Artemisinin, found in the traditional Chinese medicine (TCM) Artemisia annua, has demonstrated remarkable efficacy in therapeutics and holds significant potential as a pharmaceutical drug in cancer. Until now, there have been no systematic scientometrics studies to analyze the research trend of artemisinin and its derivatives in cancer.

Small cell lung cancer (SCLC) is a highly aggressive disease associated with poor patient survival rates. The addition of an anti-programmed death ligand 1 antibody to platinum combination chemotherapy can improve its prognosis. However, only a few patients achieve a long-term response; thus, establishing new therapies for SCLC is crucial. Midkine (MDK) is a heparin-binding growth factor involved in various biological processes, including cell proliferation and chemotherapeutic resistance, in diverse cancers. MDK has garnered attention as a therapeutic and diagnostic target for several cancers; however, only a few studies have evaluated its expression and function in SCLC. This study aimed to evaluate the MDK expression in human SCLC tissue and human SCLC cell lines, and to clarify its function in tumorigenesis.

Immune checkpoint inhibitors (ICIs) are monoclonal antibodies that block inhibitory pathways that cancer cells exploit to suppress T-cell activation. Although immune-related adverse events (irAEs) linked to ICI therapy are well documented and encompass dermatologic, endocrine, gastrointestinal, hepatic, and neurologic systems, ICI-related dysautonomia remains a rare phenomenon. Management of ICI-related dysautonomia is undefined.

While cancer-associated fibroblasts (CAFs) significantly influence tumor progression, their temporal dynamics remain poorly understood. We investigated time-dependent interactions between non-small cell lung cancer (NSCLC) cells and CAFs, and evaluated rosmarinic acid (RA)'s potential to modulate these interactions. HCC827 lung adenocarcinoma cells and MRC-5 fibroblasts were co-cultured in vitro. CAF activation markers (α-SMA, FAP) and epithelial-mesenchymal transition (EMT) were assessed through morphological and molecular analyses. Xenograft models with different tumor-to-fibroblast ratios (1:1, 1:2) evaluated tumor growth dynamics and RA's therapeutic effects combined with gefitinib. Time-course analysis revealed a biphasic pattern in tumor-CAF interactions. CAF activation markers reached peak levels by day 6, followed by maximal EMT marker expression in NSCLC cells at day 8. In xenograft models, higher CAF proportions initially inhibited tumor growth but accelerated tumor progression. RA treatment significantly attenuated CAF activation markers and reversed EMT-related changes in cancer cells, leading to reduced tumor growth in CAF-enriched xenografts. The combination of RA with gefitinib demonstrated enhanced anti-tumor effects compared to gefitinib alone. CAFs exhibit temporally biphasic roles in NSCLC progression characterized by initial suppression followed by promotion of tumor microenvironment deterioration. RA effectively modulates these tumor-stromal interactions, enhances gefitinib efficacy, and delays the development of drug resistance.

Triple-negative breast cancer (TNBC) is an aggressive subtype with poor prognosis, as chemotherapy resistance leads to relapse in many patients. Carboplatin addition improves treatment response, but challenges persist.

It has been suggested that patient awareness of chemotherapy-induced side effects is not uniform and may vary according to communication quality between healthcare providers and patients, educational initiatives, and the type of cancer and chemotherapy regimen. This study aimed to assess real-world chemotherapy-induced adverse effects as reported by cancer patients in the West Bank of Palestine and to identify key predictors of these side effects.

Triple negative breast cancer (TNBC), a highly invasive breast cancer, is one of the leading causes of cancer-related mortality worldwide. Although chemotherapy remains the standard of care for TNBC, the development of chemotherapy resistance significantly limits its clinical efficacy. In this study, we identified the deubiquitinating enzyme USP44 as a contributor to chemoresistance in TNBC and investigated the potential regulatory feedback mechanisms involved. In this experimental study, we investigated the sensitivity of TNBC cells MDA-MB-231 and BT-549 to chemotherapy drugs after overexpression and knockdown of USP44 using CCK-8 reagent kit and flow cytometry analysis, respectively. Western blot was performed to evaluate the expression levels of relevant proteins. In vivo xenograft models were established to examine the effects of USP44 and its downstream targets on chemosensitivity. Co-immunoprecipitation assay and ubiquitination assay were conducted to identify interacting proteins and elucidate the underlying molecular mechanisms. Knockdown of USP44 increased the sensitivity of MDA-MB-231 and BT-549 cells to chemotherapeutic agents, accompanied by elevated levels of Cleaved PARP. In contrast, USP44 overexpression reduced drug sensitivity. Mechanistically, USP44 was found to interact with EZH2, preventing its ubiquitination and subsequent proteasomal degradation. Notably, treatment with GSK126, a specific EZH2 inhibitor, reversed the chemoresistance induced by USP44 overexpression. USP44/EZH2 signaling pathway is one of the key to causing the drug resistance of TNBC, warranting further clinical investigation.

