The metastasis of laryngeal squamous cell carcinoma (LSCC) is not only caused by the tumor itself but is also closely related to cancer-associated fibroblasts (CAFs). The epithelial-mesenchymal transition (EMT) serves as a key event during its metastasis. However, the specific mechanisms underlying LSCC metastasis remain uncertain.

Multifocal micronodular pneumocyte hyperplasia as first manifestation of tuberous sclerosis complex has rarely been reported.

Lymphoplasmacytic lymphoma/Waldenström macroglobulinemia rarely transforms into diffuse large B-cell lymphoma, and there have been no reports of cases proving clonal identity when presenting as primary central nervous system lymphoma. There are many unclear aspects regarding the mechanism by which lymphoplasmacytic lymphoma/Waldenström macroglobulinemia infiltrates the central nervous system and transforms, as well as the treatment methods for the transformed lymphoma.

"Lineage switch" is a term used to describe the phenomenon of change of lineage of acute leukemia to a different lineage. It is typically seen during therapy or at the time of relapse. More commonly, it is described in the pediatric population with an incidence of 6-9%. Lineage switches, though uncommon, can occur from acute myeloid leukemia (AML) to acute lymphoblastic leukemia (ALL (B/T)) and vice versa. The present scenario of AML to B-ALL switch is rare in an adult, with only a handful of cases described in literature. We report herein a case diagnosed as AML at 56 years of age, with NPM mutation who relapsed after 18 months post initial diagnosis. The clinicopathological features, flowcytometry, and molecular characteristics are discussed.

Succinate dehydrogenase (SDH) deficient gastrointestinal stromal tumor (GIST) is the most common type of wild type GIST characterized by lack of mutations in proto-oncogene receptor tyrosine kinase (KIT) or platelet-derived growth factor receptor alpha (PDFGR alpha) pathways. It has a unique predilection for females and young adults, with a relatively indolent prognosis and varied treatment modalities. Data regarding SDH GIST from the Indian subcontinent is sparse.

Mammographic density (MD) is a strong, heritable risk factor for breast cancer. To date, 55 independent MD-associated genetic loci have been identified through genome-wide association studies (GWASs) in women of European ancestry; however, no studies have been reported in Asian women.

Tumor-derived exosomal microRNAs mediate intercellular communication between malignant cells and distant organs and play a pivotal role in metastatic dissemination. Breast cancer brain metastasis (BCBM) poses a significant clinical challenge, with endothelial barrier dysfunction representing a critical yet poorly understood step in metastatic progression.

Histone 3 lysine 27 (H3K27) demethylation is a key post-translational modification of chromatin and plays a fundamental role in gene activation. Demethylation of H3K27 is mediated by Jumonji C domain-containing lysine demethylase 6 A (KDM6A) and its paralog, KDM6B, both of which are responsible for homeostasis, autoimmune response, infectious diseases, and cancers. To date, mounting studies dedicate the roles of KDM6A/B on tumor promotion or suppression, and there are many reviews systematically summarize the relevant mechanisms of KDM6A/B in tumor development and therapy. KDM6A and KDM6B also contribute to the regulation of therapeutic insensitivity to chemotherapy, targeted response, radiotherapy and immunotherapy. Herein, we outline the current knowledge of KDM6A/B in regulation of therapeutic resistance, and suggest that KDM6A/B holds immense potential in recovering therapeutic resistance.

Cancers can be hematological or solid, sharing many hallmarks, although their clinical behaviors are distinct. Identifying biomarkers that differentiate hematological from non-hematological malignancies could aid differential diagnosis by providing the basis for developing point-of-care diagnostic devices. In this respect, complex histone populations are secreted and detectable in biological fluids in various disease settings. To our knowledge, studies analyzing the circulating histone profile complexity by comparing healthy individuals, patients with hematological malignancies, and solid cancer patients are currently lacking.

Women with autoimmune diseases (AIDs) experience chronic immune dysregulation and hormonal fluctuations, both of which may influence breast cancer risk. However, it remains unclear whether this risk is driven mainly by its treatment or the underlying disease, highlighting the need for integrating real-world data and genetic evidence.

