of life and medication adherence. To inform symptom management strategies, this study systematically reviews research on patients' symptom experiences and coping strategies during endocrine therapy.

Lung cancer has the second highest occurrence and lowest survival rate among all cancers and incidence rates are increasing. From the tumor milieu, tumors exude chemokines and cytokines that hassle the pulmonary drug administration hinders the success of treatment. A few mutations lead to generation of lungs cancer. It has prominent levels of mutated genes such as TP53, KRAS, MET, and EGFR. Various molecular pathways involved in causing lung cancer such as PTEN/PI3K/AKT pathway, JAK/STAT pathways, RAF-MEK-ERK, PI3K-AKT-mTOR, and RALGDS-RA, PI3K, AKT, and PI3K/AKT/mTOR pathway. Inhibition of such biological pathway through active targeting, using various biological inhibitors, and blockers could help in treating and recurrence of lungs tumor. The conventional therapeutic modalities concomitant with personalized genomic nanomedicine can have potential in improving treatment regimen. This study explored the different genomic changes that occur due to the prime etiological factors, their reported treatment profile, and nanocarrier mediated therapeutic strategy by targeting tumor microenvironment (TME). Nanocarriers confront multiple obstacles in their journey to the TME therapeutic approach as leaky vasculature, large fenestration, and usually carried off from immune system and phagocytosis process. However, formulators designed a bio-functionalized carrier that enable to evade opsonization, escape immune system, modulate TME, identify reticuloendothelial system, and thus facilitates biological interaction, and enhance cellular uptake.

Photodynamic therapy (PDT), as a non-invasive treatment modality, has shown potential as an alternative to traditional therapies in lung cancer treatment. However, its clinical application is still limited by key challenges, including low photosensitizer (PS) delivery efficiency, tumor microenvironment hypoxia, and the restricted diffusion of reactive oxygen species (ROS). This review systematically discusses innovative strategies employed by nanocarrier delivery systems to overcome these bottlenecks in PDT. The first section focuses on the application and challenges of PDT in lung cancer treatment: although PDT induces localized tumor cell death through ROS generation mediated by PSs, its efficacy is hindered by the delivery barriers of hydrophobic PSs to the lung, insufficient ROS generation due to tumor hypoxia, and PS self-quenching. The second section presents nanotechnology-driven solutions: 1) using nanocarriers equipped with catalase or hemoglobin and perfluorocarbon to alleviate tumor hypoxia and enhance ROS production; 2) modifying the surface of nanocarriers with targeting ligands to improve PS accumulation in tumor tissues and reduce self-quenching effects; and 3) combining PS-loaded nanocarriers with immune checkpoint inhibitors and chemotherapy agents to synergistically enhance anti-tumor efficacy and suppress metastasis. Future research should focus on further optimizing the biocompatibility, clinical translation potential, and multimodal synergistic mechanisms of nanocarriers, to promote the widespread application of PDT in precise lung cancer treatment.

Despite the use of therapeutic modalities such as surgery, chemotherapy, and radiotherapy, breast cancer remains a potentially fatal condition for humans. The primary problems with these treatments are their low efficacy and their inevitable side effects to the surrounding healthy tissues. Overcoming these challenges has been achieved through precision therapeutics, where personalized interventions have significantly improved treatment efficacy. However, the development of nanoparticles has largely remained focused on optimizing delivery platforms based on a one-size-fits-all approach. As lipid-based, polymeric, and inorganic nanoparticles are now being engineered with greater specificity, they are increasingly suited for customization-paving the way for truly personalized drug delivery in the era of precision medicine. In this line, the current study focuses on breast cancer, and recent developments in drug delivery. The first part of this review looks at practical difference between precision medicine and precision targeting. It describes breast cancer signaling pathways, highlighting the exciting potential of nanotechnology in cancer drug delivery using precision targeting - an approach closely linked to precision medicine. We also go over how nanostructures can improve the way drugs, genes, and immunotherapy are delivered in the treatment of breast cancer. Lastly, we discuss challenges, solutions, future directions, and possibilities for the practical use of nanotechnology in the treatment of breast cancer, while introducing nano-products based on clinical trials.

Gynecological cancers represent one of the leading causes of death in women and pose a critical global health challenge. While surgery and chemotherapy remain the first-line therapies for gynecological cancers, the persistently high morbidity and mortality rates have driven the urgent exploration of novel theranostic strategies. In recent years, polymer nanoparticles (PNPs) have gained increasing attention in the diagnosis and treatment of cancer due to their superior targeting ability and delivery efficiency. This review provides an overview of PNPs and their role in tumor diagnosis and treatment, with a strategic focus on their utility in gynecological cancers. It covers drug delivery, imaging, combination therapy, and theranostic integration in gynecological cancers, and summarizes the composition, principles and characteristics of diverse polymers and their cargoes. Furthermore, this work highlights innovative applications of PNPs in gynecological cancers management, spanning chemotherapy, immunotherapy, PARPi therapy, phototherapy and other therapies. Despite promising preclinical advancements in PNPs, formidable challenges persist in their clinical translation. This review serves as a comprehensive resource for researchers and clinicians aiming to optimize gynecological cancers theranostics as well as accelerate the development and clinical translation of PNPs.

Cancer represents a complex group of diseases characterized by abnormal cell proliferation, invasion, and metastasis. These features pose significant challenges to conventional therapeutic approaches, necessitating the development of more targeted and effective treatment strategies.

