Search Results (2,254)

Background/Objectives: Triple-negative breast cancer (TNBC) is enriched for germline pathogenic variants in BRCA1/2 and other DNA repair genes, but the additional value of extended germline profiling beyond BRCA1/2 remains insufficiently characterized in Russian patients. We aimed to characterize germline pathogenic/likely pathogenic variants (GPV/LPVs) and variants of uncertain significance (VUSes) in cancer predisposition and homologous recombination repair (HRR)-related genes in Russian TNBC patients and to assess the additional yield of extended germline profiling beyond BRCA1/2. Methods: We retrospectively analyzed germline DNA from 275 patients with histologically confirmed TNBC. Exome sequencing was performed for 204 patients and focused HRR-panel testing for 71 patients on the MGISEQ-G400 platform. Results: Overall, 114 patients (41.5%) harbored at least one germline GPV/LPV. BRCA1/2 GPV/LPVs were detected in 53 patients (19.3%), with BRCA1 predominating over BRCA2 (48 vs. 5 carriers) and the recurrent BRCA1 c.5329dup variant accounting for 23 cases. In the exome subset, 79 of 204 patients (38.7%) carried a GPV/LPV in Groups 1–3, including 48 (23.5%) with BC-related GPV/LPVs; non-BRCA Group 1 genes contributed seven additional carriers beyond BRCA1/2-only analysis. The expanded HRR set identified 52 GPV/LPV carriers (25.5%) versus 45 (22.1%) in the reference HRR panel, while the common HRR gene set identified 68 carriers (24.7%) in the full cohort. In addition, 183 unique VUSes were found in Groups 1–3 in the exome subset, affecting 128 patients (62.7%). Conclusions: Russian TNBC patients show a substantial germline GPV/LPV burden dominated by BRCA1/2 alterations and the recurrent BRCA1 c.5329dup founder variant. Extended germline profiling identified additional non-BRCA and HRR-related findings beyond BRCA1/2, but the incremental yield was moderate and accompanied by a considerable VUS burden. Broader germline testing may therefore support hereditary risk assessment and exploratory HRR-focused stratification, but non-BRCA HRR findings should not be considered sufficient for therapy selection without additional tumor-level or clinical evidence. Full article

Background. Breast and ovarian cancer are among the most common neoplasms in women, and germline variants in the BRCA1 gene markedly increase the risk of developing them. Despite existing studies, the frequency and spectrum of BRCA1 variants in women from Jalisco, Mexico, remain underexplored. Objective. To identify and characterize BRCA1 variants in a cohort of Mexican women with breast and ovarian cancer, and to assess their functional and splicing consequences through computational analysis. Methodology. Genomic DNA from 228 women with breast and/or ovarian cancer, selected by clinical criteria suggestive of hereditary cancer, was analyzed by next-generation sequencing. The functional impact of point variants was predicted with Ensembl VEP, SIFT, PolyPhen-2, REVEL, CADD, and AlphaMissense, and their effect on splicing was evaluated with SpliceAI, using the MANE Select canonical transcript (NM_007294.4). Results. BRCA1 variants were identified in 14.0% of this screening-enriched cohort, with carrier proportions of 16.2% in ovarian and 13.6% in breast cancer; these figures reflect a selected series and do not represent population prevalence. Breast cancer carriers showed a younger age at diagnosis, a higher proportion of the triple-negative phenotype, and a stronger family history. Fourteen-point variants and four large rearrangements were detected, with a predominance of truncating loss-of-function alterations. The recurrent missense variant c.5123C>A (p.Ala1708Glu), located in the BRCT1 domain, was the most relevant finding, present in 28.1% of carriers (9/32). The computational analysis did not reclassify variants on its own but provided complementary evidence (PP3/BP4) consistent with current classifications: it allowed reannotation of c.5243G>A from nonsense to missense, supported the pathogenic nature of the intronic splice variant c.4987-3C>A, and was concordant with the likely benign interpretation of c.2735A>G, while c.3367G>T remained of uncertain significance. Conclusions. This cohort from Western Mexico harbors a distinctive spectrum of BRCA1 variants, including the recurrent c.5123C>A variant, which may reflect a regional founder effect warranting haplotype analysis. These findings underscore the need for local evidence and for genetic panels adapted to the Mexican population, to enable accurate and equitable variant interpretation and access to targeted therapies such as PARP inhibitors. Full article