Cisplatin (DDP) an effective DNA-damaging agent, is fundamental in treating non-small cell lung cancer (NSCLC). Resistance to DDP remains a significant challenge in the treatment of NSCLC. This study aimed to elucidate the mechanisms underlying DDP resistance, with a focus on the role of DNA repair pathways and cancer stem cells (CSCs) in NSCLC.

Breast cancer is a heterogeneous illness in terms of histologic variants, natural history of disease, clinical behaviour, and response to therapy. Triple-negative breast cancer (TNBC) is a biologically aggressive tumour with the worst prognosis among all subtypes, owing to higher grade and high proliferation capacity, and, restricted therapeutic choices. Despite numerous attempts to identify therapeutic aberrations that can be targeted, chemotherapy continues to be the primary systemic treatment for TNBC. It should be noted, however, that multiple studies have shown racial variation in the clinical behaviour of TNBCs and there remains a need to identify alternative, novel driver mutations in our ethnically diverse population, especially actionable mutations that might prove to be potential targets for precision therapy. This study was taken up with the aim to identify distinct targetable genetic alterations in TNBC patients and to report the frequencies of various subtypes.

Bladder cancer (BLCA) is a highly heterogeneous malignancy with high morbidity and mortality. Massive lactate production and hypoxia are characteristics of the tumor microenvironment (TME). However, our understanding of the clinical value of hypoxia and lactate metabolism (HLM) in BLCA remains limited.

Head and neck squamous cell carcinoma (HNSCC), the seventh most common cancer globally, has not yet seen an exploration of the specific role of hsa-miR-103a-3p. This study employs integrated bioinformatics analysis to investigate the function, regulatory patterns, and prognostic significance of hsa-miR-103a-3p in HNSCC. The Kaplan-Meier database was used for pan-cancer prognostic analysis of hsa-miR-103a-3p. Expression significance was assessed using the dbDEMC and GSE124566 dataset from GEO. TargetScan, RNA22, miRDB, and miRWalk identified potential targets, while GEPIA 2.0 provided differentially expressed genes (DEGs). Functional and pathway enrichment analyses were conducted using ShinyGO and KOBAS. Elevated hsa-miR-103a-3p expression correlated with poor overall survival and was upregulated in HNSCC tissues. Integration of four target prediction tools yielded 297 candidate genes. Among them, HOXD10, HMGA2, and THY1 showed the highest expression, whereas UBL3, AMOT, and PDK4 displayed low levels. UBE2Q1, ZFPM2, and ATXN1 demonstrated the strongest accessibility to hsa-miR-103a-3p binding. Network analysis revealed interactions with transcription factors and tumor-related genes, while enrichment highlighted involvement in upstream regulators and downstream cancer-associated pathways. This study identified 297 target genes and clarified the regulatory role of hsa-miR-103a-3p through interaction networks, transcription factor associations, and pathway enrichment. These findings suggest a potential oncogenic role for hsa-miR-103a-3p in modulating the cAMP signaling pathway, proteoglycans in cancer, and related mechanisms, thereby linking its molecular regulation to poor prognosis and potential therapeutic targeting in HNSCC.

Gastric cancer (GC) is a prevalent gastrointestinal malignancy in China. Despite advancements in multidisciplinary diagnosis and treatment strategies, the 5-year survival rate remains low at just 10-20%. A significant number of patients ultimately die from postoperative recurrence and distant metastasis. Therefore, it is crucial to investigate the core mechanisms underlying GC development and progression and to identify potential molecular targets for early diagnosis, prevention, and treatment. MAGEA11, part of the melanoma-associated antigen (MAGE) gene family, is associated with several cancers. However, its expression, function, and mechanisms in GC remain unclear. In this study, we first confirmed that MAGEA11 is highly expressed in GC through data analysis from The Cancer Genome Atlas (TCGA), univariate and multivariate Cox regression analyses, and Kaplan-Meier survival curve analysis. Our findings indicate that MAGEA11 is an independent prognostic factor for overall survival (OS) in GC patients, with higher expression levels correlating with shorter OS, disease-specific survival (DSS), disease-free interval (DFI), and progression-free interval (PFI). Next, we explored the role of MAGEA11 in GC by constructing stable cell models with MAGEA11 knockdown and overexpression. Functional assays on these models demonstrated that MAGEA11 promotes the proliferation, migration, and invasion of GC cells in vitro. Additionally, the tumor-promoting effects of MAGEA11 were verified in vivo using a GC cell tumor model. Previous studies have shown that MAGEA11 increases the transcriptional activity of the transcription factor E2F1, thereby promoting cancer progression. To verify this mechanism in GC, we conducted cell function experiments and immunohistochemistry, confirming that MAGEA11 promotes GC development by activating E2F1's transcriptional activity. These findings indicate that MAGEA11 may be a useful molecular marker for predicting GC prognosis.

