Introduction

Computer-aided detection (CADe) systems have gained attention for their use in colonoscopy, with growing evidence of increased adenoma detection rates (ADR). However, results remain inconsistent, and debate regarding their usefulness continues, including their impact on serrated lesion (SL) detection and performance across varying levels of endoscopist expertise. Given that CADe is used as a real-time assistive tool, it is crucial to confirm its efficacy in lesion detection before considering long-term outcomes.

Aims & Methods

We conducted a multinational, multicenter randomized controlled trial in the Asia-Pacific (Project CAD/NCCH2217; jRCT1032230396) to assess the efficacy of CADe in improving lesion detection during colonoscopy performed as part of colorectal cancer (CRC) screening [1]. We enrolled asymptomatic individuals aged 50–79 years undergoing either primary screening colonoscopy or colonoscopy following a positive fecal immunochemical test (FIT), who had not received colonoscopy in the past 5 years. Participants were randomly assigned (1:1) to the CADe group (colonoscopy with CADe assistance) or the standard group (colonoscopy without CADe) using a minimization method to balance age, sex, colonoscopy indication, endoscopist experience, and country/region. In the CADe group, approved CADe devices were used in accordance with each country's regulations, including EndoBRAIN-EYE, ENDO-AID, CAD EYE, and WISE VISION. All procedures were performed by endoscopists with experience of ≥500 colonoscopies. The primary endpoint was adenoma detection rate (ADR). Secondary endpoints included adenomas per colonoscopy (APC), advanced ADR (AADR), sessile serrated lesion detection rate (SSLDR), sessile serrated lesions per colonoscopy (SSLPC), scope withdrawal time, and the resection rate of non-neoplastic lesions. Planned sample size was 1400 cases (one-sided α = 0.05, 80% power).

Results

Of the 1,399 participants enrolled between December 28, 2023, and March 6, 2025, 1,373 were included in the full analysis set (688 and 685 in the CADe and standard groups, respectively). In both groups, the proportions of primary screening and post-FIT colonoscopies were 75% and 25%, respectively. No differences were observed between the CADe and standard groups in ADR (54.7% vs. 53.9%; odds ratio [OR] 1.04; 95% confidence interval [CI], 0.83–1.30, one-sided p=0.38), APC (1.17 vs. 1.24; risk ratio [RR], 0.94; 95% CI, 0.81–1.09), or AADR (5.5% vs. 7.6%; OR, 0.71; 95% CI, 0.46–1.10). The CADe group showed higher SSLDR (9.0% vs. 6.0%; OR, 1.55; 95% CI, 1.03–2.33) and SSLPC (0.11 vs. 0.07; RR, 1.65; 95% CI, 1.09–2.50). Subgroup analysis based on endoscopist experience demonstrated a higher SSLDR in the CADe group among those with 500–4,999 (10.1% vs. 5.4%) and 5,000–9,999 (11.9% vs. 3.6%) prior colonoscopies, but not among those with experience of ≥10,000 procedures (7.0% vs. 7.5%). There was no difference between groups in the non-neoplastic lesion resection rate (14.7% vs. 13.4%; OR, 1.11; 95% CI, 0.82–1.50), and the median scope withdrawal time in cases without polypectomy was 9 minutes in both groups.

Conclusion

CADe assistance did not improve adenoma detection where high ADR was already achieved with standard colonoscopy. Nevertheless, it enhanced SSL detection, except among highly experienced endoscopists, without prolonging withdrawal time or increasing unnecessary polypectomies. While our findings do not overstate the efficacy of CADe, they support a reasonable and practical role for its use in improving colonoscopy quality in CRC screening.

References

1. Sekiguchi M, et al. Protocol for a multicenter randomized controlled trial to assess the usefulness of computer-aided detection systems for colonoscopy in colorectal cancer screening in the Asia-Pacific region (project CAD/NCCH2217). Jpn J Clin Oncol. 2025; 55: 837-40.

Disclosure

The authors have no conflict of interest related with this study.

Introduction

Computer-aided diagnosis (CAD) systems are widely implemented in the medical field for the analysis of medical images. PolyDeep is a CAD system that has demonstrated its efficacy in lesion detection.

Aims & Methods

The aim of this study is to determine whether PolyDeep increases the adenoma detection rate (ADR) in the context of expert endoscopists participating in a regional, population-based colorectal cancer screening program in Spain. PolyDeep Advance 3 (NCT05513261) is a multicentric, randomized controlled clinical trial. For the primary endpoint, we aimed to assess whether the ADR is superior in PolyDeep-assisted colonoscopy compared to conventional colonoscopy. As secondary endpoints, we aimed to determine whether PolyDeep-assisted colonoscopy improves the polyp detection rate (PDR), serrated lesion detection rate (SLDR), advanced serrated lesion detection rate (ASLDR), and advanced adenoma detection rate (AADR). We included participants who underwent colonoscopy for screening (i.e. those with a positive faecal immunochemical occult blood test – FIT+) or for surveillance after resection of advanced adenomas. We compared both groups using the chi-square and t-Student test.

