tbuckley/cabot-search huggingface dataset:
The diagnostic performance and optimal strategy of cone beam CT-assisted bronchoscopy for peripheral pulmonary lesions: A systematic review and meta-analysis
Authors: Huijie Yang, Junfeng Huang, Yu Zhang, Jiaming Guo, Shuojia Xie, Ziwen Zheng, Yuqin Ma, Qilin Deng, Changhao Zhong, Shiyue Li
Journal: Pulmonology (2024)

Cone-beam computed tomography (CBCT) assisted bronchoscopy shows prospective advantages in diagnosing peripheral pulmonary lesions (PPLs), but its diagnostic value and potential influencing factors remain unclear. What is the clinical value and optimal strategy of CBCT-assisted bronchoscopy in diagnosing PPLs? The references were searched from PubMed, EmBase, and Web of Science. Studies reporting diagnostic yield and potential influencing factors of CBCT-assisted bronchoscopy were included. The navigational success rate, diagnostic rate, complication rate, and potential influencing factors were pooled by random-effects model and meta-regression. A total of 1,441 patients with 1,540 lesions from 15 studies were included in our meta-analysis. The pooled navigational success rate (97.0% vs 81.6%; odds ratio [OR] 5.12) and diagnostic rate (78.5% vs 55.7%; OR 2.51) of the CBCT-assisted group were significantly higher than those without CBCT. The complication rate of CBCT-assisted bronchoscopy was 4.4% (95%CI: 0.02-0.07). Cone-beam CT combined with r-EBUS can achieve the highest diagnostic rate. Applying positive end-expiratory pressure could improve the diagnostic rate and reduce the complication rate (p < 0.05). Lesions located in the upper lobe could achieve a higher diagnostic rate and lesions located in the right lobes could get a lower complication rate (p < 0.05). Cone-beam CT combined with r-EBUS seems to be the effective and optimal approach to ameliorate the navigation success rate and diagnostic rate of diagnosing PPLs.Clinical trial registration: This study was registered in PROSPERO (Registration Number: CRD42022378992). URL: PROSPERO (york.ac.uk).
Effects of asymmetric nasal high-flow cannula on carbon dioxide in hypercapnic patients: A randomised crossover physiological pilot study
Authors: Lara Pisani, Maria Laura Vega, Elisa Ageno, Irene Prediletto, Roberto Dongilli, Vito Catalanotti, Gilda Giancotti, Stefano Nava
Journal: Pulmonology (2024)

Nasal high flow (NHF) therapy is an established form of non invasive respiratory support used in acute and chronic care. Recently, a new high flow nasal cannula with asymmetric prongs was approved for clinical use. The clinical benefits of the new cannula have not yet been defined and no evidence are available on the use of asymmetric NHF support in patient with Chronic Obstructive Pulmonary Disease (COPD). We conducted a single-centre, prospective, physiologic, crossover, randomised study to investigate the effects on partial pressure of carbon dioxide (PaCO2) levels of two different nasal cannula ("asymmetric" vs "standard" nasal interface) in 20 COPD hypercapnic patients. All patients were recovering from an acute exacerbation that required hospitalisation and had persistent hypercapnia, despite having attained a stable pH. After enrolment, two 90-min trials with the asymmetric nasal high flow interface (Optiflow + Duet, Fisher & Paykel Healthcare Ltd., New Zealand) or the standard interface (Optiflow, Fisher & Paykel Healthcare Ltd., New Zealand) were randomly applied and a washout period of 60 min between the two treatments was performed for minimising the carryover effect. Study results suggested that the asymmetrical cannula did not significantly decrease PaCO2 compared with the standard cannula. Similar performances were also observed in terms of diaphragm activity, dyspnoea and patient's comfort. Interestingly, asymmetric NHF cannula performed significantly better in reducing the dead space ventilation and increasing the ventilatory efficiency in more advanced COPD patients with more severe hypercapnia higher baseline PaCO2 values (PaCO2 ≥ 65 mmHg at baseline). .
A systematic review of the impact of artificial intelligence in pancreatic cancer detection.
Authors: Jahnavi Ethakota, Bipneet Singh, Sakshi Bai, Danesh Kumar, Devin Birsingh Malik
Journal: Journal of Clinical Oncology (2025)

