Objective: To analyze the heterogeneity of response to first-line camrelizumab combined with chemotherapy in patients with esophageal squamous cell carcinoma (ESCC) by pretreatment circulating cell-free DNA (cfDNA) sequencing. Methods: A total of 30 patients with human epidermal growth factor receptor 2-negative locally advanced or advanced ESCC who received first-line camrelizumab combined with chemotherapy in the Department of Oncology, Changzhi People's Hospital, from June 2020 to April 2023 were enrolled. Follow-up was conducted until May 30, 2024, with a median follow-up duration of 15.9 months. Differences in cfDNA sequencing profiles between the ORR group (complete response + partial response, n=15), and the Non-ORR group (stable disease + progressive disease, n=15), were analyzed. Base substitution types, functional mutation categories, and mutation frequencies were compared to identify differentially mutated cfDNA genes. The associations between gene mutation status and progression-free survival (PFS) and overall survival (OS) were further evaluated. Results: In both the Non-ORR and ORR groups, the insert fragment lengths showed a unimodal distribution (160-180 bp), consistent with the typical characteristics of cfDNA. C>T transition was the predominant base substitution type (47.6% in the Non-ORR group and 45.9% in the ORR group). Missense mutation was the most common functional mutation type (80.9% in the Non-ORR group and 81.1% in the ORR group). Six differentially mutated genes were identified between the Non-ORR and ORR groups, including KLF14, ITPR1, NKTR, PRRC2B, MAGI2, and TYW1B. Mutations in KLF14, ITPR1, NKTR and PRRC2B may be associated with lack of objective response (all P＜0.05), whereas MAGI2 mutations may be associated with a better treatment response (P=0.050). Survival analysis showed that, within the sample size and follow-up period of this cohort, the median PFS of patients with TYW1B mutant-type and wild-type was not reached and 9.70 months, respectively, and the median OS was 30.90 and 17.80 months, respectively. TYW1B mutation was associated with better PFS (HR=2.658, P=0.049 7) and better OS (HR=3.029, P=0.033). Conclusions: After treatment with camrelizumab combined with chemotherapy for ESCC, molecular characteristics differ among patients with different treatment responses. TYW1B mutation is associated with improved PFS and OS. However, these findings require further validation in larger cohorts.

Objective: To investigate the efficacy and safety of combination immunotherapy in patients with locally advanced esophageal cancer. Methods: Clinical data of 212 patients with pathologically confirmed locally advanced esophageal cancer who received definitive chemoradiotherapy without surgery at the Affiliated Cancer Hospital of Xinjiang Medical University from January 2019 to January 2024 were retrospectively collected. Follow-up ended in January 2025. Patients were divided into an immunotherapy group (IO group, n=93) and a non-immunotherapy group (Non-IO group, n=119) based on whether immune checkpoint inhibitors were combined during treatment. Propensity score matching (PSM) was used to balance intergroup differences. Cox proportional hazards regression models were applied to identify independent factors influencing progression-free survival (PFS) and overall survival (OS). Results: Before PSM, among the 212 patients, the median PFS was not reached in the IO group, while it was 27.40 months in the Non-IO group. The 1-year PFS rate was significantly better in the IO group than in the Non-IO group (82.4% vs 72.3%; HR=0.65, P=0.048). The median OS was 37.37 months in the IO group and 30.17 months in the Non-IO group, with no statistically significant difference in 1-year OS rates (86.2% vs 82.6%; HR=0.66, P=0.064). After PSM, the median PFS remained unreached in the IO group (n=68), while it was 18.43 months in the Non-IO group (n=68). The IO group maintained its advantage in 1-year PFS rate (80.6% vs 73.7%; HR=0.53, P=0.017). Regarding OS, the median OS was 37.37 months in the IO group and 30.17 months in the Non-IO group, with 1-year OS rates of 84.5% and 90.8%, respectively; the difference was not statistically significant (HR=0.74, P=0.261). Multivariable analysis showed that combination immunotherapy was associated with better PFS (HR=0.49, P=0.010), but no association with OS was observed (HR=0.68, P=0.187). Additionally, N stage and smoking status were independent factors for PFS. Compared with squamous cell carcinoma, patients with non-squamous cell carcinoma had worse OS (HR=4.33, P=0.018). In terms of safety, there were no statistically significant differences between the IO group (n=68) and the Non-IO group (n=68) in the incidence of any-grade adverse events or grade ≥3 adverse events (all P＞0.05). However, the incidence of grade ≥3 lymphocytopenia was significantly higher in the IO group than in the Non-IO group (42.6% vs 19.1%; χ²=8.82, P=0.003). Conclusion: Compared with chemoradiotherapy alone, chemoradiotherapy combined with immunotherapy improves PFS in patients with locally advanced esophageal cancer, but is associated with a higher proportion of patients with severe lymphocytopenia.

