To determine the concentration of isolated DNA from archived paraffin blocks of cervical cancer using real-time PCR and to study its relationship with the storage period of samples.

To determine the molecular genetic characteristics of the epithelial neoplasia of extrahepatic bile ducts (EHD) depending on the degree of epithelial dysplasia in order to identify mutations that facilitate their differential diagnosis.

Gastric cancer (GC) remains a leading cause of cancer-related mortality worldwide, driven by late-stage diagnosis, metastatic progression, and therapeutic resistance. Src homology region 2 domain-containing phosphatase 2 (SHP2) has emerged as a critical regulator of oncogenic signaling in gastric tumorigenesis, yet its therapeutic targeting remains underexplored. In this study, we evaluated the anti-cancer efficacy of NSC 57774, a novel SHP2 inhibitor, using integrated bioinformatics and functional assays in AGS gastric cancer cells. Analysis of The Cancer Genome Atlas (TCGA) and UALCAN datasets revealed marked upregulation of SHP2 and multiple receptor tyrosine kinases in gastric cancer tissues. NSC 57774 potently inhibited cell proliferation and migration, demonstrating selective cytotoxicity towards cancer cells over non-cancerous fibroblasts. Mechanistically, NSC 57774 disrupted key oncogenic pathways including MAPK/ERK, AKT and STAT3 in a concentration- and time-dependent manner, with higher doses achieving more sustained pathway suppression. NSC 57774 suppressed NF-κB inflammatory signaling at early timepoints and induced cleaved caspase-3 across all treatment groups at 72 hours, indicative of pro-apoptotic activity. A paradoxical late-phase increase in phospho-p38 was observed at 72 hours, consistent with a compensatory pro-apoptotic stress response. Comparative analysis revealed that NSC 57774 outperformed the commercial SHP2 inhibitor NSC 87877 and doxorubicin in reducing viability and migration of gastric cancer cells. Collectively, these findings position NSC 57774 as a promising candidate for targeted gastric cancer therapy, capable of disrupting multiple signaling pathways involved in tumor progression, metastasis, and inflammation, warranting further preclinical and clinical investigation.

Pathogenic variants in BRCA1 and BRCA2 confer substantial risks of breast and ovarian cancer; however, risk for female individuals undergoing testing, particularly those with variants of uncertain significance (VUS) or negative results, remain poorly defined.

Colorectal cancer (CRC) is a leading cause of cancer-related mortality worldwide, with tumor-associated macrophages (TAMs), predominantly M2-polarized, shaping a tumor-promoting microenvironment. ETS proto-oncogene 2 (ETS2) is aberrantly upregulated in CRC, but its role in exosome-mediated intercellular communication and TAM polarization remains unclear. Here, public datasets and single-cell RNA sequencing were analyzed to characterize ETS2 expression and cellular distribution in CRC. Co-culture of THP-1-derived M0 macrophages with CRC cells (LoVo and HCT-116), combined with isolation of tumor-derived exosomes, was used to assess exosome-mediated ETS2 transfer and macrophage M2 polarization. CRC cell proliferation, migration, apoptosis, CD8⁺ T cell apoptosis, and macrophage M2 polarization were evaluated by CCK-8, EdU incorporation, flow cytometry, RT-qPCR, and Transwell assays. Chromatin immunoprecipitation and dual-luciferase reporter assays confirmed transcriptional activation of pre-mRNA processing factor 4 (PRPF4) by ETS2, and a xenograft mouse model was used to assess in vivo effects. ETS2 expression was elevated in CRC tissues and TAMs and correlated positively with M2 polarization. Silencing ETS2 inhibited CRC cell proliferation and migration, promoted apoptosis, reduced macrophage M2 polarization, and decreased CD8⁺ T cell apoptosis. Mechanistically, ETS2 activated PRPF4 transcription, and PRPF4 overexpression reversed the inhibitory effects of ETS2 knockdown. CRC-derived exosomes mediated ETS2 transfer to macrophages, promoting M2 polarization, and in vivo PRPF4 overexpression significantly rescued tumor growth suppressed by ETS2 knockdown. These findings indicate that exosomal ETS2 promotes CRC progression and M2 macrophage polarization via PRPF4, highlighting the ETS2/PRPF4 axis as a potential therapeutic target.

