World journal of clinical oncology最新文献

Gastric cancer (GC) remains a major health challenge worldwide, with Helicobacter pylori (H. pylori) infection playing a key role in its development. H. pylori creates a mutagenic environment in the stomach by causing chronic inflammation, oxidative DNA damage, inducing DNA double-strand breaks, and disrupting DNA repair mechanisms and cell cycle checkpoints. Cytotoxin-associated gene A is the main carcinogenic component of H. pylori and interacts with signaling pathways to promote carcinogenesis. Deleted in malignant brain tumors 1 (DMBT1), a potential tumor suppressor gene, shows variable expression patterns in GC. DMBT1 is frequently downregulated in well-differentiated gastric adenocarcinomas but upregulated in other GC types. The correlation between DMBT1 expression and H. pylori infection is important, as maintained DMBT1 expression in precancerous states may protect against gastric carcinogenesis, while its downregulation may facilitate tumor progression. DMBT1 functions as a pattern recognition receptor that binds to H. pylori and other pathogens and modulates inflammatory and immune responses. H. pylori colonization of gastric mucosa can induce an inflammatory microenvironment, which influences tumor suppressor gene expression, including DMBT1. Understanding the interactions between DMBT1 and H. pylori may reveal new therapeutic targets and preventive strategies for H. pylori-associated gastric disease.

Background: Internal mammary (IM) lymphadenopathies in breast cancer indicate a worse prognosis than axillary metastases, yet they are rarely assessed. Accurate staging is essential for treatment planning. Robotic biopsy offers a promising alternative to video-assisted thoracic surgery for precise histological sampling. This article outlines a systematic robot-assisted dissection approach to enhance staging accuracy and optimize breast cancer management.

Case summary: At our institution, robotic lymphadenectomy of the IM chain was performed in 5 patients between July 2020 and December 2024. Patients were positioned in a 30° semi-supine position with a roll under the shoulder to elevate the chest. The camera port was inserted in the fifth intercostal space along the mid-axillary line, allowing a 0°, 12 mm robotic camera to inspect the chest cavity; CO₂ insufflation (8 L/minute, 8-10 mmHg) facilitated lung collapse and pneumo-mediastinum formation for improved dissection. Under direct vision, two additional operative ports were placed: One in the third intercostal space (anterior axillary line) and another in the fifth intercostal space (3-4 cm lateral to the parasternal line). The mean operative time was 118 minutes, with a median hospital stay of two days. No major complications occurred. Histology confirmed breast carcinoma metastases in three patients, while two had benign disease.

Conclusion: Robotic biopsy of IM lymph nodes is safe, feasible, and provides key information on breast cancer management, with very rare contraindications.

The γδT cells are an emerging class of immune effectors with potent antitumor activity, bridging innate and adaptive immunity. Their unique ability to recognise stress-induced ligands independently of major histocompatibility complex restriction makes them attractive candidates for cancer immunotherapy. However, the clinical application of γδT cells requires efficient in vitro expansion strategies to generate large numbers of functional cells. This mini-review explores the latest advancements in γδT cell expansion protocols, focusing on key activation stimuli, cytokine support, and culture conditions that optimise proliferation and cytotoxicity.

Background: Krüppel-like factor-5 (KLF5) is a zinc-finger transcription factor related to tumor progression. However, the relationship between KLF5 and lung cancer remains to be identified.

Aim: To investigate the clinical value of KLF5 and interference with KLF5 mRNA transcription on the effects of biological behaviors in lung squamous-cell carcinoma (LUSC).

Methods: Lung KLF5 mRNA data were extracted from bioinformatics databases. Blood and tissues from a cohort of patients with benign or malignant lung diseases were collected with ethical committee consent to validate KLF5 expression via multiplex immunofluorescence and immunohistochemistry, Western blot, Enzyme-Linked Immunosorbent Assay or quantitative polymerase chain reaction. Furthermore, KLF5 mRNA was silenced in lung A549 cells to validate biological behaviors in vitro and nude mouse xenograft growth in vivo, respectively.

Results: A cohort of bioinformatics databases revealed high KLF5 mRNA expression in LUSC (P < 0.001) but lower KLF5 mRNA expression in lung adenocarcinoma. Upregulated KLF5 in the lung or sera of patients with lung cancer (P < 0.001) were confirmed that related to poor differentiation, lymph node or distant metastasis. Furthermore, the incidence of KLF5 levels greater than 500 ng/mL in LUSC patients was 86.7%, which was significantly greater (P < 0.001) than that in cases with benign lung diseases (13.3%) or healthy controls. Functionally, silencing KLF5 mRNA with a specific shRNA significantly suppressed A549 cell proliferation, decreased cell migration, increased the ratio of G2 phase cells in vitro, and inhibited the growth of nude mouse xenografts in vivo.