Objective: To investigate the expression of miR-527 in bladder urothelial cell carcinoma tissues (UCC) and cell lines, and to explore the mechanism by which miR-527 inhibits bladder cancer cell migration and promotes apoptosis through targeting Bcl-2. Methods: The expression of miR-527 in bladder UCC was analyzed using The Cancer Genome Atlas database. The expression of miR-527 in bladder UCC cell lines was verified by real-time quantitative reverse transcription polymerase chain reaction. The relationship between miR-527 and its target gene Bcl-2 was validated using a dual-luciferase reporter assay. miR-527 inhibitor and miR-527 mimic were constructed for cell transfection. Cell migration and apoptosis were assessed using wound healing assay and flow cytometry. Protein expression was detected by Western blot. In vivo tumorigenesis and the expressions of Bcl-2 and Ki-67 were evaluated using a nude mouse cell-derived xenograft model and immunohistochemistry. Results: Analysis of The Cancer Genome Atlas database revealed that miR-527 expression was significantly higher in bladder cancer tissues than in normal bladder tissues, whereas Bcl-2 protein expression was significantly lower. Dual-luciferase reporter assay confirmed that miR-527 directly targeted Bcl-2. Inhibition of miR-527 significantly upregulated Bcl-2 mRNA and protein levels (both P＜0.01), enhanced cell migration, and reduced apoptosis [migration rate: (100.00±0.00)% in the miR-527 inhibitor group vs. (47.74 ± 2.18)% in the T24 control group; apoptosis rate: (2.68±1.28)% vs. (11.82±5.19)%; both P＜0.05]. Overexpression of miR-527 produced opposite effects [migration rate: (45.22±3.66)% in the miR-527 overexpression group vs. (100.00±0.00)% in the UMUC-3 control group; apoptosis rate: (11.74±0.64)% vs. (3.81±0.75)%; both P＜0.05]. In animal experiments, overexpression of miR-527 significantly inhibited tumor growth and reduced the expressions of Bcl-2 and Ki-67 in tumor tissues, whereas inhibition of miR-527 promoted tumor growth, increased tumor cellular atypia, and enhanced the expressions of Bcl-2 and Ki-67. Conclusions: miR-527, as a tumor-associated gene, is highly expressed in bladder cancer tissues. Overexpression of miR-527 inhibits the growth and migration of bladder cancer cells and induces apoptosis by negatively regulating the Bcl-2.

With the rapid development of image-guided minimally invasive therapeutic techniques, percutaneous cryoablation has become increasingly important in the comprehensive management system of pulmonary tumors due to its advantages such as good repeatability and minimal damage to surrounding structures. This consensus was developed by a working group consisting of multidisciplinary experts from respiratory and critical care medicine, interventional radiology, thoracic surgery, oncology, and ultrasound. Based on a systematic search of relevant domestic and international literature, synthesis of the latest guidelines and consensus statements, and combined with clinical practice experience in China, the group formulated 10 consensus recommendations through multiple rounds of expert discussion and voting. The contents cover the indications and contraindications of percutaneous cryoablation for lung tumors, pre-procedural biopsy strategies, application scenarios and timing of intervention in advanced lung cancer, key technical points of cryoablation, management principles for lesions of different numbers and sizes, as well as key practical aspects such as post-operative follow-up and evaluation processes and prevention and treatment strategies for complications. This consensus clarifies the role of percutaneous cryoablation in the comprehensive management of lung tumors and emphasizes that it should be performed in a standardized manner under the evaluation of a multidisciplinary team (MDT) to optimize the whole-course management pathway for patients with lung cancer. High-quality clinical research is still needed in the future to further refine standardized operating procedures and evidence-base, thereby providing references for clinical practice.