685 Background: Pancreatic cancer is the fourth leading cause of cancer deaths in the United States, and early detection remains a significant challenge. Screening the general population is not feasible, but the rise of artificial intelligence (AI) has introduced new possibilities for improving early diagnosis and patient outcomes. Methods: A systematic literature search was conducted using PubMed, Google Scholar, and MEDLINE using MeSH terms Artificial intelligence or AI, and diagnosis and pancreatic carcinoma or pancreatic adenocarcinoma. Prisma guidelines were adhered to, and a total of 19 studies resulted, 6 of them were retrospective studies, 4 of them were literature reviews, and 4 of them were randomized trials. The rest were duplicates. The inclusion criteria for this study is AI being used in the diagnosis, only in pancreatic cancer, within the last 5 years, only in English, and only retrospective studies were included. Results: One study used Digital Imaging Processing (DIP) for analyzing Endoscopic ultrasound (EUS) images from 153 pancreatic cancer patients, yielding a sensitivity of 97.98% and a specificity of 94.32%. Two studies explored Computer Aided Diagnosis (CAD) models applied to PET/CT and EUS images, achieving a sensitivity of 95.23% and specificity of 97.51% in PET/CT scans and 83.3% and 93.3% in EUS images, respectively. Another study used a Faster R-CNN model to analyze CT images from 338 pancreatic cancer patients showed high diagnostic accuracy in much less time. Additionally, two studies utilized Natural Language Processing (NLP) for identifying family histories of pancreatic cancer and detecting pancreatic cysts, with the latter achieving sensitivity and specificity rates of 99.9% and 98.8%. Conclusions: The current strategies for early diagnosis of pancreatic cancer focus on serum biomarkers and EUS-guided Fine Needle Aspiration (EUS-FNA) and sensitivity varies but depends on the physician's expertise. AI is showing promise in improving pancreatic cancer diagnosis by enhancing early detection and accuracy. Techniques like deep learning, NLP-based models, Faster R-CNN, and CAD systems analyze medical data and images more effectively than manual methods. AI holds the potential to shape the future of pancreatic cancer diagnosis and improve patient outcomes.
Survival disparities in small intestine carcinoid tumors: A SEER-based analysis.
Authors: Adit Dharia, Rahul Borra, Supriya Peshin, Haik Ser-Manukyan, Abdulah Amer Mahayni, Sainarayana Mangu, Dharmik M. Patel, Salman Muddassir
Journal: Journal of Clinical Oncology (2025)

653 Background: Small intestine carcinoid tumors (SI-carcinoids) are rare neuroendocrine neoplasms with variable survival outcomes. This study examines the impact of age, sex, race, income, and geographic location on overall survival (OS) in patients with SI-carcinoid tumors. Methods: A retrospective cohort study was conducted using the Surveillance, Epidemiology, and End Results (SEER) registry 22 to identify patients aged 20 and above with SI-carcinoid tumors from 2000 to 2021. Kaplan-Meier survival analysis and log-rank tests were used to assess differences in survival. Cox proportional hazards models estimated hazard ratios (HR) for Overall Survival (OS). Results: 20,777 patients were included, with 7,029 deaths recorded. Median OS varied significantly by age, sex, race, income, and tumor site. Patients aged 60-85 had a median OS of 10 months (95% CI: 9.75-10.42), while those over 85 had 2.92 months (95% CI: 2.67-3.33). Females had better OS (13.92 months; 95% CI: 13.42-14.42) than males (12.83 months; 95% CI: 12.42-13.25). Non-Hispanic Black patients had worse OS (12.33 months; 95% CI: 11.50-13.33) compared to Non-Hispanic Whites (13.25 months; 95% CI: 12.92-13.67). Patients earning less than $50,000 had worse OS (11.42 months; 95% CI: 10.67-12.42) than those earning $100,000–$120,000 (15.42 months; 95% CI: 14.25-17.83). Geographic disparities were noted, with nonmetropolitan areas showing worse OS (11.42 months; 95% CI: 10.83-12.92) compared to large metropolitan areas (14.00 months; 95% CI: 13.50-14.42). Cox models confirmed age (HR for 85+ years: 21.99; 95% CI: 17.40-27.81), male sex (HR: 1.12; 95% CI: 1.07-1.17), and Black race (HR: 1.29; 95% CI: 1.18-1.42) were linked to worse OS. Tumor site also affected OS, with ileal tumors showing better survival compared to duodenal tumors (HR: 0.89; 95% CI: 0.84-0.94). Conclusions: Age, sex, race, income, and geographic location significantly affect OS in patients with small intestine carcinoid tumors, highlighting the need for tailored interventions for vulnerable groups.
Clinicopathological factors related to survival in gastroenteropancreatic neuroendocrine tumors (GEP-NET): 20 years experience in the American British Cowdray Medical Center.
Authors: Susy Wuotto Alvarado, Raquel Gerson-Cwilich, Fidel David David Huitzil Melendez, Guillermo Olivares, Ivonne Salcedo, Alberto Villalobos, Juan Alberto Serrano, Alvaro Aguayo, Monica Isabel Meneses-Medina, Christian Patricio Camacho Limas, Daniela Shveid Gerson, Vanessa Rosas Camargo, Carlos Arturo Camberos-Mercado, José Fabián Martínez-Herrera, Alejandro Noguez-Ramos
Journal: Journal of Clinical Oncology (2025)