Conclusion: KLF5 is a novel diagnostic biomarker or potential therapeutic target for LUSC.

Background: Polycythemia vera (PV) is a myeloproliferative neoplasm characterized by excessive blood cell production, which increases the risk of thrombosis. Ropeginterferon alfa-2b (RI) offers potential advantages over standard therapy (ST; including phlebotomy, hydroxyurea, and aspirin) by achieving hematologic and molecular responses. However, its comparative efficacy and safety remain understudied. We hypothesized that RI would improve hematologic and molecular outcomes but may differ in safety profiles compared to ST.

Aim: To evaluate the efficacy and safety of RI vs ST in patients with PV, focusing on hematologic response, molecular response, adverse events (AEs), and thrombotic risk.

Methods: This Preferred Reporting Items for Systematic Reviews and Meta-Analyses-compliant meta-analysis included randomized controlled trials comparing RI to ST in adult PV patients. PubMed, EMBASE, ClinicalTrials.gov, and ScienceDirect were searched from inception to July 2025. Outcomes included complete hematological response (CHR), molecular response, AEs leading to discontinuation, JAK2V617F allele burden, thrombotic events, and phlebotomy frequency. Pooled odds ratios (ORs) and MD with 95% confidence intervals (95%CIs) were calculated using random-effects models. Risk of bias was assessed with Cochrane RoB 2; evidence certainty was evaluated via GRADE.

Results: Five studies involving 477 RI and 456 ST patients were included. RI significantly improved CHR (OR = 2.14, 95%CI: 1.18-3.88, P = 0.002) and molecular response (OR = 4.37, 95%CI: 0.99-19.38, P = 0.05), with substantial heterogeneity (I² = 76% and I² = 93%, respectively). AEs leading to discontinuation were higher with RI (OR = 3.89, 95%CI: 1.90-7.97, P = 0.0002; I² = 0%). No significant differences were observed in JAK2V617F allele burden (MD = -7.46, 95%CI: -21.12 to 6.20, P = 0.28; I² = 90%) or thrombotic events (OR = 0.93, 95%CI: 0.45-1.90, P = 0.83; I² = 0%). RI reduced phlebotomy frequency (MD = -1.52, 95%CI: -2.37 to -0.67, P = 0.0005; I² = 0%). Most studies had low to moderate risk of bias; evidence certainty was moderate for CHR and AEs, low for molecular response and thrombotic events, and very low for allele burden.

Conclusion: RI offers superior hematologic and molecular responses compared to ST in PV but is associated with higher discontinuation rates due to AEs. Comparable thrombotic risk and reduced phlebotomy needs highlight its potential, though tolerability requires careful management. The high heterogeneity in certain outcomes and potential for publication bias warrant cautious interpretation of these findings. Further long-term studies are needed to optimize dosing and patient selection.

Catalase (CAT) is a kind of tetrameric protein in the human body, play as a key regulator for controlling oxidative stress. The main function of CAT is to regulate the concentration of hydrogen peroxide (H₂O₂) by catalyzing the decomposition of H₂O₂. At present, it is reported that CAT is also involved in regulating the oxidative stress in tumor cells, and its expression level is significantly related to the development of breast cancer (BC). In addition, CAT with different expression patterns, was related in the proliferation, invasion, treatment and prognosis of BC cells. Meanwhile, BC is a common and well-known cancer among women worldwide, and its incidence has been increasing in recent years. Therefore, in-depth study of CAT in the pathogenesis and progression of BC is of great significance for the future treatment and diagnosis. The present review summarized the effects of oxidative stress on cancer cells, and emphasized the key role of CAT in the development of BC, which provides a key clue for promoting research on BC and selecting therapeutic targets.

Gastric carcinoma (GC) is one of the most common and deadly cancers worldwide, ranking fifth in incidence and third in cancer-related mortality. Despite significant advancements in surgical techniques and chemotherapy, the overall prognosis for GC remains poor, primarily due to late-stage diagnosis. Current diagnostic tools, such as endoscopy and biopsy, are invasive and are often utilized only after symptoms arise, leading to missed opportunities for early intervention. Traditional serum tumour markers, such as carcinoembryonic antigen and carbohydrate antigen 19-9, demonstrate limited sensitivity and specificity, particularly in the disease's early stages. GC often diagnosed at advanced stages due to a lack of early, specific biomarkers. Chronic inflammation plays a significant role in gastric carcinogenesis, particularly in cases of Helicobacter pylori-associated gastritis. Pro-inflammatory cytokines have gained attention as potential non-invasive serum biomarkers for early diagnosis and disease monitoring. In recent years, numerous studies have explored the potential of serum cytokines-such as interleukin (IL)-6, tumour necrosis factor-alpha, IL-8 and interferon-gamma-as biomarkers for detecting gastric cancer. Future research integrating cytokine profiling with imaging, endoscopic, or genomic data may revolutionize how we screen and manage GC.

