Costus speciosus is a medicinal plant with a long history in Indian Ayurvedic medicine, recognized for its diverse bioactive properties, including antibacterial, anticancer, anti-inflammatory, and antidiabetic effects. This review highlights its therapeutic potential, particularly in cancer treatment, where its bioactive compounds exhibit cytotoxic effects against breast, ovarian, and uterine cancers. These compounds have shown the ability to induce apoptosis, regulate the cell cycle, and inhibit cancer progression, offering a promising alternative to conventional chemotherapy with potentially fewer side effects. Additionally, C. speciosus demonstrates antioxidant, antimicrobial, and antidiabetic properties, expanding its clinical applications. Despite its promising pharmacological profile, further research is required to understand the molecular mechanisms underlying its therapeutic effects and ensure the safety and efficacy of its various extracts for therapeutic use.

Intra-arterial chemotherapy (IAC) has emerged as the primary treatment option for retinoblastoma management. It enables the localized delivery of a higher concentration of chemotherapeutic agents (melphalan, carboplatin and topotecan) in the ophthalmic artery, enhancing tumour control and potentially avoiding the need for enucleation. Nevertheless, procedure-related complications have raised concerns. In this article, we outline the various technical considerations for performing safe IAC and minimizing procedure-related complications.

Recent advances in deep learning and machine learning have greatly increased the capabilities of extracting features for evaluating the response to anti VEGF treatment in patients with Diabetic Macular Edema (DME). In this review, we explore how these algorithms can be used for discriminating between responders and non-responders to anti vascular endothelial growth factor (VEGF) injections. Electronic databases, including PubMed, IEEE Xplore, BioMed, JAMA, and Google Scholar, were searched, and reference lists from relevant publications were also considered from inception till August 31, 2023, based on the inclusion and exclusion criteria. Data extraction was conducted according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. The results focus on keywords such as DME, OCT, anti VEGF, and patient responses after anti VEGF injections. The article measures the effectiveness of different machine learning and deep learning algorithms, including linear discriminant analysis (LDA), ResNet-50, CNN with attention, quadratic discriminant analysis (QDA), random forest (RF), and support vector machines (SVM), in analyzing eyes that could tolerate extended interval dosing. According to a review of 50 relevant papers published between 2016 and 2023, the algorithms achieved an average automated sensitivity of 74% (95% CI: 0.55-0.92) in detecting treatment responses.

Pseudoxanthoma elasticum (PXE) is an inherited mineralization disorder that leads to calcification of elastic fibers. The ocular characteristics arise due to the calcification of Bruch's membrane, which is located between the retinal pigment epithelium and the choriocapillaris. Despite major scientific progress in understanding the underlying pathological mechanism in recent years, no causal treatment has so far been established. Therefore, the management of patients is currently limited to the treatment of secondary complications, such as intravitreal anti-vascular endothelial growth factor (VEGF) injections in cases of exudative neovascularization. This article discusses upcoming studies that aim to reduce ectopic mineralization. To confirm the diagnosis and possible inclusion in such studies a second assessment should therefore be carried out in a specialized center for PXE.

Antibody-drug conjugates (ADCs) have emerged as a transformative therapeutic modality in oncology, offering unprecedented precision in targeting tumor cells while sparing healthy tissues. In bladder cancer, a malignancy with high recurrence rates and limited treatment options, ADCs have demonstrated remarkable efficacy by targeting specific tumor-associated antigens such as NECTIN-4 and Human Epidermal Growth Factor Receptor 2 (HER2). This review provides a comprehensive evaluation of the current landscape of ADC-based therapies for bladder cancer, focusing on their mechanisms of action, clinical efficacy, and safety profiles.

Lung cancer remains a leading cause of cancer-related mortality, necessitating improved treatment strategies. This study collectively highlights the valuable potential of marine sponges as a source for discovering new anti-tumor agents.

Imidazole is a five-membered heterocyclic system featuring two nitrogen heteroatoms at the 1- and 3-positions of the ring. The imidazole scaffold is particularly suited for kinase inhibition concepts. This further confirms that this scaffold is a privileged structure in the development of anticancer drugs. Considering these key factors and the recent focus of scientists on imidazole compounds, we discuss the anticancer activities of imidazole-containing hybrids and related compounds, highlighting articles published in 2023 that serve as a basis for medicinal chemistry leads. From a chemical perspective, the present review emphasizes hybrid molecules with an imidazole ring in the side chain, imidazole-centered hybrid molecules, condensed imidazole hybrids, hybrid compounds containing two or more imidazole rings, polycyclic imidazole hybrids, imidazole-containing metal complexes, and benzimidazole hybrids.

