Discover. Oncology最新文献

Purpose: In colon cancer patients with tumor-associated inflammatory adhesions (TAIA), the preoperative clinical staging is cT4b, but postoperative pathology reveals that the tumor has not invaded surrounding organs (non-pT4b). We aimed to investigate the impact of TAIA on prognosis and treatment strategies for colon cancer patients.

Methods: Colon cancer patients from the Surveillance, Epidemiology, and End Results (SEER) database (2010 to 2019) and Chinese multicenter cohort were included to compare survival differences between the TAIA and non-TAIA groups. A Cox proportional hazards model was used to evaluate independent risk factors for survival in colon cancer patients. Additionally, we analyzed the impact of adjuvant chemotherapy on survival in TAIA patients.

Results: A total of 112,659 colon cancer patients from the SEER database and 881 colon cancer patients from the Chinese database were included in this study. After PSM, both cohorts found that patients in the TAIA group exhibited worse overall survival (P < 0.05) and cancer-specific survival (P < 0.05). Additionally, the Cox multivariate proportional hazards model identified TAIA as an independent risk factor for cancer-specific survival in colon cancer patients (SEER: HR 1.45, 95% CI: 1.40-1.50, P < 0.001; China: HR 2.108, 95% CI: 1.473-3.015, P < 0.001). Subsequently, 36,496 TAIA patients from the SEER database and 229 TAIA patients from a Chinese multicenter database were independently divided into adjuvant chemotherapy and control groups. After PSM, both databases indicated better survival in the adjuvant chemotherapy group.

Conclusion: Colon cancer patients with TAIA have a poorer prognosis. Adjuvant chemotherapy can improve the prognosis of TAIA patients.

This case report describes a 37-year-old female with a history of cesarean section and uterine leiomyoma resection, who presented with recurrent dyspnea and palpitations. Echocardiography revealed a hyperechoic, mobile mass (3.9 × 2.2 cm) in the right atrium (RA) extending into the inferior vena cava (IVC), accompanied by global cardiomegaly, severe tricuspid regurgitation, and mildly reduced left ventricular function. Elevated tumor markers (CA125, CA199, CA50) and NT-proBNP were noted. Transvaginal ultrasound identified a large pelvic mass, while PET-CT demonstrated multiple pulmonary and pelvic lesions with mild FDG uptake, suggestive of benign intravascular leiomyomatosis with metastases. Pathological biopsy of pulmonary and pelvic lesions confirmed smooth muscle-derived tumors consistent with leiomyoma, supported by immunohistochemistry (SMA+, Desmin+, h-caldesmon+). This case highlights the characteristic ultrasonographic features and underscores the importance of a multidisciplinary diagnostic approach for intravascular leiomyomatosis involving cardiac structures.

This case report describes an adult with high-risk DLBCL (IPI score 4) treated with R-CHOP combined with JK5G and JK21 postbiotics for gut microbiome modulation. The patient achieved significant tumor regression while maintaining stable hematological parameters. Microbial analysis demonstrated enrichment of beneficial genera (Veillonella, Bacteroides, Roseburia), potentially linked to postbiotic intervention. Notably, the regimen exhibited excellent tolerability without leukopenia or severe toxicities, suggesting postbiotics may enhance chemotherapy efficacy through microbiome-immune interactions while mitigating adverse effects. These findings warrant further investigation into postbiotics as adjuvant therapy for optimizing DLBCL treatment outcomes.

Background: Lung cancer is the most prevalent tumor and frequently present with distant metastases, with the bone being one of the most common affected sites. However, bone metastases leading to complete resorption of the hip joint and pelvis are extremely rare. This case aimed to report an extensive destruction of the hip and pelvis in metastatic lung adenocarcinoma, and conduct a literature review to explore the factors influencing the diagnosis and treatment decisions of bone metastasis.

Case presentation: A 56-year-old woman presented with progressive pain in her left hip joint and pelvis accompanied by impaired mobility for over one year. X-ray and computed tomography (CT) scan of left hip joint and pelvis showed extensive bone metastasis. A chest X-ray displayed disorganized lung texture in both lungs and multiple bilateral lung nodules of variable sizes. Surgical biopsy of the left iliac bone and histology examination indicated bone metastasis originating from lung adenocarcinoma, which was confirmed using immunohistochemical analysis. Due to multiple extensive metastases throughout the body, the patient was treated conservatively. Targeted therapy with almonertinib mesilate was administered; however, and the patient eventually passed away one week later.

