Solute carrier family 2 member 3 (SLC2A3), a key glucose transporter, has been implicated in tumor metabolism and immune regulation, but its specific role in kidney renal clear cell carcinoma (KIRC) remains largely unclear.

By stabilizing actin filaments and recruiting non-muscle myosin II, the closely related tropomyosin (Tpm) isoforms Tpm3.1 and Tpm3.2 support actin-dependent processes including membrane dynamics, cell migration, and cytokinesis. Actin dynamics are essential for B cell function, but the roles of Tpm3.1 and 3.2 (collectively termed Tpm3.1/3.2) in B cells have not been explored. Moreover, new treatments are needed to limit the growth and dissemination of diffuse large B-cell lymphoma (DLBCL), the most prevalent B-cell malignancy.

Small cell lung cancer (SCLC) is challenging to manage due to its high malignancy and early metastatic spread. Although initial chemoradiotherapy responses are common, resistance rapidly develops, and long-term efficacy remains limited. Immune checkpoint inhibitors (ICIs) overcome previous survival barriers, extending overall survival (OS) and progression-free survival (PFS) in extensive-stage SCLC. Nevertheless, absolute clinical benefits remain modest. To address efficacy limitations, current research focuses on optimizing first-line strategies by exploring multimodal regimens (e.g., adding targeted therapy or radiotherapy to chemoimmunotherapy) and advancing molecular subtyping for precision oncology. Furthermore, emerging therapies such as DLL3-targeted agents, bispecific antibodies (bsAbs), antibody-drug conjugates (ADCs), and chimeric antigen receptor T-cell (CAR-T) therapy continue to demonstrate clinical progress. This review synthesizes advances in SCLC management, focusing on mechanisms and clinical applications of multimodal strategies and novel therapies. It provides guidance for clinical decisions, research directions, and survival improvement.

Conventional open thyroidectomy (COT) results in visible neck scarring. Transaxillary endoscopic thyroidectomy (TET) comprises gasless (suspension-assisted) and gas-inflated approaches, both of which offer superior scar concealment. This study aimed to compare the efficacy and safety of these two endoscopic techniques for treating papillary thyroid carcinoma (PTC).

This study investigates the relationship between the systemic immune-inflammation index (SII) and all-cause mortality (ACM) risk in individuals with stages IIIB-IV epidermal growth factor receptor (EGFR)-mutated lung adenocarcinoma.

Bone metastases (BM) are a frequent and clinically relevant manifestation in patients with metastatic pheochromocytomas and paragangliomas (mPPGL).

The prognosis for patients with hepatocellular carcinoma (HCC) remains suboptimal, despite the rapid advancement of anti-cancer immunotherapy. Chimeric antigen receptor (CAR) T cell therapy targeting glypican-3 (GPC3) has been developed for HCC; however, clinical trials have demonstrated heterogeneous responses among patients and limited CAR-T cell infiltration. Locoregional administration has emerged as a promising strategy for CAR-T therapy against solid tumours, yet its potential for HCC treatment has not been thoroughly explored.

Follicular dendritic cell sarcoma (FDCS) is an uncommon malignant neoplasm that arises from follicular dendritic cells (FDCs). The mediastinum is a more unusual site of FDCS. In this document, we detail a case involving the complete surgical removal of FDCS located in the mediastinum. A 28-year-old woman presented with symptoms of right chest pain. Accompanying symptoms include chest tightness, shortness of breath, and faintness. Chest computed tomography was performed and revealed abnormal enhancement in the mediastinal region. An excisional biopsy was carried out, and through the aid of immunohistochemistry (IHC), a diagnosis of FDCS was confirmed. Following surgery, the patient underwent radiotherapy for 27 sessions. The patient was followed up by the oncology service for 6 years and was still alive at the time of drafting this report. This exceedingly uncommon case underscores the challenges in making a differential diagnosis and emphasizes the significance of diagnostic indicators, including histopathology and IHC, in establishing a diagnosis. Clinicians should be alert to the possibility of encountering this disease and take into consideration various characteristics to avoid misdiagnosis.

Non Hodgkin's Lymphoma (NHL) consists of heterogeneous group of malignant lymphoid neoplasms that are closely related, but present a gamut of morphological, genetic and clinical features. In India, age adjusted incidence rate for NHL was found out to be 2.9/100000 in men and 1.5/100000 in women.