656 Background: Neuroendocrine neoplasms (NEN) are a diverse group of tumors originating from neuroendocrine cells found throughout the body. Their “rarity”, heterogeneity, and non-specific presentation contribute to limited reliable epidemiological data, especially in developing countries such as Mexico. This study aims to analyze the clinical and pathological features of gastroenteropancreatic neuroendocrine tumors (GEP-NET) and their association with survival in a third-level center in Mexico. Methods: A retrospective cohort study at the American British Cowdray Medical Center, in Mexico City, was conducted. We included all histopathological confirmed GEP-NET from 2004 to 2024. Clinical, biochemical, and radiological features at diagnosis were analyzed. Survival was estimated using Kaplan-Meier and Log-Rank test. Results: We identified 110 NENs, of which 89% were GEP-NET, 56.1% were female, and the median age was 57.7 (SD 13.8) years. The clinical stage was metastatic (50%), localized (37.7%), and locally advanced (6.1%). The primary sites were the pancreas (49%), small bowel (23.5%), gastric (10.2%), colon (7.1%), rectum (5.1%), appendix (3.1%), and unknown (2%). ECOG performance status were 0-1 in 96.9%. In the metastatic setting, liver involvement was 96.2%, mainly high hepatic burden (59.6%). Symptoms were abdominal pain (34.6%), diarrhea (16.3%), and bowel obstruction (6.1%). Functioning tumors were 26.8%, and carcinoid syndrome was found in 9.2%. Grades 1, 2, and 3 were 62.9%, 34%, and 3.1% respectively. The median of Ki-67 was 6.4%. At diagnosis, Ga-68 PET/CT scan, serum CgA, and urinary 5-HIIA were performed in 98.2%, 39.7%, and 16.3% of patients. Among metastatic patients, 87.1% received at least one line of systemic treatment, primarily with somatostatin analogs (62.9%). In all population, the median follow-up was 42.5 months and the median overall survival (OS) was 164.9 (SD 12.2) months. Univariate analyses showed that primary site (p=0.02), Ki-67 &lt;5% (p=0.02), CgA &lt;700 ng/ml (p=0.03), and low hepatic burden (p=0.01) were statistically significantly associated with OS. Conclusions: This study provides critical insights into GEP-NET characteristics in a Mexican population, highlighting clinical, biochemical, and radiological factors associated with better survival.
Bifunctional anti-PD-L1/TGF-βRII agent SHR-1701 plus chemotherapy as first-line treatment for advanced esophageal squamous cell carcinoma (ESCC): Survival results of a phase II trial.
Authors: Yi Wang, Hong Liu, Qingwei Wang, Naian Qiao, Jianbo Wang, Bingxu Tan, Bo Cheng, Yunxia Chu, Changhong Zhao, Xiaoyu Chen, Yufeng Cheng
Journal: Journal of Clinical Oncology (2025)