The publication focuses on the innovative applications of PROTAC (proteolysis-targeting chimera) technology in modern pharmacotherapy, with particular emphasis on cancer treatment. PROTACs represent an advanced therapeutic strategy that enables selective protein degradation, opening new possibilities in drug design. This technology shows potential in the treatment of cancers, viral infections (such as HIV and COVID-19), and chronic diseases including atherosclerosis, Alzheimer's disease, atopic dermatitis, and Huntington's disease. Promising results from clinical studies on the compound ARV-471 confirm the effectiveness of this approach. New types of PROTACs, like TF-PROTAC and PhosphoTAC, are designed to enhance the effectiveness, stability, and absorption of treatment drugs. The conclusions of the review highlight the broad therapeutic potential of PROTACs in various diseases and their relevance for the future of therapies, particularly in oncology.

Cancer is the second leading cause of death worldwide. Late diagnosis, low drug selectivity, high toxicity, and treatment resistance are challenges associated with pharmacological interventions. The commonly used therapies include surgery, radiotherapy, hormonal therapy, immunotherapy, and chemotherapy. Recently, Cu complexes have been studied owing to their biological functions and effects on tumor angiogenesis. In this review, we examined 23 types of cancer and revealed the use of cell lines. The synthesis of Cu complexes with ligands such as phenanthroline and thiosemicarbazones has also been reported. Such co-ligation is promising because of its high cytotoxicity and selectivity. Compared with cisplatin, Cu complexes, especially mixed complexes, showed better interactions with DNA, generating reactive oxygen species and inducing apoptosis. Nanoformulations have also been adopted to improve the pharmacological activity of compounds. They enhance the efficacy of complexes by targeting them to the tumor tissue, thereby improving their safety. Studies have also explored Cu complexes with clinically relevant pharmacophores, suggesting a "hybrid chemotherapy" against resistant tumors. Overall, Cu complexes have demonstrated therapeutic versatility, antitumor efficacy, and reduced adverse effects, showing great potential as alternatives to conventional chemotherapy and justifying future clinical investigations to validate their use.

Extracellular vesicles (EVs) are lipid bilayer-enclosed particles secreted by cells and ubiquitously present in various biofluids. They not only mediate intercellular communication but also serve as promising drug carriers that are capable of delivering therapeutic agents to target cells through their inherent physicochemical properties. In this review, we summarized the recent advances in EV isolation techniques and innovative drug-loading strategies. Furthermore, we emphasized the distinct advantages and therapeutic applications of EVs derived from different cellular sources in cancer treatment. Finally, we critically evaluated the ongoing clinical trials utilizing EVs for drug delivery and systematically assessed both the opportunities and challenges associated with implementing EV-based drug delivery systems in cancer therapy.

There is significant inter-individual variability in the prevalence and severity of cisplatin-induced ototoxicity, which is greatly influenced by genetic and non-genetic factors that predispose the patient to the development of hearing loss. Currently, the focus should be on identifying patients who are more likely to develop ototoxicity based on genetic and non-genetic factors, as therapies to combat ototoxicity are limited or still under study. The severity of hearing loss and the time of its onset may be influenced by certain genetic polymorphisms or the dose administered, age, sex, diet, the administration of other drugs with ototoxic potential, and association with radiotherapy of the head and neck. Knowing the risk factors allows the doctor to manage each case in a personalized manner, preventing hearing damage, especially in the long term. With the help of PubMed and Scopus, we searched for relevant studies documenting the genetic and non-genetic risk in patients treated with cisplatin. This review article is a synthesis of the literature that points out the importance of these factors, encouraging genetic screening and improving quality of life in patients treated with cisplatin.

The genotoxic drug doxorubicin (Dox) remains one of the most powerful chemotherapeutic options available for a wide range of cancers including breast, ovarian, and other cancers. However, emerging evidence links Dox treatment with chemotherapy-induced cognitive impairment, a condition that is popularly referred to as Dox-induced neurotoxicity or "chemobrain", which limits the use of the drug. There are no specific treatments for Dox-induced neurotoxicity, only interventions to mitigate the neurotoxic effects of the drug. Accumulating evidence indicates that DNA damage, oxidative stress, dysregulation of autophagy and neurogenesis, inflammation, and apoptosis play central roles in Dox-induced neurotoxicity. Additionally, germline mutations in the tumour suppressor genes breast cancer susceptibility genes 1 and 2 (BRCA1 and BRCA2) increase the risk of breast, ovarian, and related cancers. BRCA1 and BRCA2 are distinct proteins that play crucial, unique roles in homologous recombination-mediated double-stranded break repair. Furthermore, BRCA1 and 2 mitigate oxidative stress in both neural cells and brain microvascular endothelial cells, which suggests that they have a critical role as regulators of pathways central to the development of Dox-induced neurotoxicity. Despite research on the effects of Dox on cognitive function, there is a gap in knowledge about the role of BRCA1 and BRCA2 in Dox-induced neurotoxicity. In this review, we discuss existing findings about the role of different mechanisms and the role of BRCA1 and BRCA2 in Dox-induced neurotoxicity, along with future perspectives.