Results

Between November 2023 and May 2024, we recruited 857 patients, of whom 30 were excluded. The baseline characteristics of the 827 patients included in the analysis were similar (male: 59.3%, screening colonoscopy: 66.7%, mean age: 61.7 ± 6.5 years, withdrawal time: 10:49 ± 04:32 minutes, colorectal cancer incidence: 2.8%). However, there were significant differences between both groups in the Boston Bowel Preparation Scale (conventional colonoscopy: 7.7 ± 1.3 vs. PolyDeep-assisted colonoscopy: 7.4 ± 1.3, p = 0.01). Regarding ADR, we did not find statistically significant differences between conventional and PolyDeep-assisted colonoscopy (57.7% vs. 60.8%, p = 0.4). Similarly, for the secondary endpoints, there were no significant differences in PDR (68.7% vs. 69.6%, p = 0.8), SLDR (32.0% vs. 29.4%, p = 0.5), ASLDR (5.3% vs. 5.1%, p = 1.0), or AADR (24.5% vs. 23.6%, p = 0.8). In Table 1, we described lesion detection rates between both groups by indication (i.e., FIT+ or surveillance).

Conclusion

In the context of expert endoscopists PolyDeep did not increase the ADR.

Introduction

Liver cancer ranks as the sixth most common malignant tumor worldwide and the third leading cause of cancer-related deaths. Hepatocellular carcinoma (HCC), accounting for approximately 90% of primary liver cancers, is among the most lethal malignancies, with a mortality-to-incidence ratio as high as 0.92. Metastasis remains a pivotal determinant of HCC patient prognosis and therapeutic efficacy, making in-depth exploration of its underlying mechanisms a critical foundation for improving clinical outcomes. Ribosomes, composed of ribosomal RNA (rRNA) and ribosomal proteins (RPs), are central to protein synthesis. Emerging evidence highlights that ribosomal heterogeneity influences tumor biology through differentially regulating protein translation. However, the specific mechanisms by which ribosomal proteins contribute to HCC metastasis remain poorly characterized, underscoring a significant gap in oncological research.

Aims & Methods

We performed a screen for ribosomal genes associated with survival in HCC patients using multiple databases through a comprehensively bioinformatics analysis. We estimated the correlation between RPS8 expression and clinicopathological features of patients in HCC. We explored the biological function of RPS8 in HCC cells via lentiviral in vitro. We further assessed the tumorigenicity of RPS8 using both subcutaneous tumor formation in nude mouse and orthotopic liver tumorigenesis in NCG mouse. multi-omics were applied for exploring the mechanism of RPS8 in HCC.

Results

Comprehensive pathological evaluation of HCC clinical specimens revealed overexpression of RPS8 in tumor tissues, which exhibited significant associations with higher tumor stage, poorly differentiated histology , microvascular invasion,and reduced overall survival.Functional studies demonstrated that knockdown of RPS8 suppressed proliferation, migration, and invasion in HCC cell lines . Overexpression of RPS8 could enhance the malignant behavior of HCC cells. Moreover, RPS8 depletion reduced subcutaneous tumor volume and orthotopic liver tumor metastasis to lungs. Mechanistically, proteomic analysis and RIP-seq revealed interferon-stimulated gene 15 (ISG15) exhibited the most significant downregulation at the protein level upon RPS8 knockdown and RPS8 directly binds to ISG15 mRNA. GO and KEGG analysis indicate that RPS8 promotes HCC invasion and metastasis by modulating cell motility and migration. Among the top five differentially expressed proteins, CCDC25, a neutrophil extracellular trap (NET) repceptor, exhibited the most significant downregulation upon RPS8 knockdown. ISG15 can bind with target proteins to form ISGlation, thus preventing the ubiquitinlation. Bioinformatic predictions have identified six potential ubiquitination modification sites in CCDC25. Additionally, molecular docking analyses suggest the presence of potential ubiquitination modification sites within the binding interface between ISG15 and CCDC25. We then performed CCDC25 overexpression in RPS8-knockdown HCC cells and CCDC25 knockout in RPS8-overexpressing HCC cells. Downregulation or upregulation of CCDC25 partially reversed the oncogenic effects of RPS8 respectively, supporting CCDC25 as a critical downstream mediator of RPS8-driven HCC progression. Finally, we found that NETs from HCC patients could promote in vivo metastasis of control cells, but showed less efficacy in RPS8-knockdown cells.

Conclusion

Ribosomal protein RPS8 promotes HCC metastasis through upregulating ISG15 to stabilize NETs receptor CCDC25 protein. These findings provide a promising therapeutic strategy targeting .