Recent advances in molecular genetic research, driven by the development of genomic analysis technologies, have significantly improved treatment outcomes for leukemia. In recent years, mounting evidence indicates that germline genetic background influences drug sensitivity and the risk of adverse effects, underscoring the growing importance of personalized treatment strategies. In particular, the NUDT15 polymorphism, which determines sensitivity to 6-mercaptopurine, has garnered significant attention. Notably, a low-activity variant of this polymorphism, prevalent in Asian countries, has been shown to substantially increase the risk of bone marrow suppression and other adverse effects. Pre-treatment analysis of the NUDT15 polymorphism has demonstrated utility in dose adjustment, helping to mitigate the risk of treatment-related toxicities. Studies have also explored the relationship between genetic background and late complications of leukemia treatment. Optimization of therapeutic strategies based on pharmacogenetic insights holds promise for minimizing complications while maximizing treatment efficacy for each individual patient.

Colorectal cancer (CRC) is a malignant tumor of the digestive system with high incidence rate and mortality. Tanshinone IIA (Tan IIA) plays an anti-cancer role in a variety of cancer cells. Here, we aimed to elucidate the therapeutic effects and potential mechanism of Tan IIA in CRC.

Small cell lung cancer (SCLC) accounts for approximately 15% of all lung cancer cases and is characterized by high malignancy, rapid progression, and poor prognosis. Here, we report a case of a 58-year-old female patient who was initially diagnosed with extensive-stage SCLC (ES-SCLC) with liver metastasis. The patient underwent etoposide and cisplatin (EP) chemotherapy combined with local radiotherapy and achieved a complete response. The progression-free survival reached 48 months, and upon relapse, the patient received EP chemotherapy combined with the programmed cell death protein 1 (PD-1) inhibitor, tislelizumab, as immunotherapy. During the treatment period, the patient experienced immune-related pancreatitis, but the symptoms were relieved with timely intervention and treatment. As of January 2, 2024, the patient's overall survival exceeded 95 months. This case highlights the potential efficacy of the combination of chemotherapy and immunotherapy in recurrent ES-SCLC patients and underscores the importance of close monitoring and management of immune-related adverse reactions. The study provides valuable insights into the application of personalized treatment in lung cancer management and offers new possibilities for extending patient survival.

Resistance to poly(ADP‒ribose) polymerase inhibitors (PARPis) remains a significant challenge in ovarian cancer (OC) treatment. TTK protein kinase (TTK) has been implicated in cisplatin resistance in OC, but its role in PARPi resistance remains unclear. In this research, we found that TTK inhibition overcome olaparib resistance in HR-proficient OC cells, whereas TTK promotes olaparib resistance in HR-deficient OC cells. Mechanistically, TTK directly interacts with RPA2, facilitating phosphorylation of its S33 residue to activate the ATR signaling pathway. Knocking down RPA2 increased olaparib sensitivity in OC cells. Additionally, TTK-mediated resistance to olaparib through the RPA2/ATR signaling pathway was confirmed via both in vitro and in vivo models. In conclusion, TTK inhibition overcomes olaparib resistance in HR-proficient OC cells, in part by suppressing RPA2-S33 phosphorylation and attenuating ATR signaling. TTK inhibitors offer a promising strategy to increase the therapeutic efficacy of PARPis in OC patients.

Gastrointestinal cancer (GIC) ranks among the most fatal malignancies globally and is characterized by a significant propensity for metastasis. While surgical intervention can effectively cure GIC in its early stages, a substantial number of cases are diagnosed at advanced stages, where the response to current therapeutic options is markedly diminished. Increasing evidence highlights the pivotal role of circadian rhythm, an intrinsic 24-hour cyclical system regulating biological activities to adapt to the alternations of day and night in the progression, metastasis, and development of chemoresistance in GIC. Recent studies have disclosed that the modulation of key circadian rhythm genes (such as BMAL1 and PER1) can suppress tumor advancement through multiple pathways. This review compiles the most recent research concerning the circadian rhythm and its influence on GIC progression. It elucidates the role of circadian genes in the initiation, metastasis, metabolism, inflammatory response, and therapeutic resistance in GIC, including both chemotherapy and targeted therapies. Furthermore, the review discusses the current implementation and future outlook of therapeutic strategies based on circadian modulation in the treatment of GIC.