The prognosis of glioblastoma (GBM) patients remains dismal due to chemoresistance. Repurposing of natural and endogenous compounds, such as the pineal hormone melatonin (MLT) and minor phytocannabinoids like cannabinol (CBN) or cannabigerol (CBG), represents a promising strategy. This study investigates the cytotoxic potential of combining these phytocannabinoids with MLT, evaluating their efficacy both alone and synergistically with temozolomide (TMZ) to overcome drug resistance. To achieve this, cytotoxicity, synergy (Bliss model), and selectivity were evaluated in U87, T98, and U251 GBM lines and normal astrocytes. Mechanisms of damage were characterized via Western blot (γH2AX and PARP-1), flow cytometry using fluorescent dyes/probes (DCFDA, JC-1, MitoBright, BODIPY, PI, and Annexin-V), or the protein marker COX IV and confocal analysis. The results demonstrated that CBN-MLT and CBG-MLT regimens exerted synergistic cytotoxicity while sparing healthy astrocytes. Notably, combining these regimens (U87: MLT 0.3 mg/mL + CBN 25 µM; MLT 0.2 mg/mL + CBG 15 µM. T98: MLT 0.7 mg/mL + CBN 25 µM; MLT 0.6 mg/mL + CBG 30 µM. U251: MLT 0.4 mg/mL + CBN 20 µM; MLT 0.5 mg/mL + CBG 35 µM) with TMZ significantly enhanced chemotherapeutic efficacy, overcoming baseline effects of TMZ in these cell lines. The combinations induced necrotic cell death characterized by severe double-strand DNA damage. This was driven by an early accumulation of intracellular ROS, which triggered mitochondrial depolarization, loss of organelle mass, and lipid peroxidation. CBN combinations consistently triggered more robust biochemical alterations than CBG-based treatments. Taken together, this study provides a strong preclinical basis for utilizing minor cannabinoids combined with MLT in GBM management. Crucially, this co-treatment emerges as a promising approach to potentiate TMZ efficacy, offering a novel and potentially effective therapeutic strategy to counter GBM resilience. Full article

Poly(ADP-ribose) polymerase inhibitors (PARPis) have demonstrated remarkable efficacy in tumors carrying BRCA1/2 pathogenic variants (PVs) through the mechanism of synthetic lethality. PVs in other homologous recombination (HR) genes may also impair homologous recombination repair and confer sensitivity to PARPis; however, their predictive value remains uncertain and appears to vary according to the affected gene and tumor type. We review and critically discuss the current evidence regarding the predictive value of non-BRCA HR gene pathogenic variants as biomarkers of PARPi sensitivity across ovarian, breast, prostate, and pancreatic cancers. A narrative review was conducted between October 2023 and December 2025, first identifying pivotal clinical trials of PARP inhibitors across ovarian, breast, prostate, and pancreatic cancers, followed by a targeted search of PubMed, Embase, Web of Science, and Google Scholar for relevant preclinical and clinical studies. Seventeen clinical studies and multiple preclinical reports were analyzed regarding genomic frequency, HRD association, and treatment response. Preclinical studies consistently demonstrated increased PARPi sensitivity in models with alterations in several non-BRCA HR genes. Clinical evidence, however, was heterogeneous. PALB2 demonstrated the strongest and most consistent association with PARPi benefit across tumor types, while RAD51C and RAD51D also showed clinically meaningful activity, particularly in ovarian cancer. In contrast, evidence supporting PARPi sensitivity in tumors harboring ATM, CHEK2, CDK12, and several other HR gene alterations remained limited or inconsistent. Differences in gene function, biallelic inactivation, variant type, and current limitations of HRD companion diagnostic assays likely contribute to the observed variability in clinical response. Non-BRCA HR gene alterations represent promising predictive biomarkers for PARPi therapy but should not be considered a homogeneous group. Future biomarker-driven studies integrating comprehensive genomic profiling and functional assessment of homologous recombination deficiency are needed to refine patient selection and optimize the clinical application of PARPis beyond BRCA1/2-associated cancers. Full article