References

1.Kang J, Brajanovski N, Chan KT et al. Ribosomal proteins and human diseases: molecular mechanisms and targeted therapy. Signal Transduction and Targeted Therapy 2021; 6.
2. Larionova TD, Bastola S, Aksinina TE et al. Alternative RNA splicing modulates ribosomal composition and determines the spatial phenotype of glioblastoma cells. Nature Cell Biology 2022; 24:1541-1557.
3.Kang JA, Kim YJ, Jeon YJ. The diverse repertoire of ISG15: more intricate than initially thought. Experimental & Molecular Medicine 2022; 54:1779-1792.
4.Yang L, Liu Q, Zhang X et al. DNA of neutrophil extracellular traps promotes cancer metastasis via CCDC25. Nature 2020; 583:133-138.
5.Zhan X, Wu R, Kong XH et al. Elevated neutrophil extracellular traps by HBV‐mediated S100A9‐TLR4/RAGE‐ROS cascade facilitate the growth and metastasis of hepatocellular carcinoma. Cancer Communications 2022; 43:225-245.

Introduction

Radiation proctopathy (RP) is a common late complication of pelvic radiotherapy, affecting up to 20% of patients treated for pelvic malignancies. It manifests as rectal bleeding, anaemia, urgency, and diarrhoea, significantly reducing quality of life. Argon Plasma Coagulation (APC) remains the standard endoscopic therapy but has notable limitations, including high recurrence rates, the need for multiple sessions, and risks such as ulceration and perforation.
PuraStat, a synthetic self-assembling peptide hydrogel, offers an innovative alternative by creating a transparent matrix that promotes haemostasis and mucosal healing without thermal injury. While small series have shown benefit, robust real-world evidence is lacking.

Aims & Methods

We assessed real-world outcomes of PuraStat in RP at a UK tertiary centre (2023–2024). Consecutive patients with chronic radiation-induced rectal bleeding were included and treated by a single endoscopist. Patients were stratified into two cohorts:
1. De novo PuraStat – no prior APC (n=50)
2. APC→PuraStat – persistent or recurrent symptoms despite APC (n=50)
PuraStat was applied during flexible sigmoidoscopy, either as monotherapy or following APC. The primary outcome was resolution or improvement of rectal bleeding. Secondary outcomes included the number of repeat endoscopic interventions within 6 months and treatment-related adverse events.

Results

A total of 100 patients were included (median age: 74 years, range 64–85; 52% male). Most had prostate or gynaecological cancer treated with pelvic radiotherapy.
- De novo PuraStat (n=50): All achieved symptomatic relief, with marked bleeding reduction and endoscopic improvement. Follow-up sigmoidoscopy showed mucosal healing or mild residual proctitis in 92%. Mean repeat sessions: 1.3 (range 0–3) over 6 months.
- APC→PuraStat (n=50): These patients had undergone a median of 3 APC sessions with limited success. PuraStat led to complete symptom control in all cases, reducing the need for frequent interventions (mean: 1.5 sessions over 6 months).
No adverse events (e.g., perforation, infection, severe pain) were reported in either group. Patients with severe radiation-associated vascular ectasia (RAVE) and refractory bleeding demonstrated excellent response to PuraStat.

Conclusion

This large real-world series demonstrates that PuraStat is a safe, effective, and well-tolerated therapy for radiation proctopathy, whether used as first-line treatment or following APC failure. It provided rapid and sustained bleeding control, significantly reduced the need for repeat endoscopic interventions, and promoted mucosal healing without the risks associated with thermal therapies. Importantly, PuraStat showed consistent efficacy even in patients with severe radiation-associated vascular ectasia (RAVE) and those refractory to conventional modalities, highlighting its role as both a frontline and salvage option. These findings position PuraStat as a valuable addition to the therapeutic armamentarium for radiation-induced rectal bleeding. Larger prospective, multicentre studies and cost-effectiveness analyses are warranted to validate these results and define its optimal place in treatment algorithms.

Table 1: Treatment Outcomes by Group

References

1- White K, Henson CC. Endoscopically delivered PuraStat for the treatment of severe haemorrhagic radiation proctopathy: Service evaluation of a new endoscopic treatment for a challenging condition. Frontline Gastroenterol. 2021;12(1):37–42. doi:10.1136/flgastro-2020-101735
2-Van de Wetering FT, Verleye L, Andreyev HJN, Maher J, Vlayen J, Pieters BR, et al. Non-surgical interventions for late rectal problems (proctopathy) of radiotherapy in people who have received radiotherapy to the pelvis. Cochrane Database Syst Rev. 2016;(4):CD003455. doi:10.1002/14651858.CD003455.pub2
3-Andreyev HJN, Davidson SE, Gillespie C, Allum WH, Swarbrick E. Practice guidance on the management of acute and chronic gastrointestinal problems arising as result of treatment for cancer. Gut. 2012;61:179–192. doi:10.1136/gutjnl-2011-300563
4-Dahiya DS, Kichloo A, Tuma F, Albosta M, Wani F. Radiation proctitis and management strategies. Clin Endosc. 2022;55(1):22–32. doi:10.5946/ce.2020.288
5-Rustagi T, Mashimo H. Endoscopic management of chronic radiation proctopathy. World J Gastroenterol. 2011;17(41):4554–4562. doi:10.3748/wjg.v17.i41.4554
6-Lenz L, Rohr R, Nakao F, Libera E, Ferrari A. Chronic radiation proctopathy: A practical review of endoscopic treatment. World J Gastrointest Surg. 2016;8(2):151–158. doi:10.4240/wjgs.v8.i2.151