Objective: To investigate the anti-tumor effect of knockdown of telomerase reverse transcriptase (TERT) in melanoma and its potential clinical value. Methods: Employed TERT knockdown strategy and evaluated the expression of target gene by Western blot analysis and RT-qPCR. The in vitro effects of TERT knockdown strategy were evaluated by cell proliferation, apoptosis, migration and invasion assays in A375 cells line, and the in vivo effects were evaluated via a xenografts mouse tumor model. Results: Following TERT knockdown, a significant downregulation of both mRNA transcripts and protein expression were observed (P＜0.001). Knockdown of TERT inhibited the proliferation, migration, and invasion of melanoma cells in vitro, while enhancing apoptosis and inducing significant G0/G1 phase cell cycle arrest [The values for cell viability, number of invasive cells, 24-hour wound healing rate, apoptosis ratio, and G0/G1 phase ratio in the Con group were (100.00±6.51)%, (270.22±19.31) cells, (49.72±1.90)%, (7.13±0.36)%, and (46.69±0.45)%, respectively; in the Neg group, they were (95.80±5.33)%, (260.67±16.52) cells, (52.32±1.68)%, (7.23±0.70)%, and (47.48±0.15)%, respectively; and in the shRNA group, they were (60.80±5.29)%, (106.67±14.11) cells, (20.75±4.64)%, (12.76±0.48)%, and (59.77±0.64)%, respectively, all P＜0.05]. The results of subcutaneous tumorigenesis experiment in nude mice indicated that stably knockdown TERT in melanoma cells attenuated the tumorigenicity. Conclusion: TERT silencing effectively suppresses melanoma progression and metastasis, demonstrating its potential as a novel therapeutic target for melanoma treatment.

Epidermal growth factor receptor (EGFR) mutation is the most common driver mutation in non-small cell lung cancer (NSCLC) among Asian populations. For patients with resectable EGFR-mutant NSCLC, the high risk of postoperative recurrence remains a major clinical challenge. The neoadjuvant treatment paradigm has shifted from conventional chemotherapy to precision therapies centered on EGFR-tyrosine kinase inhibitors (TKIs), aiming to downstage tumor and eradicate micrometastases before surgery, thereby improving surgical outcomes and long-term survival. This article systematically reviews the evolution and recent advances in neoadjuvant therapy for EGFR-mutant NSCLC. As of December 2025, osimertinib-based regimens, whether used as monotherapy or in combination with chemotherapy, have emerged as potential options in this field and are supported by high-level evidence-based medicine. The article also discusses the limitations of immunotherapy in the EGFR-mutant NSCLC population and the future development trends of combination strategies, emphasizing that biomarker-guided individualized therapy represents the corner direction moving forward.