Gastrointestinal malignancies, particularly pancreatobiliary and gastroesophageal cancers, are associated with poor prognosis due to their frequent late-stage diagnosis. Many of these tumors contribute to anorexia-cachexia syndrome and malnutrition, further exacerbating disease progression. Inflammation plays a crucial role in tumor proliferation, and growing evidence suggests that gut microbiome significantly influence inflammatory responses and clinical outcomes in these patients. Additionally, the gut microbiome contributes to carcinogenesis through multiple mechanisms, including DNA damage, activation of oncogenic pathways, and modulation of immune responses. The emerging field of nutritional interventions highlight the microbiome's impact on anticancer drug responses, affecting both chemotherapy and molecular-targeted treatments. Given its pivotal role, microbiome modulation through probiotics, fecal microbiome transplantation, and antibiotics represents a promising approach for cancer prevention and treatment. In this review, we explore the intricate interplay between gut microbiome, inflammation, and nutritional status in gastrointestinal cancers, emphasizing potential therapeutic strategies to improve patient outcomes.

Melanoma is an aggressive type of skin cancer notorious for its resistance to chemotherapy, radiotherapy and immunotherapy, which greatly impacts its lethality. The hedgehog (HH) signaling cascade, originally known for its roles in embryonic development, regulates growth, proliferation and cancer stem cell (CSC) self-renewal. The glioma-associated oncogene homolog (GLI) transcription factors play crucial roles in melanoma. However, oncogenic B-Raf proto-oncogene, serine/threonine kinase (BRAF) steals the spotlight by driving the aberrant activation of HH-GLI1/2 signaling. Oncogenic BRAF-driven HH-GLI1/2 signaling imparts invasive phenotype to melanoma cells and sustains CSC self-renewal. Interestingly, the transcriptional activities of GLI1 and GLI2 are suppressed by acetylation, a process that is counteracted by the deacetylating actions of histone deacetylase (HDAC) 1/2. Therefore, inhibiting HDAC1/2 might keep GLI proteins in inactive acetylated form, thus representing an attractive druggable target. Notably, both HDAC1 and HDAC2 are induced by HH signaling, creating a positive feedback loop where HH signaling upregulates the expression of both HDAC1 and HDAC2. Selective inhibition of BRAF/HH/HDAC/GLI signaling axis is likely to unravel new therapeutic opportunities in melanoma. However, the precise contribution of oncogenic BRAF-driven HH signaling to therapy resistance and CSC renewal remains unclear and requires thorough investigation. In this article, we endeavored to explore the crosstalk between oncogenic BRAF and HH signaling, and the pivotal role this interaction plays in the self-renewal of melanoma stem cells. A better understanding of the molecular mechanisms governing these interactions is essential for improving melanoma treatment strategies and identifying new therapeutic targets.

The urgent necessity for enhanced risk stratification to improve the efficiency of colonoscopy screening is underscored by the fact that colorectal cancer (CRC) continues to be a primary cause of global cancer mortality. Conventional models mostly rely on generalized obesity markers including body mass index (BMI), which does not effectively represent oncogenic risk linked with abdominal obesity. Liu et al undertook a large-scale case-control study comprising 6484 first-time colonoscopy patients at a prominent Chinese hospital between 2020 and 2023 to overcome this restriction. Age, male sex, smoking status, and raised waist-hip ratio (WHR) were found by multivariate logistic regression as independent predictors of advanced colorectal neoplasia (ACN). In a validation cohort of 1891 individuals, a new 7-point risk scoring model was created and stratified into low- (5.0%) ACN prevalence, moderate- (10.3%) and high-risk (17.6%). With C-statistic = 0.66 the model showed better discriminating ability than the Asia-Pacific Colorectal Screening (APCS) score (C-statistic = 0.63) and the BMI-modified APCS model. These results fit newly published data showing central obesity as a major carcinogenic driver via pro-inflammatory visceral adipokine channels. With the use of WHR, patient risk classification is greatly improved, providing a practical tool to make the most of screening resources in the face of rising CRC incidence rates. Finally, multi-ethnic validation is necessary for the WHR-based scoring model to be considered for integration into global CRC preventive frameworks, since it improves the accuracy of ACN risk prediction.