411 Background: Recently, several clinical trials have demonstrated synergistic efficacy by combining immune checkpoint inhibitors (ICIs) with chemotherapy. However, only a subset of patients (pts) derived benefits. Combining ICIs with agents blocking immunosuppressive pathway may expand the clinical benefit of ICIs to more pts. Transforming growth factor β (TGF-β) participates in tumor immune escape. SHR-1701, a novel bifunctional fusion protein consisting of a monoclonal antibody targeting PD-L1 fused with the extracellular domain of TGF-β receptor II, was evaluated in a phase II trial (ChiCTR2000039909) to assess its efficacy and safety when combined with chemotherapy for pts with unresectable locally advanced, recurrent or metastatic ESCC in China. Methods: This trial enrolled treatment-naive pts with histologically or cytologically confirmed unresectable locally advanced, recurrent, or metastatic ESCC. Eligible pts received SHR-1701 (30mg/kg, iv, d1, q3w) in combination with up to six cycles of albumin-bound paclitaxel (125mg/m 2 , iv, d1, d8, q3w) and cisplatin (75mg/m 2 , iv, d1, q3w). For those without progressive disease, maintenance treatment was administered with SHR-1701 monotherapy until disease progression or unacceptable toxicity. The primary endpoint was objective response rate (ORR). Secondary endpoints included progression-free survival (PFS), overall survival (OS), disease control rate (DCR) and safety. Results: At the data cut-off, March 1, 2024, 24 pts had received at least one dose of the study treatment and were included in both the intention-to-treat (ITT) analysis and safety analysis sets. 3 and 12 pts achieved confirmed complete and partial responses, respectively. The confirmed ORR was 62.5% and DCR was 87.5%. With a median follow-up of 20.8 months (95% CI, 15.5-NR), the median duration of response was 9.1 months (95% CI, 6.9-NR). The median PFS was 10.8 months (95% CI, 7.8-NR) and the median OS was 26.1 months (95% CI, 8.6-NR). 12-month PFS and OS rates were 41.4% (95% CI, 22.5-76) and 64.8% (95% CI, 47.8-87.9), respectively. Grade 3-4 treatment-related adverse events occurred in 11 (45.8%) pts and no treatment-related death was observed. Conclusions: The results highlighted that SHR-1701 plus chemotherapy as first-line therapy maintained long-term, durable survival benefit in pts with advanced ESCC. Clinical trial information: ChiCTR2000039909.
Mediation of the liver protective effect of the anti-cancer drug candidate namodenoson via adiponectin.
Authors: Pnina Fishman, Avital Bareket-Samish
Journal: Journal of Clinical Oncology (2025)

604 Background: Namodenoson (CF102) is a small, orally available, anti-cancer drug candidate, currently in pivotal phase 3 clinical study for the treatment of hepatocellular carcinoma. Adiponectin is a positive cytokine released by adipocytes and endothelial cells, known to induce liver-, cardio-, and neuro-protective effects. We evaluated the potential role of adiponectin as the mediator of the observed namodenoson-induced protective effects. Methods: Proteins extracted fromN1S1 tumor-bearing mice and from murine adipocyte culture treated with namodenoson or vehicle were analyzed using Western blot. Apoptosis was determined in the N1S1 tumor-bearing mice using the TUNEL assay. The effect of namodenoson on hepatic ischemia/reperfusion (IR) was evaluated in Wistar rats by temporarily clamping the hepatic vasculature; the effect on hepatic inflammation was evaluated in Con. A-induced hepatitis in mice. The STAM murine in-vivo model was used to study the effect of namodenoson on metabolic dysfunction-associated steatohepatitis (MASH). Adiponectin levels were determined in the serum of patients in the phase 2 trial evaluating namodenoson vs placebo in patients with metabolic dysfunction-associated steatotic liver disease (MASLD)/MASH. Results: The anti-cancer effect of namodenoson was attributed to its capability to bind to the A3 adenosine receptor, inducing inhibition of PI3K and subsequent de-regulation of the Wnt/β-catenin and NF-kB signal transduction pathways, resulting in apoptosis of liver tumor cells. At the same time, namodenoson demonstrated a liver protective effect manifested by prevention of hepatic IR injury, suppression of liver inflammation, and induction of anti-fibrotic and anti-steatotic effects. In adipocyte cell culture, namodenoson stimulated adiponectin production. An increase in adiponectin levels was also shown in the murine MASH model (STAM). These in-vitro and in-vivo results were consistent with translational data from the phase 2 study of namodenoson in MASLD/MASH where upregulation of adiponectin was observed with namodenoson (mean change from baseline of 539 ng/mL for namodenoson 12.5 mg BID vs -78 ng/mL for placebo, P = 0.032). Conclusions: The anti-cancer effect of namodenoson combined with its protective effects, position it as a unique drug inducing a dual effect in patients with advanced liver cancer.
Birth cohort effects in appendiceal adenocarcinoma incidence across the United States.
Authors: Andreana Natalie Holowatyj, Mary Kay Washington, Richard M Goldberg, Caitlin C. Murphy
Journal: Journal of Clinical Oncology (2025)