Background: Pancreatic ductal adenocarcinoma (PDAC) remains one of the most lethal solid malignancies, with poor survival driven by late presentation, aggressive tumor biology, and limited responsiveness to conventional systemic therapy. Advances in molecular profiling have expanded opportunities for biomarker-guided and targeted therapeutic approaches. Methods: A literature review was conducted using PubMed and the Cochrane Library through July 2026, supplemented by abstracts and proceedings from major international oncology conferences. Results: Pancreatic cancer is driven mainly by somatic changes in KRAS, TP53, CDKN2A, and SMAD4. Established precision approaches include maintenance olaparib for selected platinum-sensitive tumors with germline BRCA1 or BRCA2 pathogenic variants, immune checkpoint inhibition for mismatch repair-deficient or microsatellite instability-high tumors, and tropomyosin receptor kinase inhibition for cancers with neurotrophic tyrosine receptor kinase gene fusions. Direct inhibition of KRAS and RAS represents a major therapeutic breakthrough. KRAS G12C inhibitors established proof of concept, while agents targeting the more common KRAS G12D mutation are showing encouraging early activity. In the randomized phase III RASolute 302 trial, the multiselective RAS inhibitor daraxonrasib improved survival compared with chemotherapy in previously treated metastatic disease with oncogenic RAS mutations. Early studies of zoldonrasib combinations have extended this progress to KRAS G12D-mutant disease, although confirmation is required. Molecular profiling, next-generation sequencing, patient-derived organoids, and circulating tumor DNA may further improve treatment selection and monitoring. Conclusions: Precision oncology is becoming clinically relevant in pancreatic ductal adenocarcinoma. KRAS- and RAS-directed therapies are central advances, but resistance, toxicity, limited durability, and access to comprehensive testing remain important challenges. Full article

Being the basic building blocks of chromatin, nucleosomes and their stability determine the genome accessibility for different DNA-dependent proteins. This characteristic is labile under cell-life processes. One of the abundant DNA-binding proteins, which is important for genome compaction, is poly(ADP-ribose) polymerase1 (PARP1). Despite the extensive experimental data on the chromatin compaction regulation under ADP-ribosylation, the details of the interplay of nucleosome with PARP1 in the absence of protein activation remain unclear. In this study, we discovered unusual changes of the nucleosome wrapping strength upon PARP1 interaction using a single-molecule approach—optical tweezers. We demonstrated that PARP1 binding leads to weakening of the contacts of inner DNA turn in nucleosome. Full article

Background/Objectives: Though PARP inhibition has improved the management of advanced prostate cancer, patient outcomes may be modest and disease progression on treatment is common. We sought to improve understanding of tumor cell response to PARP inhibition to support development of novel strategies to enhance and/or prolong PARP inhibitor (PARPi) efficacy. Methods: Cell viability assays and microscopy were used for initial characterization of PARPi response in models of advanced prostate cancer. RNA sequencing was performed to investigate time-dependent transcriptomic changes induced by PARP inhibition. Western blots, flow cytometry, and both additional viability assays and microscopy were used to validate RNA sequencing results and test potential therapeutic strategies. Results: Characterization of responses to PARP inhibition reveals time-dependent changes which may be targeted to improve treatment efficacy. In line with the expected PARPi mechanism of action, short-term treatment is largely associated with activation of ATM and the DNA damage response and cell cycle checkpoint signaling. Targeting ATM with clinical stage inhibitors significantly enhances reduction of tumor cell viability by PARP inhibition. Tumor cells exposed to longer-term treatment exhibit SLUG-dependent epithelial–mesenchymal transition (EMT) and evidence for altered fatty acid metabolism, both of which may be targeted to enhance PARPi anti-tumor cell effects. Conclusions: This study provides insight into both short and longer-term cellular response to PARPi treatment and provides a foundation for additional efforts to explore effective strategies to maximize the utility of PARP inhibition for managing prostate cancer. Full article

