World journal of clinical oncology最新文献

Background: Rectal cancer management is currently evolving with the advent of different neoadjuvant treatment strategies and organ preservation strategies. A significant proportion of patients could achieve complete clinical response after neoadjuvant treatment, which often translates to pathologic complete response (pCR) as assessed on surgical specimens after curative intent surgery. Endoscopy plays a significant role in assessing treatment response to neoadjuvant therapies.

Aim: To explore the role of endoscopy in predicting subsequent pCR after neoadjuvant treatment in rectal cancer patients.

Methods: An extensive literature review was undertaken to identify the criteria used for assessment of endoscopic response and their ability to predict pCR.

Results: Fifteen studies were identified through literature review. The most commonly used endoscopic criteria for evaluation included the presence of a flat white scar and the absence of nodularity or telangiectasia. Information on the timing of endoscopic assessment in relation to neoadjuvant treatment protocols were also extracted from the studies. In most studies, the diagnostic accuracy for predicting pCR exceeded 0.8. The main limitations identified were the retrospective design of included studies included and a moderate risk of bias.

Conclusion: Endoscopy can be a key prognostic factor in predicting pCR to neoadjuvant treatment in rectal cancer despite significant limitations in currently available data.

Background: Although chronic-phase chronic myeloid leukemia (CP-CML) is treatable and nearly curable in about 50% of patients, accelerated-phase chronic myeloid leukemia (AP-CML) shows concerning drug resistance, while blast crisis chronic myeloid leukemia (BC-CML) is highly lethal. Advances in whole exome sequencing (WES) reveal pan-cancer mutations in BC-CML, supporting mutation-guided therapies beyond Breakpoint cluster region-Abelson. Artificial intelligence (AI) and machine learning (ML) enable genomic stratification and drug repurposing, addressing overlooked actionable mutations.

Aim: To stratify BC-CML into molecular subtypes using WES, ML, and AI for precision drug repurposing.

Methods: Included 123 CML patients (111 CP-CML, 5 AP-CML, 7 BC-CML). WES identified pan-cancer mutations. Variants annotated via Ensembl Variant Effect Predictor and Catalogue of Somatic Mutations in Cancer (COSMIC). ML (principal component analysis, K-means) stratified BC-CML. COSMIC signatures and PanDrugs prioritized drugs. Analysis of variance/Kruskal-Wallis validated differences (P < 0.05).

Results: In this exploratory, hypothesis-generating study of BC-CML patients (n = 7), we detected over 2500 somatic mutations. ML identified three BC-CML clusters: (1) Cluster 1 [breast cancer susceptibility gene 2 (BRCA2), TP53]; (2) Cluster 2 [isocitrate dehydrogenase (IDH) 1/2, ten-eleven translocation 2]; and (3) Cluster 3 [Janus kinase (JAK) 2, colony-stimulating factor 3 receptor], with distinct COSMIC signatures. Therapies: (1) Polyadenosine-diphosphate-ribose polymerase inhibitors (olaparib); (2) IDH inhibitors (ivosidenib); and (3) JAK inhibitors (ruxolitinib). Mutational burden, signatures, and targets varied significantly across clusters, supporting precision stratification.

Conclusion: This WES-AI-ML framework provides mutation-guided therapies for BC-CML, enabling real-time stratification and Food and Drug Administration-approved drug repurposing. While this exploratory study is limited by its small sample size (n = 7), it establishes a methodological framework for precision oncology stratification that warrants validation in larger, multi-center cohorts.

Neurotransmitter-mediated regulation plays a multi-dimensional role in the tumor microenvironment, profoundly influencing key processes such as tumor immune evasion, metabolic reprogramming, and metastasis. However, the upstream regulatory mechanisms linking neural inputs to immune evasion and metabolic reprogramming remain incompletely understood. We systematically summarize current evidence from molecular, cellular, and immunological studies to elucidate how neurotransmitter-dependent mechanisms drive dynamic changes in the tumor microenvironment through the regulation of tumor cells and immune cells, and map the complex interaction networks between the nervous system and tumor progression. We propose a unifying "neuro-metabolic-immune axis" framework that highlights the dual role of neurotransmitters in suppressing anti-tumor immunity and facilitating tumor adaptation. By mapping this axis, we reveal new insights into tumor ecology and identify neural pathways as promising therapeutic targets. Targeting these pathways may enhance immunotherapy and disrupt tumor-supportive metabolism, offering new directions in precision oncology.

Cancer rehabilitation is a critical component of comprehensive cancer care, aiming to improve the quality of life for cancer survivors by addressing physical, psychological, and social challenges following treatment. In India, with rising cancer incidence and a growing survivor population, the need for effective rehabilitation services is more pronounced than ever. However, despite significant progress in cancer treatment, rehabilitation remains an underdeveloped and underutilized area of care in the country. This mini-review explores the current status of cancer rehabilitation in India, highlighting existing gaps in healthcare infrastructure, access, and awareness. It examines the scope of rehabilitation services-including physical therapy, psychosocial support, palliative care, and vocational rehabilitation-and identifies regional variations in service availability. Furthermore, the mini-review outlines challenges faced by healthcare providers, such as a shortage of trained professionals, limited funding, and cultural stigmas surrounding cancer. Future perspectives on cancer rehabilitation in India emphasize the need for policy reforms, integration of rehabilitation into national cancer care programs, and promotion of multidisciplinary care teams. The article concludes with recommendations for expanding cancer rehabilitation services to meet the evolving needs of survivors and to enhance their long-term well-being in India.

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.