Cholangiocarcinoma (CCA) progression involves dysregulated cell cycle control, but core regulatory networks and their roles in tumor heterogeneity remain elusive. We integrated bulk transcriptomics (TCGA-CHOL and GEO cohorts) and single-cell RNA-seq (GSE138709) to identify survival-related genes (SRGs) driving CCA. Through limma, WGCNA, and PPI analysis, we identified seven SRGs (CDK1, ASPM, CCNB1, KIF2C, TOP2A, BUB1, DLGAP5) enriched in G2/M-phase pathways. Single-cell analysis revealed specific SRG upregulation in malignant epithelial subpopulations (PHGR1-Epi/UBE2C-Epi), with pseudotime trajectories demonstrating dynamically increased SRG expression during dedifferentiation. Functional validation confirmed CCNB1 as a core regulator: siRNA knockdown in HuCCT1/RBE cells significantly suppressed proliferation and clonogenicity. This study is the first to define a G2/M-phase gene module promoting CCA progression and map its single-cell dynamics, highlighting CCNB1 as a therapeutic target. Our results reveal SRGs as a coordinated oncogenic network underlying tumor aggressiveness, providing mechanistic insights for future SRG-targeted therapies.

Clear cell renal cell carcinoma (ccRCC) is the most common subtype of renal cell carcinoma (RCC). Although we have made many achievements in the therapy of RCC with the progress of medicine, the clinical management of metastatic RCC remains a daunting challenge. SWI/SNF chromatin remodeling complex-related genes (SCRGs) are significantly associated with tumor progression and cancer cell evolution in ccRCC. This study aimed to investigate the prognostic significance of SCRGs in ccRCC to elucidate its molecular subtype characteristics. Using 29 known SCRGs, 532 ccRCC patients from the TCGA-KIRC cohort were classified into two subtypes (SCRGcluster A and SCRGcluster B). Patients in SCRGcluster B exhibited a significantly poorer prognosis compared to those in SCRGcluster A. Functional enrichment and immune microenvironment profiles significantly differed between the subtypes, with SCRGcluster B showing higher levels of immune infiltration. Five core genes (TMCC3, TOP2A, EPS8, PIK3R3, KCNK5) were identified through the integration of multiple machine learning approaches and multivariate Cox regression analysis. A novel prognostic model based on these core genes was validated in an external cohort. Additionally, single-cell data analysis revealed the expression patterns of these core genes in ccRCC. In vitro experiments demonstrated that KCNK5 is underexpressed in ccRCC cell lines and tissues, and that its overexpression suppresses malignant phenotypes. Specifically, KCNK5 overexpression significantly inhibited the proliferation, migration, and invasion capabilities of ccRCC cell lines. Although the precise functional mechanisms of these core genes in ccRCC are not yet fully elucidated, this study provides new insights for the treatment of ccRCC.

The PEST-containing nuclear protein (PCNP) has been reported to play paradoxical roles in tumorigenesis. While PCNP functions as a tumor suppressor in neuroblastoma and lung adenocarcinoma, it has been identified as a tumor promoter in ovarian cancer. However, the underlying mechanisms driving these contrasting effects remain unclear. Gene Expression Profiling Interactive Analysis (GEPIA) was employed to analyze relevance of PCNP expression with prognosis in HCC. To evaluate the role of PCNP in hepatocellular carcinoma (HCC), we analyzed the expression of PCNP in 87 HCC tissues and 80 adjacent normal tissues. Correlation between PCNP and ubiquitin-like with PHD and ring finger domains 2 (UHRF2) was transcriptionally detected, and then their effects on malignant behaviors, including proliferation, invasion, tumor formation in vitro and in vivo were evaluated. According to tissues array results, it is found that PCNP was significantly upregulated in HCC tissues, which was further confirmed in HCC cell lines by western blotting. Importantly, both the cytoplasmic and nuclear PCNP fractions were correlated with pathological grade, T staging, clinical staging and recurrence, and patients with a high level of PCNP had lower overall survival and disease-free survival and a higher recurrence rate than those with a low PCNP level, indicating that PCNP might be an independent prognostic factor for HCC patients. Functional investigations revealed that PCNP knockdown inhibited malignant behaviors, including proliferation, invasion, colony formation and tumor formation, in vitro and in vivo. Pearson correlation analysis indicated a positive association between PCNP and UHRF2, with evidence that PCNP transcriptionally upregulates UHRF2. Furthermore, ectopic overexpression of PCNP activated the ErbB3/Ras/Raf1 signaling pathway through upregulation of UHRF2. Our findings suggest that PCNP promotes HCC progression by activating the ErbB3/Ras/Raf signaling pathway through upregulation of UHRF2. Consequently, PCNP holds potential as both a diagnostic biomarker and a therapeutic target for hepatocellular carcinoma.

