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Objective To investigate the efficacy and differences between endoscopic mucosal resection (EMR) and endoscopic submucosal dissection (ESD) in the treatment of early colorectal cancer and precancerous lesions. Methods A retrospective analysis was conducted on the clinical information of 655 patients who underwent endoscopic treatment for intestinal lesions at the Department of Gastroenterology, Jiangning Hospital, Nanjing, from January 2020 to May 2024, with postoperative pathology indicating early colorectal cancer or high-grade intraepithelial neoplasia. The efficacy was analyzed by grouping according to surgical method and lesion morphology. Results EMR has been shown to suitable for lesions with a diameter ≤2 cm and protruding lesions, while ESD has been shown to suitable for lesions with a diameter ＞2 cm and laterally spreading lesion. The incidence of intraoperative complications in the ESD group was significantly higher than that in the EMR group ［21.5% (55/256) vs 7.5%(30/399), χ2=26.933, P＜0.01］. For Is-type, Isp-type and Ip-type of protruded lesions, the incidence of intraoperative complications of ESD was significantly higher than that of EMR（P0.05). For Ip-type lesions, the overall hospital stay was significantly shorted with EMR treatment (P＜0.05). There was no significant difference in curative resection rates for Is-type, Isp-type, and Ip-type lesions treated with EMR (P＞0.05), but the proportion of Ip-type lesions with a diameter ＞2 cm was significantly higher than that of Is-type and Isp-type lesions (P＜0.05). Conclusion Both EMR and ESD have their advantages in the treatment of early colorectal cancer and precancerous lesions, but for Ip-type lesions with larger diameters, EMR treatment is safe and effective.

The incidence and mortality of gastric cancer are in the forefront of the tumor, and the prognosis is poor, especially in the middle and advanced stage. Even with comprehensive treatment, the 5- year survival is very low. The development of precision medicine has extended the survival of patients, and fibroblast growth factor receptor (FGFR) has gradually become a popular target for the treatment of gastric cancer. In this paper, the common FGFR alteration types in gastric cancer and the exploration of FGFR inhibitors in the field of gastric cancer were reviewed, and the challenges were analyzed.

Objective To investigate the predictive effect of circulating tumor cell (CTC) combined with neutrophil to lymphocyte ratio (NLR) on efficacy of advanced gastric cancer. Methods The clinicopathological data of 36 patients with advanced gastric cancer who received firstline treatment in Jiangning Hospital Affiliated to Nanjing Medical University and Jiangsu Cancer Hospital from June 2022 to January 2023 were collected. The optimal cutoff values of CTC and NLR were calculated using X-tile software, and the patients were divided into high CTC group (CTC>15, n=21) and low CTC group (CTC≤15, n=15), high NLR group (NLR>2.32, n=20) and low NLR group (NLR≤2.32, n=16). COX regression analysis and survival curve were used to analyze the relationship between CTC, NLR and progression free survival (PFS). Receiver operating characteristic (ROC) curves compared the predictive power of CTC, NLR, and the combination in predicting the outcome of advanced gastric cancer. Results Multivariate COX regression analysis showed that CTC (HR=7.441, P=0.045) and NLR (HR=4.690, P=0.011) were associated with PFS in patients with advanced gastric cancer. Patients in CTC group and low NLR group had longer PFS than those in high CTC group and high NLR group, respectively (P

Objective To evaluate the diagnostic value of abnormal prothrombin (des-gamma-carboxy prothrombin, DCP), Golgi protein 73 (GP73) and α-hydroxybutyrate dehydrogenase (α-HBDH) in the patients with alpha-fetoprotein（AFP）-negative primary hepatocellular carcinoma (PHCC). Methods A retrospective analysis was conducted on the patients with hepatitis B virus (HBV) infection treated in Second Hospital of Nanjing from January 2021 to December 2022, including 88 PHCC patients with negative AFP (PHCC group), 84 patients with hepatitis cirrhosis (cirrhosis group) and 75 patients with chronic hepatitis B (hepatitis group). At the same time, 67 healthy persons were served as control group. The serum DCP, GP73 and α-HBDH levels were detected and compared among these groups to assess the diagnostic efficacy of the three indicators (alone or in combination) for AFP-negative PHCC by drawing receiver operating characteristic (ROC) curve. Results The levels of DCP, GP73 and α-HBDH in PHCC group were significantly higher than those in cirrhosis group, hepatitis group and control group (P＜0.05), respectively. In the diagnosis of AFP-negative PHCC, the area under ROC (AUC) of combined detection of DCP, GP73 and α-HBDHwas 0.889, which was higher than that of DCP (0.804), GP73 (0.748) and α-HBDH (0.800) individually, and there were significant differences (Z =3.087, 3.350, 3.042, P＜0.01). The sensitivity (92.04%), specificity (96.03%) and accuracy (91.09%) of combined detection were the highest, followed by those of alone DCP (56.82%, 91.82%, 79.35%, respectively). Conclusion DCP, GP73 and α-HBDH have certain value in diagnosing AFP-negative PHCC, and the combined detection is helpful to improve the diagnostic efficiency.