Despite guideline-directed therapies, most patients with advanced oesophageal squamous cell carcinoma (ESCC) derive limited benefit and are unable to tolerate iterative treatment modifications. Therefore, timely identification of resistant cases and the provision of alternative therapeutic options are urgently needed.

Cell death is a fundamental process essential to all living organisms, with apoptosis serving as one of the most crucial pathways across various stages of life. Dysregulation of apoptosis is closely associated with numerous diseases, particularly cancer. PUMA (p53 upregulated modulator of apoptosis) is a key mediator of apoptotic cell death. It is activated in response to a wide range of internal and external signals. Beyond its established role in apoptosis, PUMA also regulates other forms of cell death, including necroptosis, autophagy, and ferroptosis, underscoring its critical role in cancer cell death, especially during chemotherapy. However, PUMA activation is frequently impaired in many cancers, leading to resistance to cell death and treatment failure. This review highlights recent advancements in understanding the regulation of PUMA expression at multiple levels, including epigenetic, transcriptional, post-transcriptional, and post-translational mechanisms. It also examines the influence of diverse cellular regulators, such as epigenetic modifiers, transcription factors, non-coding RNAs, kinases, and ubiquitin ligases in modulating PUMA activity. Additionally, we discuss PUMA's role in cancer progression, its impact on the effectiveness of anti-cancer therapies, and its potential as a prognostic biomarker for therapeutic resistance. Finally, we propose critical questions to inspire future research, aiming to deepen the understanding of PUMA regulation and its significance in cancer therapy.

Despite decades of therapeutic development, osteosarcoma survival remains poor. Although berberine (BBR) shows anti-tumor activity, its efficacy is limited. We addressed this through structural modification and machine learning-guided discovery, developing a novel derivative: 9-O-methoxyethylberberrubine bromide (B1).

Mitochondrial unfolded protein response (UPRmt) is implicated in lung adenocarcinoma (LUAD), and our study accordingly aims to establish a model incorporating UPRmt-related genes (MRGs) for predicting the therapeutic response and prognosis in LUAD.

Although antibody-conjugated drugs have achieved success in clinical practice for cancer treatment, challenges remain in developing a highly efficient drug delivery system with specific accumulation in tumors and reduction in side effects. With improved pharmacokinetics, strong covalent bonding and quick binding reactions, a pre-targeting approach via molecular pairs represents an attractive platform for two-step delivery system construction.

The complex invasiveness and heterogeneity of glioblastoma multiforme (GBM) hinder the complete eradication of the tumor. The invasion of the basement membrane (BM) occurs before the spread to the meninges and the metastasis of glioma cells, increasing the recurrence rate of the disease, leading to poor patient prognosis.

Immune checkpoint inhibitors targeting PD-1 show limited efficacy in non-small cell lung cancer (NSCLC) due to primary resistance. KIF20A, a cell cycle regulator implicated in chemotherapy resistance, may influence tumor immunity, but its role in anti-PD-1 resistance remains unclear.

Crotonoside (CTS) is a primary bioactive component found in Croton. current research has mainly focused on leukemia, with few reports in other cancers. Considering the traditional use of Croton, this study aims to evaluate the anti-colorectal cancer (CRC) activity of CTS and reveal its potential mechanisms. First, results in vitro show that CTS can markedly suppress CRC cell proliferation, invasion and migration, and EMT pathway (P < 0.01). Then, RNA-seq analysis was employed to identify the core target and potential mechanism of CTS against CRC, and the results suggested KIF20A is a core target. Bioinformatic analysis showed that KIF20A is overexpressed in CRC and associated with a worse prognosis (P < 0.01). KEGG and GO enrichment analyses indicated that anti-CRC activity of CTS is linked to the cell cycle. Next, Results confirmed that CTS can promote the expression of CDK1 and Cyclin B1 (P < 0.01), and induces G2/M phase arrest to exert anti-CRC effects (P < 0.01). Then, a subcutaneous tumor model was established in vivo to evaluate the anti-CRC activity of CTS; the results showed that CTS significantly inhibited CRC tumor growth and reduced both tumor weight and volume (P < 0.01). CTS can suppress the expression of Ki67, E-cadherin, vimentin, and KIF20A (P < 0.05), and promote the expression of Cyclin B1 and CDK1 (P < 0.01). In addition, molecular docking analysis revealed that the binding energy of CTS to KIF20A was - 7.9 kcal/mol, and CETSA assay showed that CTS treatment attenuated the thermal degradation of KIF20A protein. These results showed CTS can bind KIF20A tightly. Finally, overexpression of KIF20A reverses the anti-CRC effect of CTS. In summary, this study confirms that CTS can target and inhibit KIF20A, thereby inducing cell G2/M phase arrest and exerting anti-CRC effects.