Well-differentiated liposarcoma (WDLPS) and dedifferentiated liposarcoma (DDLPS) are characterized by recurrent MDM2-centered amplification of chromosome 12q13-15, yet this diagnostic label reduces a complex structural lesion to a binary result. An architecture-resolved 12q amplicon platform requires an MDM2-centered dosage anchor plus direct evidence of nontrivial topology or carrier state; cargo, regulatory, and functional data define progressively higher-resolution features. When only MDM2 amplification is documented, the lesion is best described as diagnostic 12q amplification rather than a fully resolved platform. This review presents an evidence-graded architecture-to-function framework that separates direct WDLPS/DDLPS observations from mechanisms inferred from broader amplification biology. Disease-specific evidence supports heterogeneous 12q carriers, including ring, giant marker, rod-shaped, discontinuous, and neochromosome-like structures, as well as enhancer coamplification or altered 3D contacts. In contrast, chromothripsis, telomere crisis/BFB remodeling, ecDNA-like dynamics, and enhancer hubs are treated as extrapolated or testable mechanisms unless directly validated in liposarcoma. Conclusions are weighted by methodological resolution: cytogenetics/FISH define diagnostic amplification and visible carrier classes; MLPA or array-based assays define dosage and discontinuity; WGS with long-read or optical mapping is needed for junction-level architecture; and single-cell/spatial assays mainly resolve cellular-state or ecosystem context unless paired with structural readouts. MDM2-p53 and CDK4-RB remain central outputs, whereas selected cargo, lineage state, metabolism, and tumor-microenvironment programs are interpreted as evidence-ranked cooperating or downstream modules. Clinically, architecture-aware interpretation is proposed as a prospective framework for sampling, model design, biomarker development, and trial stratification, not as an established basis for routine management.

Fibroadenoma is the most common benign fibroepithelial lesion of the breast; it occurs most frequently in adolescents and women of reproductive age. While fibroadenoma is considered a non-invasive lesion with a good prognosis, some fibroadenomas may show rapid growth, recurrence, stromal hypercellularity, epithelial proliferative changes and even show radiological overlap with phyllodes tumour and breast carcinoma resulting in significant diagnostic dilemmas. In recent years, molecular pathology and biomarker studies have led to better understanding of the biology of fibroadenomas, and their ability to differentiate between fibroadenomas and malignant breast lesions. This review will provide a comprehensive overview of biomarkers involved in the diagnosis, prognosis, prediction, molecular, genetic, epigenetic, functional, circulating and imaging of breast fibroadenoma and breast cancer. The key biomarkers such as MED12 mutation, Ki-67, p53, Bcl-2, ER/PR, HER2, VEGF, MMPs, γ-H2AX, ctDNA, circulating tumour cells and transcriptomic classifiers are discussed in the context of tumour proliferation, apoptosis, angiogenesis, invasion, genomic instability and malignant transformation risk. The retrieved relevant literature was from 2000 to 2025 from the databases of PubMed, Scopus, Web of Science, and Google Scholar. The review further emphasizes the growing significance of liquid biopsy, radiomics, artificial intelligence, digital pathology, and the integration of multi-omics techniques for enhancing lesion classification, diagnostic accuracy, and personalized risk assessment. Many challenges still exist such as a lack of standardised cut off values for biomarkers, overlap between fibroadenoma and phyllodes tumour, a lack of molecular panels specifically designed for fibroadenoma and a lack of long-term validation studies. Further incorporation of molecular profiling, imaging biomarkers, computational pathology, and precision oncology approaches into the future could greatly enhance the risk stratification and handling of benign and malignant fibroepithelial breast lesions.

Treatment choices for metastatic non-small-cell lung cancer (NSCLC) after first-line targeted therapy progression are heterogeneous. This study aimed to characterize real-world treatment patterns and outcomes of advanced NSCLC harboring actionable genomic alterations (AGAs) in second- (2 L) or third-line (3 L) settings. This retrospective cohort study across six Chinese centers included stage IV NSCLC patients with confirmed AGAs. Therapies were divided into six categories: targeted monotherapy (T), targeted combinations (T+), chemotherapy monotherapy (C), chemotherapy combinations (C+), anti-angiogenic monotherapy (A), and other regimens (O). The primary outcome was the treatment pattern. Secondary outcomes included biomarker testing and effectiveness. A total of 658 patients were enrolled, with the majority harboring EGFR mutations (n = 590, 89.7%). In the 2 L-enrolled group (n = 602), T use declined from 75.3% in the 1 L setting to 49.3% in 2 L, while utilization of A + C increased to 16.5%. Within the EGFR-mutant subgroup, therapeutic sequences were highly dependent on 1 L TKI generation and T790M resistance status. Over half (51.1%) of T790M-negative patients continued T in 2 L following progression on 1 L first- or second-generation TKIs. Among the 3 L-enrolled patients (n = 56), A + C (35.7%) and C (14.3%) were predominant. The overall median real-world progression-free survival for the 2 L-enrolled group was 7.4 months in the 2 L setting (7.5 months for the EGFR-mutant subgroup) and 5.4 months in 3 L. This multicenter real‑world cohort predominantly comprised patients with EGFR‑mutant NSCLC, with smaller numbers of other AGA subtypes. Targeted therapies remain the cornerstone of later-line advanced NSCLC management. The prevalent real-world reliance on continued TKI therapy, even in T790M-negative patients, highlights the clinical dilemma of limited post-resistance options and the need to integrate emerging novel therapeutics.

