This study is based on using a novel sex-structured mathematical model to assess the effectiveness of vaccination and Pap screening against HPV and related cancers in South Korea. In addition to its disease-free equilibrium (DFE) being locally-asymptotically stable when the associated control reproduction number is less than one, the model could have one or three endemic equilibria, for a special case with negligible disease-induced mortality, if the reproduction number exceeds one. It's shown, using a Krasnoselskii sublinearity argument, that this special case has a unique and locally-asymptotically stable endemic equilibrium, when the reproduction number is larger than one, if, additionally, the HPV vaccine is assumed to be perfect. The DFE of a simplified version of the model, which is calibrated using HPV-related cancer data in Korea, is globally-asymptotically stable when its reproduction number is less than one. Simulations of the full model showed that, although vaccine-derived herd immunity (needed for HPV elimination) cannot be achieved in Korea under the current vaccination coverage of females (of 88%), it can be achieved if, additionally, at least 65% of males are vaccinated at steady-state. While the current combined vaccination-screening strategy (termed Strategy A) will fail to eliminate HPV, extended strategies that include increased coverage of female vaccination (termed Strategy B) or additionally vaccinating boys (termed Strategy C) could lead to such elimination in Korea. The implementation of boys-only vaccination strategy induces a significant spillover benefit in reducing cervical cancer burden, which exceeds the corresponding spillover benefit achieved by implementing a girls-only vaccination strategy.

Epigenetic regulation is a fundamental mechanism controlling gene expression and cellular function, primarily mediated through reversible modifications such as DNA methylation, histone acetylation, and chromatin remodeling. Dysregulation of critical epigenetic enzymes, including histone deacetylases (HDACs), DNA methyltransferases (DNMTs), and bromodomain and extraterminal domain (BET) proteins, has been closely associated with tumor initiation, progression, metastasis, immune evasion, and resistance to conventional therapies. Targeting these epigenetic regulators with small-molecule inhibitors or degraders has emerged as a promising therapeutic strategy, capable of reprogramming aberrant transcriptional networks and reshaping the tumor microenvironment. Beyond direct cytotoxic effects, epigenetic drugs have demonstrated the ability to enhance antitumor immunity by restoring antigen presentation, promoting immunogenic cell death, modulating cytokine profiles, and reversing local immune suppression. Recent preclinical and clinical studies have highlighted the potential of combining epigenetic therapies with immune checkpoint inhibitors to achieve synergistic antitumor responses and overcome resistance mechanisms. This review provides a comprehensive summary of the mechanisms of action, pharmacological characteristics, and clinical applications of epigenetic drugs, with a focus on innovative combination strategies and ongoing translational advancements. We also discuss future directions, emphasizing the need to improve drug specificity, minimize off-target effects, integrate personalized immunotherapeutic approaches, and identify predictive biomarkers to optimize patient selection and clinical outcomes. Overall, epigenetic therapy represents a versatile and evolving avenue for precision oncology with broad implications for tumor control and immunomodulation.

Lung cancer remains a leading cause of cancer-related mortality worldwide. Cuproptosis, a new form of programmed cell death, is emerging as a key regulator in tumor progression. In this review, we talk about the interplay between cuproptosis, non-coding RNAs (ncRNAs), and epigenetic modifications in lung cancer. We performed an extensive review of recent literature to explore the function of ncRNAs in the regulation of cuproptosis, their effects on tumor microenvironment remodeling, immune response regulation, and drug sensitivity. ncRNAs were found to modulate cuproptosis by influencing copper metabolism, apoptosis, and oxidative stress response. Specific ncRNA signatures possess prognostic biomarker and therapeutic target potential in lung cancer. In addition, ncRNA-mediated epigenetic regulation has significant influence on deciding lung cancer formation and treatment outcome. The integration of non-coding RNAs related to cuproptosis into therapies offers great promise for the improvement of lung cancer prognosis. Further studies are needed to validate these findings and promote their implementation in clinical practice.