90 Background: Appendiceal adenocarcinoma incidence rates are increasing across all age groups, sexes and histological subtypes in the United States. Birth cohort patterns of appendiceal adenocarcinomas can provide us with new, etiologic clues into these rising rates but have not been examined for this rare malignant tumor type. We estimated appendiceal adenocarcinoma incidence rates across birth cohorts in the United States. Methods: Using the National Cancer Institute’s Surveillance, Epidemiology, and End Results (SEER) Program data from eight population-based cancer registries, we identified a total of 4,858 persons aged 20+ years when diagnosed with a pathologically-confirmed primary appendiceal adenocarcinoma (non-mucinous, mucinous, goblet cell, signet ring cell carcinoma) between 1975 and 2019. Birth cohorts (1900-1904 to 1990-1994) were created using five-year age groups and time periods. The ratio of age-specific incidence rates was estimated in each birth cohort relative to the 1945-1949 birth cohort and reported as incidence rate ratios (IRRs) with 95% confidence intervals (CI). Results: Compared to persons born in 1945-1949, appendiceal adenocarcinoma incidence rates more than tripled among persons born in 1980-1984 (IRR 3.41, 95%CI 2.54-4.56) and quadrupled among persons born in 1985-1989 (IRR 4.62, 95%CI 3.12-6.82). For all tumor histological types, age-specific appendiceal adenocarcinoma incidence rates increased across successive birth cohorts after 1945-1949—although to varying degrees reported across histological types (e.g., 1980-1984: mucinous adenocarcinoma: IRR 2.71, 95% CI 1.73-4.26; non-mucinous adenocarcinoma: IRR 2.60, 95% CI 1.46-4.63; goblet cell adenocarcinoma: IRR 4.95, 95% CI 2.77-8.85). Conclusions: There are strong, yet distinct birth cohort effects for appendiceal adenocarcinomas across histological subtypes that remain unexplained. These patterns signal that recent exposure changes may be influencing this increasing disease risk for Generation X and Millennials now entering mid-adulthood. With the trend toward more non-operative management of appendicitis, another significant consideration for providers is to keep occult appendiceal tumors in the differential diagnosis of patients who present in this way. The current absence of appendiceal cancer prevention and screening modalities emphasizes the importance of efforts to support earlier detection in a rare malignancy where clinical trials have been historically very limited. Moreover, as similar trends have been reported in other gastrointestinal cancers, this is also suggestive of potential shared exposures contributing to this rising cancer burden across generations.
Prognostic implications and therapeutic response in GNAS-mutated colorectal adenocarcinoma: A retrospective cohort analysis.
Authors: Faran Polani, Whitney Rose Swain, Bobby Se, Jamie Randall, Timothy Lewis Cannon
Journal: Journal of Clinical Oncology (2025)

244 Background: GNAS, a key regulator of the G-protein signaling pathway, is frequently mutated in colorectal adenocarcinomas and other malignancies. Despite its role in tumorigenesis, GNAS mutations remain understudied, with no established targeted therapies. Exploring the impact of GNAS alterations on therapeutic response and outcomes in colorectal cancer (CRC) is crucial for developing effective treatment strategies. Methods: We reviewed 531 CRC cases from our institutional Molecular Tumor Board database, identifying 8 patients with GNAS mutations. The prevalence ofGNASmutations in our cohort was 1.5%, which aligns with reported rates of 2-5% in various CRC cohorts. Comprehensive clinicopathologic data, including tumor histology, staging, treatment outcomes, and response rates, were analyzed. A detailed evaluation was conducted on stage IV patients to assess their response, progression-free survival (PFS), and overall survival (OS) in comparison to historical stage IV CRC benchmarks. Results: The cohort included 8 patients with a median age of 61 years (range: 33-73 years), with balanced gender representation (50% male, 50% female). The racial distribution was 50% Black or African American, 25% White, and 12.5% Asian or Pacific Islander. The majority of patients (62.5%) were diagnosed at stage IV, with primary tumor sites predominantly in the sigmoid colon and cecum. Among the 5 stage IV patients, while no patients achieved a complete or partial response, 3 exhibited stable disease, resulting in a 60% disease control rate (including stable disease). The median progression-free survival (mPFS) was 9 months, reflecting the duration of disease control before progression, while the median overall survival (mOS) was 15 months. These outcomes are notably lower than historical benchmarks for stage IV CRC, where response rates typically range from 40-50% with mOS of 20-24 months, highlighting the potentially adverse prognostic impact of GNAS mutations. Conclusions: Patients with GNAS-mutated colorectal adenocarcinoma appear to represent a unique subset with poorer therapeutic outcomes, even when achieving stable disease. The observed disease control in the absence of objective responses underscores the complexity of treating GNAS-mutated tumors and highlights the urgent need for targeted therapies tailored to this molecular subtype. Further research into the biological mechanisms underlying GNAS mutations and their impact on CRC treatment resistance is warranted to improve patient outcomes.