After discovering the molecular changes leading to cancer occurrence and progression, the revolutionary changes have occurred in the treatment of non-small cell lung cancer (NSCLC) . The targeted therapy has become the first-line treatment for the advanced NSCLC patients with epidermal growth factor receptor (EGFR) mutation and anaplastic lymphoma kinase (ALK) fusion gene. With the rapid development of targeted drugs, the clinical studies on uncommon mutations or fusions of ROS1, MET, RET, HER2 and BRAF V600E in NSCLC are progressing rapidly, providing more options and opportunities for treatment in the patients with NSCLC.

Gene therapy and antibody approaches are crucial auxiliary strategies for hepatocellular carcinoma (HCC) treatment. Previously, we established a survivin promoter‐regulated oncolytic adenovirus that has inhibitory effect on HCC growth. The human sulfatase‐1 (hSulf‐1) gene can suppress the growth factor signaling pathways, then inhibit the proliferation of cancer cells and enhance cellular sensitivity to radiotherapy and chemotherapy. I131‐metuximab (I131‐mab) is a monoclonal anti‐HCC antibody that conjugated to I131 and specifically recognizes the HAb18G/CD147 antigen on HCC cells. To integrate the oncolytic adenovirus‐based gene therapy and the I131‐mab‐based radioimmunotherapy, this study combined the CArG element of early growth response‐l (Egr‐l) gene with the survivin promoter to construct a radiation‐inducible enhanced promoter, which was used to recombine a radiation‐inducible oncolytic adenovirus as hSulf‐1 gene vector. When I131‐mab was incorporated into the treatment regimen, not only could the antibody produce radioimmunotherapeutic effect, but the I131 radiation was able to further boost adenoviral proliferation. We demonstrated that the CArG‐enhanced survivin promoter markedly improved the proliferative activity of the oncolytic adenovirus in HCC cells, thereby augmenting hSulf‐1 expression and inducing cancer cell apoptosis. This novel strategy that involved multiple, synergistic mechanisms, including oncolytic therapy, gene therapy and radioimmunotherapy, was demonstrated to exert an excellent anti‐cancer outcome, which will be a promising approach in HCC treatment. Highlights: ► A radiation‐induced oncolytic adenovirus is constructed as hSulf‐1 gene vector.► I131‐metuximab boosts oncolytic adenoviral proliferation in hepatocellular carcinoma.► I131‐metuximab increases adenovirus‐mediated hSulf‐1 expression in cancer cells.► Oncolytic adenovirus and I131‐metuximab synergistically increase antitumor effect. [ABSTRACT FROM AUTHOR]

Gene therapy and antibody approaches are crucial auxiliary strategies for hepatocellular carcinoma (HCC) treatment. Previously, we established a survivin promoter-regulated oncolytic adenovirus that has inhibitory effect on HCC growth. The human sulfatase-1 (hSulf-1) gene can suppress the growth factor signaling pathways, then inhibit the proliferation of cancer cells and enhance cellular sensitivity to radiotherapy and chemotherapy. I(131)-metuximab (I(131)-mab) is a monoclonal anti-HCC antibody that conjugated to I(131) and specifically recognizes the HAb18G/CD147 antigen on HCC cells. To integrate the oncolytic adenovirus-based gene therapy and the I(131)-mab-based radioimmunotherapy, this study combined the CArG element of early growth response-l (Egr-l) gene with the survivin promoter to construct a radiation-inducible enhanced promoter, which was used to recombine a radiation-inducible oncolytic adenovirus as hSulf-1 gene vector. When I(131)-mab was incorporated into the treatment regimen, not only could the antibody produce radioimmunotherapeutic effect, but the I(131) radiation was able to further boost adenoviral proliferation. We demonstrated that the CArG-enhanced survivin promoter markedly improved the proliferative activity of the oncolytic adenovirus in HCC cells, thereby augmenting hSulf-1 expression and inducing cancer cell apoptosis. This novel strategy that involved multiple, synergistic mechanisms, including oncolytic therapy, gene therapy and radioimmunotherapy, was demonstrated to exert an excellent anti-cancer outcome, which will be a promising approach in HCC treatment., (Copyright © 2012 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.)