To overcome the clinical limitations of melittin, a potent anticancer host defense peptide, by developing a multifunctional, virus-like particle (VLP)-based delivery system that enhances tumor targeting, immune activation, and therapeutic safety.

Non-melanoma skin cancers (NMSC) are the most common malignancies worldwide. While early-stage lesions can be definitively treated with local therapies, advanced stage cutaneous squamous cell carcinoma (cSCC) often requires systemic treatments such as PD-1 inhibitors. These treatments may be administered for prolonged durations; this practice may lead to an unnecessary physical and financial toxicity. The purpose of this study was to evaluate the patterns of disease progression after anti-PD-1 therapy discontinuation in this group of patients.

This study aimed to assess the cost-effectiveness of capecitabine versus active monitoring in stable or responding metastatic colorectal cancer (mCRC) after 16 weeks of first-line therapy.

Antiangiogenic tyrosine kinase inhibitors (TKIs) are associated with elevated hemoglobin [Hb] levels, potentially influencing prognosis in advanced hepatocellular carcinoma (HCC) patients. However, the impact of altitude on Hb dynamics and its prognostic significance remains underexplored. This study aimed to assess altitude-related Hb changes and their relationship with treatment outcomes in patients following TKI treatment.

Stratifin/14-3-3σ (SFN) is a new diagnostic biomarker of interstitial lung disease (ILD) with a diffuse alveolar damage (DAD) pattern as well as a predictor of resistance to anticancer therapy. Despite the potential clinical benefit of SFN, its impact on therapeutic efficacy of immune checkpoint inhibitors (ICIs) and ICI-induced interstitial lung disease (ICI-ILD) in patients with non-small cell lung cancer (NSCLC) receiving cancer immunotherapy is unknown.

Lung cancer is the second most common cancer worldwide, with persistently high morbidity and mortality rates. Despite years of research in the field, a complete cure for this disease remains elusive. Current clinical treatment options primarily include chemotherapy, surgery, and targeted drugs. However, these treatments are often limited by the highly metastatic nature of lung tumors and the development of drug resistance, resulting in suboptimal therapeutic outcomes. Ferroptosis is an iron-dependent cell death mechanism driven by lipid peroxidation, offers promising potential to overcome drug resistance in lung cancer. Recent advances in nanotechnology have enabled targeted delivery and precise regulation of ferroptosis pathways, addressing the limitations of conventional therapies. This review systematically summarizes current strategies utilizing nanomedicine to induce ferroptosis in lung cancer, with a focus on key molecular targets, such as GPX4, System Xc-, and FSP1, as well as innovative delivery platforms including metal nanoparticles, nanozymes, and responsive liposomes. Unique challenges in pulmonary drug delivery, such as mucociliary clearance and oxidative microenvironments are also discussed, along with lung cancer-specific solutions like inhalable systems and tumor microenvironment remodeling. Furthermore, we compare ferroptosis nanotherapies across different cancers to highlight the distinctive innovations in lung cancer. This article provides a comprehensive overview of recent progress and proposes optimized strategies to enhance therapeutic efficacy, offering insights into the translational potential of ferroptosis-based nanomedicine in lung cancer treatment.

Patients with gastrointestinal tract cancer reported suboptimal adherence to oral anticancer agents (OAAs), reducing the therapeutic benefit. According to the Common-Sense Model of Self-Regulation, patients' medication perceptions decide adherence. However, how perceptions of OAAs influence adherence remains unknown among this population. This study explored this relationship.

The introduction of genetic tests based on next-generation sequencing techniques into veterinary cancer diagnostics provides information on molecularly targeted therapies useful for dogs. However, there is still a lack of in vitro studies describing the effect and mechanism of action of such anti-cancer drugs in companion animals. Our study aimed to demonstrate in vitro activity of a commonly used PARP inhibitor, olaparib, in canine lymphoma and leukemia cells as well as to indicate its potential uses in anti-cancer therapy based on the mutational status of DNA damage related genes. Canine lymphoma and leukemia cell lines were incubated with olaparib alone and in combination with doxorubicin, and the impact of a single drug and combinations on cell viability, proliferation, induction of apoptosis, and DNA damage were assessed.