P-glycoprotein (P-gp), a transmembrane efflux pump encoded by the ABCB1/MDR1 gene, is a major contributor to multidrug resistance in hematological malignancies. These malignancies, arising from hematopoietic precursors at various differentiation stages, can manifest in the bone marrow, circulate in the bloodstream, or infiltrate tissues. P-gp overexpression in malignant cells reduces the efficacy of chemotherapeutic agents by actively expelling them, decreasing intracellular drug concentrations, and promoting multidrug resistance, a significant obstacle to successful treatment. This review examines recent advances in combating P-gp-mediated resistance, including the development of novel P-gp inhibitors, innovative drug delivery systems (e.g., nanoparticle-based delivery), and strategies to modulate P-gp expression or activity. These modulation strategies encompass targeting relevant signaling pathways (e.g., NF-κB, PI3K/Akt) and exploring drug repurposing. While progress has been made, overcoming P-gp-mediated resistance remains crucial for improving patient outcomes. Future research directions should prioritize the development of potent, selective, and safe P-gp inhibitors with minimal off-target effects, alongside exploring synergistic combination therapies with existing chemotherapeutics or novel agents to effectively circumvent multidrug resistance in hematological malignancies.

The growing global demand for phytochemicals as bioactive sources is prompting scientists to develop methods that link their sensory properties to their mechanisms of action in cancer treatment. Recent techniques for tracking the actions of small plant metabolites (SPMs) from single-cell plant sources to their molecular anticancer biomarkers could provide valuable insights in this field. Among the critical methods discussed in this review are the real-time tracking of cell components through stable isotope probing (Sis) and microspectroscopy, which has attracted the attention of biotechnologists. Additionally, the precise pathways required for studying new insights into functional materials are discussed, based on high-resolution and accurate technologies, which could aid their functional categorization. Notably, the molecules under study have recently garnered attention for their anticancer applications due to advancements in effective evaluation techniques that surpass traditional methods. In December 2020, the Food and Drug Administration (FDA) authorized 89 SPMs as safe anticancer natural molecules. In conclusion, by combining spatiotemporal techniques and SPMs' mechanisms, they could facilitate the development of more exceptional, bio-efficient materials.

Monoclonal antibodies targeting specific cell surface antigens have emerged as a promising therapeutic approach for acute myeloid leukemia (AML), thus widening the treatment landscape of this heinous disease. These antibodies have been designed to selectively target and eliminate leukemic cells while limiting damage to the normal hematopoietic counterpart. Among the potential targets on AML cells, CD33, CD123, and CD47 have shown the major potential in preclinical and clinical trials. Additionally, conjugation of monoclonal antibodies with cytotoxic agents has further enhanced their therapeutic efficacy. Nonetheless, challenges such as antigen heterogeneity, resistance mechanisms, and the immunosuppressive tumor microenvironment remain significant barriers to achieving durable remission in AML patients. This review explores the mechanisms of action, current clinical developments, and ongoing trials into the role of monoclonal antibodies in AML, highlighting their potential to improve clinical outcomes when used alone or in combination with conventional therapies, making them thus able to become, in the near future, a cornerstone in the treatment of AML.

Lung cancer is among the most common malignancies globally, is frequently associated with a poor prognosis, and is the second leading cause of cancer-related mortality in both genders. Resistance to treatment, heterogeneity, and invasiveness make lung cancer one of the most challenging tumors to combat. Drug repurposing is considered an advantageous strategy for expediting and economizing drug discovery, as it involves rebranding an existing drug for a new therapeutic use. Since depression is a prevalent psychiatric illness among individuals diagnosed with lung cancer, various selective serotonin reuptake inhibitors (SSRIs) used for the treatment of depression were examined for their possible use in lung cancer treatment as repurposed drugs. Herein, we evaluated the efficacy of SSRIs, both alone and in combination with various anticancer agents, in the treatment of lung cancer along with their mechanisms of action. The innovative approach of repurposing SSRIs offers hope by simplifying the drug discovery process and potentially revealing new therapeutic options for lung cancer. Exploring SSRIs' effects on lung cancer treatment may unlock unexpected avenues for combating this aggressive disease.