Breast cancer (BC) is the most commonly diagnosed malignant disease in women worldwide. Resistance to neoadjuvant chemotherapy (NAC) still limits treatment efficacy despite the enormous progress in systemic therapy. Because pathological complete response (pCR) is strongly associated with favorable clinical outcomes, especially in triple-negative and HER2-positive breast cancer, the discovery of reliable predictive biomarkers before treatment has become a key clinical goal. This narrative review summarizes the available evidence of genetic and transcriptomic biomarkers associated to responses to conventional anthracycline, taxane and platinum-based NAC. Current evidence suggests biomarkers can be broken down into three interconnected biological pathways. Dysregulation of immune and interferon signaling, including interferon-stimulated genes (ISG15, IFIH1, MX1, OAS family, IFI27, and IFITM1), affects chemotherapy response by modulating immune activation, apoptosis, and DNA damage tolerance. Second, alterations in DNA damage response (DDR) pathways for BRCA1, TP53, PARP1, ATM, and CHK1 affect the cells' vulnerability to genotoxic stress and contribute to the subtype-specific differences in treatment efficacies. Third, dysregulated cell cycle components (CCND1, CDK4/6, RB1, and E2F1) affect proliferation, checkpoint control, and susceptibility to chemotherapy-induced apoptosis. These pathways act in concert, rather than as independent mechanisms, to influence NAC sensitivity. Available data suggest that no single biomarker has sufficient predictive accuracy for all breast cancer subtypes. Subtype-specific multi-gene models integrating immune, DDR and cell-cycle biomarkers represent a more powerful tool to predict pCR and improve patient stratification before NAC. Further prospective clinical validation is needed before these biomarkers can be implemented in routine clinical practice.

To evaluate the proportion of expressed programmed cell death ligands-1 (PD-L1) in epithelial ovarian carcinoma patients, and the association with the clinicopathological, surgical outcomes, and oncologic outcomes. To compare PD-L1 protein expression with messenger ribonucleic acid (mRNA) expression.

Poly(ADP-ribose) polymerase inhibitors (PARPi) have shown limited efficacy in gastric cancer, primarily due to the rarity of inherent homologous recombination (HR) deficiency. The nuclear Arp2/3 complex was recently implicated in DNA double-strand break repair via HR. Here, we investigate whether pharmacological inhibition of Arp2/3 can induce a functional HR-deficient state to synergize with PARPi in gastric cancer cells.

Recent research has identified pyroptosis as a distinct form of programmed cell death that is strongly correlated with tumor outcomes. However, its value as a prognostic biomarker in clear cell renal cell carcinoma (ccRCC) is not yet fully established.

Colorectal cancer (CRC) is a leading cause of cancer-related morbidity and mortality worldwide; thus, understanding its molecular mechanisms is critical for developing novel therapeutic targets. Long non-coding RNAs (lncRNAs) play crucial isoform-specific roles in cancer. While oncogenic lncRNA LINC00673 is known to be involved in multiple malignancies and possesses five distinct transcript variants, the functional role of LINC00673-V4-a highly expressed transcript variant in CRC-remains largely unexplored. This study investigated how LINC00673-V4 drives CRC proliferation by modulating the Hippo-Yes-associated protein (Hippo-YAP) signaling pathway.

Accurate identification of actionable somatic variants is essential for therapeutic stratification in colorectal cancer (CRC). While next-generation sequencing (NGS) enables comprehensive genomic profiling, targeted approaches may provide faster and more practical alternatives for routine diagnostics.

Cervical cancer (CC) is a prevalent malignancy in women. RNA-binding motif single-stranded interacting protein 3 (RBMS3) acts as a tumor suppressor in many cancer types, but its role and underlying regulatory mechanisms in CC remain unclear.

Kidney renal clear cell carcinoma (KIRC) is the most common subtype of renal cell carcinoma, accounting for 75-80% of cases. Although Prohibitin 1 (PHB1) has been implicated in tumorigenesis, its role in KIRC remains unclear. This study aimed to investigate the expression, function, and underlying mechanisms of PHB1 in KIRC.

G protein-coupled receptor 19 (GPR19) is an orphan G protein-coupled receptor with emerging relevance in cancer; however, its role in breast cancer remains poorly understood. Given the high frequency of tumor protein p53 (TP53) alterations in aggressive breast cancer, particularly triple-negative breast cancer (TNBC), we investigated the clinical significance, biological function, and molecular mechanism of GPR19 in TP53-mutant breast cancer.

Lung adenocarcinoma (LUAD) is the most common subtype of non-small cell lung cancer and remains a major cause of cancer-related mortality. Despite advances in targeted therapies, tumor heterogeneity and acquired resistance frequently undermine clinical outcomes. This study aimed to identify novel oncogenic drivers and underlying mechanisms in LUAD.

While mitochondrial dysfunction and immune cell dysregulation have been established as important contributors to the pathogenesis of osteosarcoma (OS), the prognostic value of mitochondria-related genes (MRGs) and immune-related genes (IRGs) in OS remains poorly understood.

Methyltransferase-like 9 (METTL9) has been implicated in tumor progression, yet its clinical significance, functional roles, and immunoregulatory functions in lung adenocarcinoma (LUAD) remain unclear. This study aimed to integrate multi-omics datasets and experimental evidence to systematically evaluate the expression profile, prognostic value, molecular mechanisms, and tumor microenvironment (TME)-related functions of METTL9 in LUAD.