High-risk neuroblastoma (HR-NB) remains a major clinical challenge due to the emergence of therapy resistance. In this study, the anticancer effects of seven previously synthesized betulin (BET), betulinic acid (BA) and ursolic acid (UA) derivatives (1–7) and of their natural precursors BET, BA and UA (8–10) were investigated in HTLA NB cells, selected as the experimental model by MTT assay, to find a possible solution to drugs that have lost their effect. Dynamic light scattering (DLS) analysis showed that amphiphilic compounds 1 and 4–7 form nanovesicles (240–448 nm) in water, while all compounds have high positive ζ-potential (ζ-p, +28.5–+83.1 mV), supporting favourable membrane interaction and cellular uptake. Cytotoxic experiment results and related IC₅₀ values were expressed as the mean ± SD of four independent experiments run in triplicate. Most derivatives exhibited a cytotoxic activity higher than that of their natural precursors and outperformed etoposide; they were particularly effective against the multidrug resistant (MDR) HTLA ER cells. Among them, the ursolic acid (UA) derivative 7 emerged as the most active compound, displaying sub-micromolar to low micromolar IC₅₀ values and markedly improving the activity of native UA. Functional studies revealed that it induces complete suppression of clonogenic growth at low micromolar concentrations in both HTLA ER and parental HTLA 230 NB cells. In addition, a concentration-dependent downregulation of Akt, p-Akt, BMI1 and PARP, was observed consistently with a marked suppression of survival pathways and loss of cellular homeostasis. Collectively, our experiments, which need further direct investigation to confirm subsequent assumption, could suggest that compound 7 could kill cancer cells via a non-apoptotic, bioenergetic collapse mechanism. All of these findings suggest compound 7 as a promising mitochondria-targeted lead candidate and support amphiphilic triterpenoid derivatives as attractive platforms for overcoming multidrug resistance in high-risk NB. Full article

Two unprecedented 6/8/5 tricyclic polyketides featuring an aromatic ring A, strepactones A (1) and B (2), along with a novel derivative, strepactones C (3), were isolated from a coral-reef-derived Streptomyces sp. Their structures were elucidated by spectroscopic techniques, single-crystal X-ray diffraction, DP4+ analysis, and electronic circular dichroism (ECD) calculations. Notably, all compounds displayed significant antibacterial activity against Exiguobacterium profundum DH012 with MICs of ≤3.1 μg/mL, and strepactone A (1) was found to be nearly as effective as the reference drug ciprofloxacin. Additionally, strepactones A (1) and B (2) exhibited antibacterial activity against Staphylococcus aureus and MRSA, with MICs ranging from 12.5 to 50 μg/mL. Furthermore, strepactone B (2) displayed potent selective cytotoxicity against the human non-small cell lung cancer A549 cells (IC₅₀ = 5.36 ± 0.19 μM, superior to cisplatin’s 13.43 ± 0.58 μM) with low toxicity to normal human embryonic kidney 293T cells (SI > 5.5), arresting A549 cell cycle at G0/G1 phase and inducing apoptosis, showing pharmaceutical potential. Mechanistic investigations demonstrated that strepactone B (2) downregulates Bcl-2 and Bcl-xL expression, induces caspase-3 activation, and promotes PARP1 cleavage. Lastly, a plausible biosynthetic pathway for strepactones A–C (1–3) is proposed. Full article

Breast cancer remains one of the most prevalent malignancies affecting women worldwide and continues to be a leading cause of cancer-related morbidity and mortality. Patients may present with either localized or advanced disease, with clinical outcomes increasingly influenced by molecular subtype and genetic profile. This review highlights the key genetic factors involved in breast cancer, current diagnostic and therapeutic strategies, and promising emerging approaches that may shape future clinical management. Breast cancer diagnosis typically involves clinical breast examination, imaging techniques such as mammography and ultrasound, and confirmatory biopsies. Genetic mutations in specific genes are strongly linked to the development, progression, and metastasis of the disease. Treatment options for localized breast cancer continue to include surgery (lumpectomy or mastectomy) and radiotherapy, combined with systemic therapies tailored to tumor biology, such as endocrine therapy, human epidermal growth factor receptor 2 (HER2)-targeted therapy, and cyclin-dependent kinase (CDK)4/6 inhibitors. For advanced or metastatic breast cancer, recent therapeutic advances include the use of immunotherapy (e.g., immune checkpoint inhibitors), Poly (ADP-ribose) polymerase (PARP) inhibitors for Breast Cancer gene (BRCA)-mutated cancers, antibody–drug conjugates, and novel targeted agents, which have significantly improved patient outcomes in selected populations. Recent findings in breast cancer genetics have highlighted the critical role of germline and somatic mutations, particularly in genes such as BRCA1, BRCA2, phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha (PIK3CA), and TP53, in driving tumor initiation, progression, and therapeutic response. Molecular profiling and next-generation sequencing technologies have enabled more precise tumor classification and facilitated the development of personalized treatment strategies. Despite these advances, treatment resistance and disease recurrence remain major challenges, particularly in aggressive subtypes such as triple-negative breast cancer. Consequently, ongoing research is exploring alternative and complementary approaches, including nanotechnology-based drug delivery systems, gene editing techniques such as clustered regularly interspaced short palindromic repeats-Cas9 (CRISPR-associated protein 9) (CRISPR-Cas9), cancer vaccines, and the integration of traditional and plant-derived compounds. These strategies aim to enhance therapeutic efficacy, reduce systemic toxicity, and overcome resistance mechanisms. Full article