Receptor-interacting serine/threonine-protein kinase 1 (RIPK1) is crucial in regulating inflammation, apoptosis, and necroptosis. Accumulating evidence highlights RIPK1 as a promising therapeutic target for various human diseases, including neurodegenerative disorders, autoimmune diseases, and cancer. In tumour cells, RIPK1 suppresses immunogenic cell death, promotes an immunosuppressive tumour microenvironment, which facilitates immune evasion, metastatic progression, and therapeutic resistance, contributing to an immunologically cold tumour phenotype. Therefore, targeting RIPK1 represents a promising therapeutic approach to overcome immune checkpoint blockade resistance and convert tumours into an immunologically hot phenotype. In this review, we summarise the biological functions of RIPK1 and elaborate on its roles in cancer progression in terms of the tumour immune microenvironment, tumour metastasis, and chemoresistance. Furthermore, we enumerate several identified RIPK1-targeted inhibitors with potential for cancer therapy. Although RIPK1 has been proposed as a potential anticancer target, there are still great opportunities and challenges that require further investigation.

Sonodynamic therapy (SDT) has emerged as a promising approach for treating hepatocellular carcinoma (HCC) by combining sonosensitizers with low-intensity ultrasound. However, SDT alone could not achieve satisfactory results. Here, we developed novel nanobubbles loaded with hematoporphyrin monomethyl ether (HMME@NBs) and evaluated its therapeutic potential in combination with the glycolytic inhibitor lonidamine (LND) against HCC. The HMME@NBs was successfully prepared with particle size of 410.58 ± 20.07 nm and zeta potential at -8.38 ± 1.12mV. The encapsulation efficiency and loading efficiency of HMME was 80.6% and 7.12%, respectively. Both in vitro and in vivo studies demonstrated that while SDT and LND monotherapies inhibited the growth of HepG2 cells and xenograft tumors in nude mice, the combination therapy exhibited the most significant inhibitory effect. Multi-omics analysis of tumor tissues revealed substantial alterations in metabolites and gene expression, with key pathways such as glutathione metabolism implicated in the treatment response. Our findings highlight the enhanced antitumor efficacy of HMME@NBs-mediated SDT combined with LND, supported by mechanistic insights from transcriptomic and metabolomic profiling. This synergistic strategy holds great potential for HCC treatment.

Paragangliomas are rare neuroendocrine tumors originating from extra-adrenal chromaffin tissue. Their clinical manifestations are variable, often depending on the tumor's size, location, and catecholamine secretion. While most functional paragangliomas present with hypertension, a small subset can remain normotensive, making diagnosis more challenging.

We report the case of a 45-year-old woman with no notable medical history, who presented with vague abdominal discomfort and episodic palpitations. Notably, she exhibited no documented hypertension. Biochemical evaluation revealed markedly elevated urinary normetanephrines. Cross-sectional imaging identified a 4.5 cm para-aortic mass, which was further confirmed by ^123I-MIBG scintigraphy. After adequate preoperative alpha- and beta-blockade, she underwent open surgical resection. Histopathological analysis confirmed paraganglioma, demonstrating characteristic zellballen architecture and immunohistochemical positivity for chromogranin A, synaptophysin, and S100. Her postoperative recovery was uneventful. At 12-month follow-up, she remained asymptomatic with normal catecholamine levels and no signs of recurrence. Genetic testing was offered but declined.

This case emphasizes the diagnostic difficulty posed by normotensive functional paragangliomas, which may be overlooked in the absence of classical hypertension. Biochemical screening and functional imaging are crucial even in atypical presentations. Preoperative pharmacologic preparation and expert surgical management are key to minimizing intraoperative risk and ensuring favorable outcomes.

Clinicians should maintain a high index of suspicion for paragangliomas in patients with suggestive symptoms, regardless of blood pressure status. A multidisciplinary approach and long-term follow-up are vital, particularly for extra-adrenal tumors, with consideration of genetic counselling in all cases.

Burkitt lymphoma (BL) is a rapidly progressing tumor that requires urgent diagnosis and treatment. It is the first human neoplasm linked to a viral cause and is classified into three subtypes: sporadic, endemic, and immunodeficiency-associated.