Objective: To investigate the effects of miR-1910-3p on proliferation, invasion, epithelial-mesenchymal transition (EMT) and in vivo tumor growth of lung adenocarcinoma (LUAD) cells. Methods: Bioinformatics analysis was performed using The Cancer Genome Atlas (TCGA) database and the Starbase database to compare the expression of miR-1910-3p between LUAD tissues and adjacent normal tissues. In vitro experiments were conducted using human LUAD cell lines (H1299, A549) and normal lung epithelial cells (BEAS-2B). The expression level of miR-1910-3p was verified by real-time quantitative polymerase chain reaction (RT-qPCR). H1299 and A549 cells were transfected with liposomes to establish miR-1910-3p overexpression (mimic group), knockdown (inhibitor group) and negative control (NC group) cell models. Cell proliferation was assessed using the Cell Counting Kit-8 (CCK-8) assay and plate colony formation assay. Cell invasion was evaluated by Transwell invasion assay. The protein expression changes of EMT markers (E-cadherin, N-cadherin, Vimentin, Snail) were quantitatively analyzed by Western blot. For in vivo experiments, a subcutaneous xenograft model was established in nude mice, and tumor growth was monitored on days 7, 14, 21 and 28. At the end of the experiment, the nude mice were euthanized and the tumors were harvested for analysis. Results: Bioinformatics analysis showed that the expression level of miR-1910-3p was significantly higher in LUAD tissues than in adjacent normal tissues (P＜0.01). RT-qPCR results confirmed that compared with BEAS-2B cells, the relative expression levels of miR-1910-3p were significantly upregulated in A549 and H1299 LUAD cell lines (both P＜0.05). CCK-8 assay results showed that compared with the mimic NC group, overexpression of miR-1910-3p significantly enhanced the proliferative activity of A549 cells [mimic NC group (111.00±7.69)% vs. miR-1910-3p mimic group (119.70±7.54)%, P＜0.01] and H1299 cells [mimic NC group (113.40±15.21)% vs. miR-1910-3p mimic group (118.3±18.82)%, P＜0.01]; conversely, compared with the inhibitor NC group, knockdown of miR-1910-3p significantly inhibited the proliferative activity of A549 cells [inhibitor NC group (115.90±11.39)% vs. miR-1910-3p inhibitor group (111.90±8.83)%, P＜0.05] and H1299 cells [inhibitor NC group (113.20±15.34)% vs. miR-1910-3p inhibitor group (109.60±12.53)%, P＜0.05]. Plate colony formation assay showed that compared with the mimic NC group, overexpression of miR-1910-3p significantly enhanced the colony formation ability of A549 cells [mimic NC group (18.96±1.92)% vs. miR-1910-3p mimic group (37.33±3.66)%, P＜0.01] and H1299 cells [mimic NC group (22.86±2.78)% vs. miR-1910-3p mimic (42.33±2.58)%, P＜0.01]; conversely, compared with the inhibitor NC group, knockdown of miR-1910-3p significantly inhibited the colony forming ability of A549 cells [inhibitor NC group (19.46±3.33)% vs. miR-1910-3p inhibitor group (10.79±2.86)%, P＜0.01] and H1299 cells [inhibitor NC group (22.63±1.27)% vs. miR-1910-3p inhibitor group (12.96±1.45)%, P＜0.01]. Western blot analysis showed that compared with the mimic NC group, overexpression of miR-1910-3p significantly upregulated the expression of N-cadherin, Vimentin and the transcription factor Snail, while downregulating the expression level of E-cadherin (all P＜0.05). Transwell invasion assay showed that compared with the mimic NC group, overexpression of miR-1910-3p significantly enhanced the invasion ability of A549 cells [mimic NC group (333.00±35.68) vs. miR-1910-3p mimic group (521.67±46.92), P＜0.01] and H1299 cells [mimic NC group (341.67 ±32.87) vs. miR-1910-3p mimic group (537.66±33.13), P＜0.01]; conversely, compared with the inhibitor NC group, knockdown of miR-1910-3p significantly inhibited the invasive ability of A549 cells [inhibitor NC group (363.67±49.24) vs. miR-1910-3p inhibitor group (211.33±27.79), P＜0.01] and H1299 cells [inhibitor NC group (351.67±24.11) vs. miR-1910-3p inhibitor group (154.33±9.29), P＜0.01]. Subcutaneous xenograft experiment in nude mice showed that compared with the mimic NC group, overexpression of miR-1910-3p significantly promoted tumor growth in vivo, manifested as an increased tumor weight and volume (both P＜0.01). In the mimic NC group, tumor weights on days 7, 14, 21 and 28 were (0.08±0.01) g, (0.18±0.03) g, (0.41±0.06) g and (0.73±0.06) g, respectively; in the the miR-1910-3p mimic group, tumor weights on days 7, 14, 21 and 28 were (0.07±0.01) g, (0.35±0.06) g, (0.72±0.08) g, and (0.96±0.09) g, respectively. In the mimic NC group, tumor volumes on days 7, 14, 21 and 28 were (132.00±1.00) mm3, (254.67±7.10) mm3, (530.67± 42.71) mm3 and (853.33±74.10) mm3; in the miR-1910-3p mimic group, tumor volumes on days 7, 14, 21 and 28 were (132.00±2.00) mm3, (425.33±29.94) mm3, (829.00±62.00) mm3, and (1 123.33±95.38) mm3, respectively. Conclusion: miR-1910-3p acts an oncogene in LUAD, promoting tumor cell proliferation, invasion and in vivo tumorigenesis by activating EMT process.