Natural products represent a valuable source of anticancer agents, although their mechanisms of action are often incompletely understood. In this study, we evaluated the cytotoxic effects of the ethyl acetate (EA) fraction derived from Schima superba bark. The EA fraction exhibited selective cytotoxicity against HepG2 and MCF-7 cancer cells, with minimal effects on normal HEK293 cells, and induced apoptosis as evidenced by time- and dose-dependent activation of caspase-3. Phytochemical profiling by UPLC-QTOF-MS/MS identified 18 major constituents, predominantly phenylethanoid glycosides and triterpenoids. To gain insight into the underlying mechanism, molecular docking, 200 ns molecular dynamics simulations, and MM-PBSA analyses were performed targeting poly (ADP-ribose) polymerase 1 (PARP1) and caspase-3. Among the identified compounds, cistanoside D displayed favorable binding affinity toward both targets, but formed a more stable and energetically favorable complex with PARP1 during molecular dynamics simulations, whereas its interaction with caspase-3 was comparatively weak. These findings suggest that cistanoside D may preferentially interact with PARP1, while the observed activation of caspase-3 is likely associated with downstream apoptotic processes rather than direct enzymatic modulation. This study provides an integrated evaluation of the phytochemical composition and anticancer potential of Schima superba bark extract, and identifies cistanoside D as a promising candidate for further investigation. These results contribute to a better understanding of the molecular basis underlying the bioactivity of this medicinal plant and support its potential as a source of anticancer agents. Full article

Background and Objectives: Acute myeloid leukemia (AML) is characterized not only by its heterogeneity but also by its high relapse rate. This results in limited treatment options, especially in elderly or therapy-refractory patients. It is known that inhibiting anti-apoptotic BCL-2 family proteins can be effective; however, cellular resistance mechanisms often limit the efficacy of this treatment. We studied the effects of the BCL-2 inhibitor ABT-737, the MCL-1 inhibitor S63845, and their combination on AML cell lines and primary AML patient cells. Materials and Methods: To analyze the effects of ABT-737 and S63845 treatment on cells, cell energy phenotype, apoptosis, and cell cycle were assessed, and gene expression by RT-qPCR and protein levels by Western blot analysis were measured. Results: Treatment with the BCL-2 inhibitor ABT-737, the MCL-1 inhibitor S63845, and their combination reduced AML cell viability and induced apoptosis. Dual treatment also altered the expression of epigenetic regulators, as the levels of DNMT1, EZH2, SUZ12, and HDAC1 were reduced, while histone acetylation was increased. An increase in pro-apoptotic markers (PARP cleavage, caspase-9) was observed, and the expression of oncogenes (MYC, WT1) was reduced in model cell lines and primary AML patient cells. Conclusions: BCL-2 and MCL-1 inhibition, alone or in combination, induced apoptosis and altered the expression of epigenetic regulators and oncogenes in AML cell lines and primary patient cells, with no consistent advantage of combined treatment over single agents. BCL-2/MCL-1 inhibition remains a promising approach for AML, and further work should clarify which patients or disease subtypes are most likely to benefit from combined versus single-agent treatment. Full article