Non-clinical pharmacological safety studies are conducted using cells and animals to ensure the safety of pharmaceuticals in humans. Following these studies, drug candidates are administered to humans during clinical trials. Safety must be sufficiently confirmed in non-clinical studies to ensure that test participants suffer no adverse health effects. However, due to species differences, low ability to extrapolate from in vitro to in vivo evaluation methods, and other problems, health hazards may unfortunately still occur. Therefore, sophisticated in vitro evaluation systems using human cells are actively being pursued. The main challenge remains the lack of a reliable methodology for extrapolating in vitro results to in vivo settings. We have attempted to extract parameters that can be predictably translated from in vitro [contractile evaluation in three-dimensional (3D) heart tissue] to in vivo (guinea pig echocardiography) conditions, using cardiac contractile dysfunction induced by anticancer drugs as an example. In this review, we introduce the in vitro methods developed to date to evaluate this cardiac contractile dysfunction, analyze the factors enabling highly accurate prediction of torsades de pointes in humans based on past proarrhythmic risk prediction methods using human induced pluripotent stem cell-derived cardiomyocytes, and apply them to evaluate cardiac contractile dysfunction caused by anticancer drugs using three-dimensional heart tissue. We also introduce the proposed strategy for this evaluation method in this section.

Ototoxicity, or hearing loss and damage to the auditory system caused by certain medications, is a significant clinical challenge. Many commonly used drugs, including antimicrobials, cancer therapies, and loop diuretics, have the potential to induce temporary or permanent ototoxicity. The underlying mechanisms are complex, involving both genetic and environmental factors. Pharmacogenomics, the study of how an individual's genetic makeup influences their response to drugs, has emerged as a promising field for understanding and mitigating ototoxicity. Developing personalized approaches to prevent and manage ototoxicity is crucial, and this is where the pharmacogenomic basis of ototoxicity becomes crucial. This review aims to provide healthcare professionals with an updated perspective on the genetics of ototoxicity by summarizing the latest research and insights in this rapidly evolving field. It presents a comprehensive overview of the mechanisms and genetic factors associated with drug-induced ototoxicity, with a particular focus on cisplatin and aminoglycoside antibiotics.

Microtubules are important components of the cytoskeleton. Traditional Chinese medicines (TCMs), including Chinese ethnic medicines, such as Uighur medicines, Li ethnic medicines, Dong ethnic medicines, Lisu ethnic medicines, and Tujia ethnic medicines, can act on microtubules and tubulin, inhibit microtubule polymerization or promote microtubule depolymerization. In this paper, we review the microtubule-binding sites, summarize the mechanisms by which the active TCM and ethnic medicine ingredients and their derivatives inhibit microtubules, and look forward to applying TCMs and ethnic medicines to inhibit microtubules for cancer treatment.

Isatin (1H-indole-2,3-dione) scaffold is an important heterocyclic building block which can be used for the design and synthesis of anti-cancer agents targeting tyrosine kinases, tubulin polymerization, carbonic anhydrases, and histone deacetylases. There are also several lines of evidences demonstrating the role of cyclin-dependent kinase 2 (CDK2) in cancer development and its potential as anti-cancer target. Here we are going to review isatin-derived CDK2 inhibitors and their potential for developing new anticancer agents. The purpose of this review is to present the importance of isatin scaffold for design of new CDK2 inhibitors from medicinal and biological viewpoints. Furthermore, the in vitro and in silico studies, and structure-activity relationships (SARs) were also discussed. The Insights derived from SARs provide crucial directions for the rational design of potent and selective isatin-based CDK2 inhibitors, which improve therapeutic efficacy and reduce side effects of anticancer chemotherapy.

Acute promyelocytic leukemia (APL) is highly malignant and progresses rapidly. In recent years, several studies have shown that oral arsenic, the primary component is realgar, could effectively alleviate APL, with therapeutic effects not inferior to those of intravenous arsenic and a higher safety profile, but currently the active substances and mechanism of realgar's anti-APL effect are unclear, making oral arsenic agents containing realgar lack sufficient scientific basis clinically. The clinical trials on oral arsenic agents containing realgar for the treatment of APL over the past 20 years were reviewed, suggesting it had good therapeutic effect and relatively high safety. Quantitative analysis was conducted on the accumulation of arsenic metabolites in different tissues during the longest 90 day period after realgar administration in rats, and it was found that dimethylarsenic (DMA) was the most predominant form of arsenic metabolites in the body. The DMA concentration slightly increased and remained stable with prolonged administration time, even if discontinuation, the DMA concentration still remained at a certain level. Distribution and accumulation of DMA were significantly higher in blood than in organs. Futhermore, DMA significantly prolonged the survival time of APL mice, induced cell apoptosis, inhibited NB4 cell proliferation, promoted the differentiation of leukemia cells, and downregulated the expression of PML-RARα fusion protein and wild-type RARα protein. The study concluded that DMA could be the main active substance of realgar and is responsible for its significant anti-APL effects, suggesting realgar has good efficacy for blood-related diseases and have low hepatorenal toxicity.

The KRAS (Kirsten rat sarcoma viral oncogene homolog) gene is recognized as the most frequently mutated oncogene in advanced non-small cell lung cancer (NSCLC). The most prevalent mutation within this gene is G12C, formally known as KRAS G12C, which leads to the substitution of glycine with cysteine at position 12 of the KRAS protein.