We report a rare case of a 5-year-old boy who presented to the Oral and Maxillofacial Surgery Department with a two-month history of bilateral maxillary swelling and pain. He had no significant medical history. An incisional biopsy confirmed the diagnosis of Burkitt's lymphoma. The patient underwent chemotherapy following the R-COPADM protocol. Despite stage III diffuse lymph node involvement, treatment was successful.

Oral and maxillofacial involvement of BL in pediatric patients are extremely rare, with an estimated prevalence of 0.5 % to 6 %. In this case, the disease extended beyond the jaws to involve the maxillary sinuses, orbit, and zygomatic bone. Histologically, the classic "starry-sky" pattern was notable in most tissue sections.

This case highlights the importance of early recognition and prompt multidisciplinary intervention in pediatric Burkitt lymphoma to prevent widespread disease progression and improve survival outcomes.

High endothelial venules (HEVs) are specialized blood vessels found primarily in lymphoid tissues, notably at the cortico-paracortical junction of lymph nodes (LNs). They play a key role in lymphocyte trafficking, facilitating the entry of lymphocytes into peripheral lymphoid organs.

Recent evidence indicates the presence of HEVs within tumor tissues, where they form part of tertiary lymphoid structures. This review aims to explore the structural and functional alterations of HEVs in tumors and LNs, and investigate their role in cancer prognosis and response to immunotherapy.

We conducted a comprehensive review of recent studies examining HEVs in tumors and LNs, with a focus on their involvement in immune responses and cancer progression. Additionally, the use of MECA-79 as a specific HEV marker was considered as a potential therapeutic target.

HEVs within tumors have been associated with improved immune surveillance and better prognosis in certain cancers. The presence of HEVs in tumors correlates with enhanced immune cell infiltration and may influence the effectiveness of immunotherapy treatments. Targeting HEVs, particularly through MECA-79, holds promise as a novel therapeutic strategy to modulate tumor immunity.

Targeting HEVs in tumor tissues represents a promising avenue for cancer therapy. Further research is needed to optimize strategies for modulating HEV function and to better understand their role in immune responses to cancer.

The human immune system has evolved to interact with various commensal and pathogenic bacteria in intricate and nuanced ways. While the diversity of bacteria presents fundamental challenges in understanding immune-microbe interactions, it also offers ample opportunities for developing effective immunomodulatory therapies. Here we show microbial product cocktails as an alternative class of immunotherapy for cancer. Using freshly resected tumors from bladder cancer patients, an immuno-comparative analysis of recruitment and enhancement assay, and an artificial intelligence-guided optimization workflow, we establish a personalized platform for identifying potent microbial product cocktails that promote recruitment, infiltration, and activation of immune cells for cancer treatment. In an orthotopic mouse bladder cancer model, microbial product cocktails demonstrate immunoenhancement and improve survival rates compared with standard bacillus Calmette-Guérin immunotherapy.

Metabolic reprogramming plays a critical role in the initiation and progression of skin cutaneous melanoma (SKCM). This study aims to construct a prognostic model based on metabolic-related genes (MRGs) to forecast patient outcomes and their response to immunotherapy. 10 machine learning algorithms within a cross-validation framework were utilized to compute prognostic risk scores based on MRGs, dividing SKCM patients into high- and low-risk groups. Further exploration included immune-related scores, immune infiltration levels, and oncological phenotype between these groups. The expression levels of six essential MRGs were assessed, and the effect of GALNT2 on proliferation and migration in SKCM cell lines was confirmed. This study has developed a new MRGs prognostic risk model that effectively predicts the survival of melanoma patients. The low-risk group exhibits higher immune scores and immune cell infiltration, which are beneficial for immunotherapy. In contrast, the high-risk group is positively correlated with the malignant phenotype of tumors, with increased MRG expression promoting tumor development. The study also identified six key genes, among which both the silencing and overexpression of GALNT2 significantly affect the proliferation and migration of melanoma cells. This study highlights the significance of MRGs in predicting patient survival and immunotherapy outcomes, providing insights for potential future targeted therapies.