Endometriosis (EMS) is a chronic gynecological condition affecting 6-10% of reproductive-age women. These lesions, albeit of benign nature, present cancer-like features, and may progress to epithelial ovarian cancer (EOC) through a multistep process. The coexistence of EMS and EOC in the presence of transitional lesions (TL) - i.e. atypical EMS/borderline lesions - is termed as endometriosis-correlated ovarian cancer (ECOC). Given the regulatory role of miRNAs in gene expression and biological pathways, we aimed to identify miRNAs that may drive or modulate the malignant transformation of ovarian EMS. Global miRNA profiling was evaluated on 81 samples (EMS, TL and ECOC) from 44 patients. Principal component analysis and unsupervised clustering revealed two distinct clusters formed by ECOC and ovarian EMS samples, whereas TL were dispersed among the other two. Differential expression analysis (DEA) of TL vs. ovarian EMS, revealed 30 significantly upregulated miRNAs. Comparison of ECOC vs. TL samples yielded 118 significantly upregulated and 77 downregulated miRNAs. Finally, DEA of ECOC vs. ovarian EMS lesions yielded 200 upregulated and 128 downregulated miRNAs. Evaluation of miRNAs commonly deregulated between the three groups showed 14 shared upregulated miRNAs (miR-429, miR-425-5p, miR-200c-3p, miR-200c-5p, miR-200b-3p, miR-200a-3p, miR-183-5p, miR-182-5p, miR-141-5p, miR-141-3p, miR-96-5p, miR-93-5p, miR-10a-5p, miR-10a-3p) with a progressive increase in expression levels, from ovarian EMS to TL and ultimately to ECOC. The identified miRNA expression profiles associated with the progression from ovarian EMS, TL and ECOC provide valuable insights into the molecular progression from benign to malignant lesions and could represent potential biomarkers for the early detection of ECOC.

SEPT9 methylation has been closely linked to breast cancer, yet its role in differentiating disease stages remains unclear. In particular, Few studies previously have examined differences in SEPT9 methylation between ductal carcinoma in situ (DCIS) and invasive ductal carcinoma (IDC), or among DCIS lesions of varying nuclear grades. This study investigated SEPT9 methylation across 105 breast cancer cases, classified into pure DCIS, DCIS with invasive components (DCIS-INV), IDC alone, and metastatic breast cancer (MBC). Methylation levels were measured using real-time PCR, and in vitro experiments were conducted using MCF-7 and T47D cell lines treated with decitabine to explore the relationship between methylation and microtubule stability. SEPT9 methylation was significantly elevated in cancer cells compared to normal breast epithelium, with positivity rates of 90.6% in DCIS-INV, 77.8% in IDC, and 79.2% in MBC, versus only 18.2% in pure DCIS. SEPT9 methylation was negtive in low-grade DCIS and positive in 28.6% of intermediate- to high-grade cases. Positive methylation was significantly associated with high Ki-67 expression and lymph node metastasis (P < 0.05), but showed no correlation with age, menopausal status, tumor size, or hormone receptor status. Additionally, decitabine treatment induced a reduction in SEPT9 methylation levels, which affects microtubule stability, suggesting a potential mechanistic link to tumor invasion. These findings indicate that SEPT9 methylation is a promising biomarker for distinguishing invasive breast cancer from DCIS and for identifying high-risk DCIS lesions with greater potential for progression.