Non-Hodgkin lymphoma (NHL) is a common malignant tumor in children, accounting for approximately 7% of all childhood malignancies, with a higher incidence rate among adolescents. After standardized treatment, the overall survival rate exceeds 80%. Lymphoblastic lymphoma (LBL), mature B-cell non-Hodgkin lymphoma (mB-NHL), and anaplastic large cell lymphoma (ALCL) account for 90% of pediatric and adolescent NHL cases. The Lymphoma Group of the Oncology Branch of the Chinese Medical Association has organized multidisciplinary experts from pediatric oncology, pediatrics, internal medicine, pathology, and radiology. Based on domestic and international evidence-based evidence and extensive clinical experience, this consensus has been developed focusing on NHL common in children and adolescents (including LBL, mB-NHL, and ALCL), covering clinical manifestations, auxiliary examinations, pathological diagnosis, clinical staging, and treatment. It aims to provide evidence-based guidance for standardized clinical practice and further improve patient survival rates.

Small cell carcinoma of the esophagus (SCEC) is a rare and highly aggressive neuroendocrine tumor with poor prognosis. Its clinical manifestations lack specificity, and diagnosis relies on gastroscopic biopsy pathology and immunohistochemistry. The use of ultrasonic gastroscope, enhanced CT or positron emission tomography-computed tomography (PET-CT), and brain MRI is recommended for accurate staging. The American Joint Committee on Cancer-tumor, node, metastasis (AJCC-TNM) staging system and the Veterans Administration Lung Study Group (VALSG) staging systems are adopted to guide the treatment. The treatment emphasizes a multidisciplinary comprehensive mode incorporating chemotherapy, radiotherapy and surgery. For patients with limited-stage disease, chemotherapy combined with local treatment (surgery or radiotherapy) is recommended. For operable patients, radical chemoradiotherapy or perioperative treatment followed by radical surgery is recommended, while patients with inoperable disease should receive radical chemoradiotherapy. For patients with extensive-stage disease, systemic chemotherapy is the mainstay, while etoposide plus platinum as the preferred regimen. If systemic treatment is effective, additional local treatment may be administered for residual lesions. Palliative treatment is recommended for symptomatic metastases. There is currently a lack of high-level evidence-based medical evidence for immunotherapy, and relevant clinical trials are recommended. This consensus aims to promote the standardized diagnosis and treatment of SCEC and to improve patients' quality of life and long-term survival through multidisciplinary collaboration.

The rearranged during transfection (RET) gene is a proto-oncogene encoding a receptor tyrosine kinase. RET gene alterations are driver events in various tumors. Pralsetinib and selpercatinib are novel, highly selective RET tyrosine kinase inhibitors (RET-TKIs). They are recommended as priority therapeutic options for RET fusion-positive non-small cell lung cancer (NSCLC) in the Chinese Society of Clinical Oncology (CSCO) Guidelines for the Diagnosis and Treatment of Non-Small Cell Lung Cancer and Thyroid Carcinoma and the Chinese Medical Association (CMA) Clinical Guidelines for Lung Cancer, as well as for radioiodine-refractory differentiated thyroid cancer with RET fusion and RET-mutant medullary thyroid carcinoma. Common adverse events asosociated with pralsetinib and selpercatinib include hypertension, liver enzyme abnormalities, neutropenia and fatigue. Studies have demonstrated that the incidence of adverse events is not associated with disease type. Given the low prevalence of RET gene alterations (＜5%), which are regarded as rare genetic mutations, clinical experience in the use pf RET-TKIs and and patient management remains limited. Base on the current status of adverse event management of RET-TKIs in China, and integrating the latest international evidence and clinical experience, the Chinese Medical Doctor Association Tumor Multidisciplinary Diagnosis and Treatment Professional Committee and the Shenzhen Medical Doctor Association Tumor Multidisciplinary Diagnosis and Treatment Professional Committee organized discussion among experts from medical oncology, respiratory medicine, radiation oncology, thoracic surgery, and other related disciplines to formulate this expert consensus on the management of adverse events of RET-TKIs.