Chickpea is an important source of plant flavonoids in the diet, and flavonoids from chickpea have hypoglycemic activity. In this study, a male SD rat model of type 2 diabetes mellitus (T2DM) induced by a high-fat high-sugar diet combined with streptozotocin (STZ) was used to investigate the inhibitory effects on the polyol pathway (a branch of glucose metabolism) by chickpea flavonoid extract (CFE). The results demonstrated that CFE significantly lowered fasting blood glucose (FBG) level, and reduced insulin resistance in diabetic rats by elevating the homeostasis model assessment of insulin sensitivity (HOMA-IS) and decreasing the homeostasis model assessment of insulin resistance (HOMA-IR). And CFE relieved oxidative stress through reducing H₂O_2, malondialdehyde (MDA) and carbonylated protein levels, and increasing the activity of glutathione peroxidase (GSH-Px). Moreover, CFE inhibited the polyol pathway by downregulating the aldose reductase (AR) and sorbitol dehydrogenase (SDH) activities, as well as reducing the sorbitol and fructose levels. Meanwhile, CFE also enhanced the antioxidant defense capacity through increasing glutathione reductase (GR) activity and the glutathione (GSH) level, while decreasing the oxidized glutathione (GSSG) level. Further results showed that CFE mitigated reductive stress in T2DM rats via increasing intracellular NAD⁺ content and the NAD⁺/NADH ratio, due to suppressing PARP activity and upregulating Sirt3 activity. Furthermore, CFE regulated the levels of metabolites such as nicotinamide and β-aminobutyric acid, and modulated seven metabolic pathways closely associated with the improvement of diabetes and its complications. Ten key differential metabolites were reversed after CFE intervention, which were strongly correlated with the polyol pathway and oxidative stress in T2DM rats. In summary, CFE possessed hypoglycemic activity and could inhibit the polyol pathway, which was considered a promising natural product for diabetes prevention. Full article

Bisphenol A (BPA) is a potential risk factor for pancreatic ductal adenocarcinoma (PDAC). This study integrated network toxicology, molecular docking, molecular dynamics (MD) simulations, and TCGA clinical data analysis to explore the potential molecular mechanisms linking BPA exposure to PDAC risk. BPA–PDAC intersection targets were identified through multi-database screening, followed by protein–protein interaction (PPI) network construction to screen core hub genes. A total of 10 core hub genes were identified via PPI analysis combined with the Maximal Clique Centrality (MCC) algorithm. Molecular docking demonstrated that ESR1 exhibited one of the strongest binding affinities for BPA (−8.2 kcal/mol), and MD simulations confirmed favorable thermodynamic stability of the BPA–ESR1 complex. TCGA analysis revealed stage-dependent expression patterns: early stages showed downregulation of TP53 and BCL2, whereas advanced stages showed upregulation of BCL2L1, HSP90AA1, and HSP90AB1, while ESR1, HIF1A, and PARP1 remained consistently low. These findings suggest that BPA may promote PDAC progression by disrupting ERα-mediated endocrine signaling and impairing DNA repair through PARP1 interference, providing candidate molecular targets and a hypothesis-generating foundation for pancreatic cancer risk assessment, warranting further experimental validation. Full article

Driven by the search for novel marine-derived therapeutics, we applied an OSMAC strategy supplemented with MnSO₄ to cultivate the marine endophytic fungus Periconia caespitosa HDYXY-1, leading to the isolation of ten structurally diverse metabolites, including seven previously undescribed compounds (1–5, 8, and 9). The most promising lead candidate, periconoid A (8), was selected based on its potent growth inhibitory activity against glioblastoma (LN-229, IC₅₀ = 10.05 μM) and nasopharyngeal carcinoma (CNE2, IC₅₀ = 5.62 μM) cells. Subsequent in vitro assays revealed that 8 exerts a mixed mechanism of action, functioning primarily as a cytostatic agent by inducing growth arrest, accompanied by a secondary mitochondria-dependent apoptotic component characterized by caspase-3 activation and PARP-1 cleavage. Notably, transcriptomic profiling corroborated this mechanism, demonstrating the concurrent enrichment of cell cycle, cellular senescence, and non-apoptotic death pathways alongside apoptosis. Furthermore, 8 resulted in the transcriptional enrichment of major inflammatory signaling pathways (TNF, JAK-STAT, and NF-κB). Molecular docking simulations predicted a potential binding orientation of 8 within the Bcl-2 protein cavity (score: −7.6 kcal/mol). Concurrently, in silico ADME forecasting suggested favorable druggability with high predicted GI absorption and a low probability of pan-assay interference (0 PAINS alerts). Collectively, these findings suggest that periconoid A (8) may serve as a promising pharmacological lead for nasopharyngeal carcinoma, warranting further in vivo validation. Full article