Conclusion: Early detection of bone metastasis and identification of the original tumor are crucial, especially when the symptoms are subtle or nonspecific. Delayed diagnosis can lead to extensive skeletal destruction, loss of function, and poor prognosis. A comprehensive diagnostic approach integrating thorough physical examination, advanced imaging modalities, and pathological analysis is essential for timely and accurate diagnosis. An optimal management requires a personalized, multidisciplinary treatment strategy that considers the patient's overall condition, the molecular profile of the primary tumor, and the anatomical complexity of the metastatic site.

Background: Lung cancer is one of the malignant tumors with high morbidity and mortality worldwide. Nuclear factor E2-ralated factor 2 (Nrf2), a critical antioxidant transcription factor, has been identified to play a significant role in the pathogenesis, progression and chemoresistance of lung cancer through its dysregulated activation. The present investigation sought to enhance our understanding of the global research landscape concerning Nrf2 in lung cancer by employing a bibliometric methodology.

Methods: The present study retrieved relevant articles and reviews concerning Nrf2 in lung cancer from the Web of Science Core Collection and Scopus databases. A comprehensive bibliometric analysis was conducted utilizing a suite of tools including Microsoft Excel, Python, CiteSpace, VOSviewer, R (bibliometrix), and Charticulator to evaluate various aspects such as publication productivity, contributing nations, affiliated institutions, prominent authors, influential journals, co-cited references, and thematic keywords.

Results: The study encompassed 1931 publications, showing a marked rise in citations from 2002 to 2025. China dominated the publication landscape, with several leading institutions contributing. Professors Masayuki Yamamoto and Shyam Biswal were identified as key contributors. Cancer Research was the most prolific journal. Nrf2 played a central role in lung cancer research, with research hotspots evolving from basic studies to clinical treatment strategies and increasing interest in specific lung cancer subtypes, reflecting the multidimensional and interdisciplinary development of the field.

Conclusion: Research on Nrf2 in lung cancer has shifted from basic cell typing to studies of oxidation and programmed cell death, and it is time to dissect upstream regulators and create targeted Nrf2 modulators for personalized treatment.

Background: Immune checkpoint inhibitors (ICIs) therapy have significantly improved survival in cancer patients. However, immune-related adverse events (irAEs) have emerged as a major challenge limiting its therapeutic efficacy. Recent studies have demonstrated that certain immune cell phenotypes and metabolites may be associated with the risk of irAEs. Nevertheless, the precise biological mechanisms for this association remain poorly understood.

Methods: Using genetic variants from large-scale genome-wide association studies (GWAS), we employed two-sample mendelian randomization (MR) to systematically investigate causal relationships among 731 immune cell phenotypes, 1400 metabolites, and the risk of both all-grade and high-grade irAEs. A two-step MR method was employed to further analyze the mediating effects of key immune cell phenotypes and metabolites in irAEs. The inverse-variance weighted (IVW) method served as the primary approach to assess causal relationships, while Cochran's Q test, MR-Egger intercept test, MR-PRESSO, and leave-one-out analysis were employed to evaluate heterogeneity and horizontal pleiotropy.

Results: Our results found that metabolites mediate several causal pathways linking immune cell phenotypes to high-grade irAEs. Specifically, etiocholanolone glucuronide levels partially mediated the causal effect of CCR2 on monocyte in high-grade irAEs, with a mediation proportion of 0.0730 (95% CI 0.0032, 0.1428; P = 0.0403). Thymol sulfate levels partially mediated the causal effect of CD39 on monocyte in high-grade irAEs, with a mediation effect estimate of - 0.0321 (95% CI - 0.0621, - 0.0021; P = 0.0358). Our analysis identified putative associations for all-grade and high-grade irAEs with 10 and 11 immune cell phenotypes and causal relationships with 30 and 36 metabolites, respectively. Sensitivity analysis confirmed the robustness of these associations.