Graphene-based materials (GBMs) have shown significant promise in cancer therapy due to their unique physicochemical properties, biocompatibility, and ease of functionalization. Their ability to target solid tumors, penetrate the tumor microenvironment (TME), and act as efficient drug delivery platforms highlights their potential in nanomedicine. However, the complex and dynamic nature of the TME, characterized by metabolic heterogeneity, immune suppression, and drug resistance, poses significant challenges to effective cancer treatment. GBMs offer innovative solutions by enhancing tumor targeting, facilitating deep tissue penetration, and modulating metabolic pathways that contribute to tumor progression and immune evasion. Their functionalization with targeting ligands and biocompatible polymers improves their biosafety and specificity, while their ability to modulate immune cell interactions within the TME presents new opportunities for immunotherapy. Given the role of metabolic reprogramming in tumor survival and resistance, GBMs could be further exploited in metabolism-targeted therapies by disrupting glycolysis, mitochondrial respiration, and lipid metabolism to counteract the immunosuppressive effects of the TME. This review focuses on discussing research studies that design GBM nanocomposites with enhanced biodegradability, minimized toxicity, and improved efficacy in delivering therapeutic agents with the intention to reprogram the TME for effective anticancer therapy. Additionally, exploring the potential of GBM nanocomposites in combination with immunotherapies and metabolism-targeted treatments could lead to more effective and personalized cancer therapies. By addressing these challenges, GBMs could play a pivotal role in overcoming current limitations in cancer treatment and advancing precision oncology.

Lung cancer, a malignant neoplasm that is globally prevalent and characterized by high incidence and mortality rates, has seen the rise of immune checkpoint inhibitors (ICIs) as a crucial systemic treatment. However, a subset of patients exhibits suboptimal responses to ICIs. Recently, studies revealed the role of vitamin D in inflammation modulation, cell differentiation, and cancer prevention. Vitamin D precisely modulates immune responses and inflammatory states within the tumor microenvironment (TME) by targeting both innate and adaptive immunity. These effects may reduce immune tolerance to ICIs and synergistically enhance their therapeutic efficacy. Here, we review vitamin D metabolism in lung cancer patients, as well as its anti-tumor mechanisms, immune regulation, and the significant promise of vitamin D in lung cancer immunotherapy and adjuvant therapeutic strategies. Further research is imperative to surmount these challenges and fully realize vitamin D's potential in improving lung cancer immunotherapy outcomes.

Multiple myeloma (MM) remains an incurable hematologic malignancy due to the inevitable development of drug resistance, particularly in relapsed or refractory cases. Post-translational modifications (PTMs), including phosphorylation, ubiquitination, acetylation, and glycosylation, play pivotal roles in regulating protein function, stability, and interactions, thereby influencing MM pathogenesis and therapeutic resistance. This review comprehensively explores the mechanisms by which dysregulated PTMs contribute to drug resistance in MM, focusing on their impact on key signaling pathways, metabolic reprogramming, and the tumor microenvironment. We highlight how PTMs modulate drug uptake, alter drug targets, and regulate cell survival signals, ultimately promoting resistance to PIs, IMiDs, and other therapeutic agents. Furthermore, we discuss emerging therapeutic strategies targeting PTM-related pathways, which offer promising avenues for overcoming resistance to treatment. By integrating preclinical and clinical insights, this review underscores the potential of PTM-targeted therapies to enhance treatment efficacy and improve patient outcomes in MM.

Chemotherapy resistance represents a formidable obstacle in oncological therapeutics, substantially compromising the efficacy of adjuvant chemotherapy regimens and contributing to unfavorable clinical prognoses. Emerging evidence has elucidated the pivotal involvement of exosomes in the dissemination of chemoresistance phenotypes among tumor cells and within the tumor microenvironment. This review delineates two distinct intra-tumoral resistance mechanisms orchestrated by exosomes: (1) the exosome-mediated sequestration of chemotherapeutic agents coupled with enhanced drug efflux in neoplastic cells, and (2) the horizontal transfer of chemoresistance to drug-sensitive cells through the delivery of bioactive molecular cargo, thereby facilitating the propagation of resistance phenotypes across the tumor population. Furthermore, the review covers current in vivo experimental data focusing on targeted interventions against specific genetic elements and exosomal secretion pathways, demonstrating their potential in mitigating chemotherapy resistance. Additionally, the therapeutic potential of inhibiting exosome-mediated transporter transfer strategy is particularly examined as a promising strategy to overcome tumor resistance mechanisms.