Chrysin belongs to natural flavonoids characterized wide spectrum of biological activity. Its use in treatment is limited by low bioavailability and rapid metabolism. The structure-activity relationship shows that introduction of substituent at C7 position of flavone scaffold increase the activity and bioavailability. In this study, a series of quinoline-chrysin hybrids was obtained. The structure of compounds was determined using spectroscopic methods. The anticancer activity of compounds was tested against neck and head squamous cell carcinoma lines (HNSCC), while the antioxidant activity was determined using DPPH method. The biological effect depends on the type of quinoline moiety. For the most active compounds, IC50 values as low as ~ 13.8 µM for anticancer activity and ~ 24.5 µM for antioxidant activity were observed. For the most active compounds, their effect on the expression levels of TP53, BAX, and BCL2 genes was examined.

Colorectal cancer (CRC) is a serious threat to human health, with an approximate 14% mutation rate in the ataxia telangiectasia-mutated (ATM) gene, which is involved in homologous recombination repair. BMN673 (talazoparib), a next-generation poly(ADP-ribose) polymerase (PARP) inhibitor, is the most potent PARP inhibitor (PARPi) reported to date, demonstrating robust anticancer activity. However, the precise mechanism underlying its action in ATM-deficient CRC remains unknown. This study demonstrated that BMN673 stimulated ATM-deficient CRC cell death via a synthetic lethal effect. RNA sequencing analysis revealed significant enrichment of the PERK-ATF4 pathway, mitophagy, and ferroptosis. Functional assays confirmed that BMN673 induced a multifaceted cell death program comprising autophagy-associated death, ferroptosis, and mitophagy, in addition to synthetic lethal. Mechanistically, BMN673 was shown to enhance activating transcription factor 4 (ATF4) transcriptional activity by suppressing poly-ADP-ribosylation (PARylation), facilitating ATF4 binding to the growth differentiation factor 15 (GDF15) promoter region and thereby inducing GDF15 transcriptional expression. Notably, GDF15 overexpression modulated the sensitivity of ATM-deficient CRC cells to BMN673 by promoting autophagy-associated cell death, ferroptosis, and mitophagy, contributing to the anticancer effect of BMN673. Additionally, combining BMN673 with radiotherapy exerted a synergistic anticancer effect on ATM-deficient CRC cells, which was prevented by autophagy inhibition. The findings identified the ATF4-GDF15 pathway as a crucial mediator of BMN673 sensitivity in ATM-deficient CRC cells, revealing therapeutic vulnerability beyond canonical DNA damage repair pathways and providing new insight for combination therapy strategies.

The Kv11.1 potassium channels and the transcription factor c-Myc both play fundamental roles in controlling cellular homeostasis. Cancers take advantage of dysregulated c-Myc and Kv11.1, however, little is known about the possible link between these proteins. In this work we found that an inverse relationship between c-MYC and Kv11.1 exists in some lung adenocarcinoma. Importantly, patients expressing an elevated level of the Kv11.1 channel present a better overall survival when compared with patients with low expression. Therefore, we evaluated the hypothesis that pharmacologic activation of the Kv11.1 channel in lung cancer may impair tumor growth. We discovered that Kv11.1 activation inhibits lung cancer growth by inducing a senescent phenotype. Moreover, we found that pharmaceutical Kv11.1 opening produced a rapid proteasomal degradation of c-Myc and that this could be antagonized by the OTUD6B deubiquitinase. We concluded that use of Kv11.1 agonists should be considered as anticancer pharmacological strategy against lung adenocarcinomas.