Conclusion: This study suggests causal relationships between immune cell phenotypes, metabolites and irAEs. Two metabolites that may act as potential mediating factors between immune cells and high-grade irAEs were identified. Of course, further investigation is warranted to validate these results.

Organoids, an emerging bioengineering approach, can replicate the structure and function of human organs in vitro, providing valuable tools for biomedical research. Patient-derived organoids (PDOs) retain the histological and genetic characteristics of the original tumor, playing a crucial role in precision oncology. Ultrasound-assisted technology, particularly multimodal ultrasound imaging, facilitates the establishment of PDOs for inoperable or rare tumors by enabling precise tumor localization, minimally invasive tissue sampling, and high-purity cell extraction.This review explores the application of multimodal ultrasound techniques in PDO development across various tumor types, highlighting their advantages in obtaining high-purity tumor cells, improving PDO culture success rates, and advancing personalized cancer treatment. Additionally, we discuss factors influencing PDO establishment, such as tumor type, sampling methods, and bioengineering advancements. By summarizing current progress and challenges, this review provides insights into optimizing ultrasound-assisted PDO construction for clinical and research applications.

Background: Collagen triple helix repeat containing 1 (CTHRC1) is an oncogene in numerous human cancers including oral squamous cell carcinoma (OSCC). However, whether and how CTHRC1 influences OSCC progression through ferroptosis has not been completely clarified.

Methods: qRT-PCR were conducted to assess CTHRC1 expression in OSCC. The proliferation of OSCC cells were assessed through 5-ethynyl-2'-deoxyuridine (EdU) assay, colony formation, and CCK-8 assays. Flow cytometry was used to analyze the apoptotic cells of OSCC cells. Ferroptosis was assessed based on the amounts of MDA, lipid ROS, intracellular Fe²⁺, and ferroptosis-related proteins. TGF-β/Smad pathway-related protein were detected by Western blot.

Results: Pronounced overexpression of CTHRC1 was observed in OSCC cell lines (SCC-9, CAL-27 and SCC-25). Knockdown CTHRC1 overtly inhibited cell proliferation but induced apoptosis in OSCC cells. Moreover, silencing of CTHRC1 could stimulate ferroptosis, as well as inhibit the activation of TGF-β/Smad pathway. Treatment with SRI-011381, a TGF-β/Smad pathway specific agonist, significantly reversed the promoting effect of CTHRC1 silencing on ferroptosis in OSCC cells.

Conclusions: Our findings indicate that knockdown of CTHRC1 stimulates ferroptosis in OSCC through inhibiting TGF-β/Smad pathway, which provides important experimental data and theoretical basis for the management, diagnosis, and treatment of OSCC.

Background: Nicotinamide adenine dinucleotide phosphate (NADPH) oxidase 2 (NOX2) plays a carcinogenic role in various tumors. Recent study has reported that the carcinogenic mechanism of NOX2 in esophageal squamous cell carcinoma (ESCC) may be associated with the regulation of B-cell translocation gene 2 (BTG2). This study aims to clarify the role of NOX2 in the progression of ESCC.

Materials and methods: NOX2 was knocked down in ESCC cell lines via siRNA transfection to assess its impact on cell function and BTG2 regulation. Tumor tissues from 66 ESCC patients were analyzed for NOX2 and BTG2 expression using immunohistochemistry to determine their clinical significance.

Results: NOX2 deficiency inhibited ESCC cell proliferation, promoted apoptosis, and caused G1 phase arrest. Following NOX2 knockdown, BTG2 mRNA expression significantly increased in TE1 and KYSE30 cells, and a notable rise in BTG2 protein expression was observed in KYSE30 cells. Immunohistochemical analysis revealed that NOX2 expression was significantly higher in tumor tissues compared to adjacent non-cancerous tissues, while BTG2 expression was markedly lower in tumor tissues. High NOX2 expression correlated with poor prognosis, whereas high BTG2 expression indicated better outcomes. Multivariate analysis indicated that abnormal NOX2 and BTG2 expressions are independent prognostic factors for ESCC.

Conclusion: The carcinogenic role of NOX2 in ESCC may be associated with the regulation of BTG2 expression. The aberrant expressions of NOX2 and BTG2 are associated with the prognosis of patients with ESCC, suggesting that NOX2 and BTG2 could serve as potential biomarkers and therapeutic targets.