OBJECTIVE:Postoperative recurrence is a common complication of percutaneous endoscopic lumbar discectomy for lumbar disc herniation,which can significantly increase the risk of reoperation.A well-performing risk prediction model can help identify high-risk groups early and prevent postoperative recurrence.This study systematically evaluated the risk prediction model for postoperative recurrence after percutaneous endoscopic lumbar discectomy to provide a reference for surgical decision-making.METHODS:The PubMed,Embase,Web of Science,CNKI,WanFang Data,VIP,and CBM were electronically searched to collect studies on the recurrence risk prediction models after percutaneous endoscopic lumbar discectomy from inception to July 1,2024.Two reviewers independently screened the literature and extracted data.The models' risk of bias,applicability,and report quality were assessed using prediction model risk of bias assessment tool(PROBAST)and Transparent Reporting of a Multivariable Prediction Model for Individual Prognosis or Diagnosis(TRIPOD)tools,respectively.Meta-analysis of postoperative recurrence rate of percutaneous endoscopic lumbar discectomy and related predictors was performed using Revman 5.4 software.RESULTS:(1)A total of 15 studies were included,all of which were retrospective studies,including 24 models for predicting the risk of recurrence after percutaneous endoscopic lumbar discectomy.(2)The PROBAST evaluation results indicated that all 15 studies exhibited a high risk of bias.Regarding applicability,two studies demonstrated a low risk,while 13 presented a high risk.(3)Regarding the TRIPOD reporting quality,the overall quality across the 15 studies was low.The primary reasons for this low compliance included the failure to report blinding,a lack of explanation for the sample size calculation method,lack of detailed description of missing data processing methods,and lack of information such as introduction to the model used.(4)Furthermore,the area under the receiver operating characteristic curve for the model ranged from 0.684 to 0.972,with the number of potential predictor variables varying from 15 to 28.(5)The results of meta-analysis showed that the postoperative recurrence rate of lumbar disc herniation patients treated with percutaneous endoscopic lumbar discectomy was 12％(95％CI=9.0％-15.0％),Modic changes(OR=6.72,95％CI=3.90-11.59),body mass index(OR=1.28,95％CI=1.10-1.49),work intensity(OR=3.22,95％CI=1.85-5.59),age(OR=2.28,95％CI=1.50-3.48),and smoking history(OR=2.65,95％CI=1.75-4.00)were independent influencing factors for postoperative recurrence of percutaneous endoscopic lumbar discectomy(all P＜0.05).CONCLUSION:The overall predictive performance of the recurrence risk prediction models after percutaneous endoscopic lumbar discectomy is satisfactory;however,the model exhibits a high overall risk of bias and applicability,coupled with low reporting quality.Additionally,there is a lack of prospective research and external validation.Future,risk prediction models should consider factors such as Modic changes,body mass index,work intensity,age,and smoking history as potential predictors.

OBJECTIVE:Postoperative recurrence is a common complication of percutaneous endoscopic lumbar discectomy for lumbar disc herniation,which can significantly increase the risk of reoperation.A well-performing risk prediction model can help identify high-risk groups early and prevent postoperative recurrence.This study systematically evaluated the risk prediction model for postoperative recurrence after percutaneous endoscopic lumbar discectomy to provide a reference for surgical decision-making.METHODS:The PubMed,Embase,Web of Science,CNKI,WanFang Data,VIP,and CBM were electronically searched to collect studies on the recurrence risk prediction models after percutaneous endoscopic lumbar discectomy from inception to July 1,2024.Two reviewers independently screened the literature and extracted data.The models' risk of bias,applicability,and report quality were assessed using prediction model risk of bias assessment tool(PROBAST)and Transparent Reporting of a Multivariable Prediction Model for Individual Prognosis or Diagnosis(TRIPOD)tools,respectively.Meta-analysis of postoperative recurrence rate of percutaneous endoscopic lumbar discectomy and related predictors was performed using Revman 5.4 software.RESULTS:(1)A total of 15 studies were included,all of which were retrospective studies,including 24 models for predicting the risk of recurrence after percutaneous endoscopic lumbar discectomy.(2)The PROBAST evaluation results indicated that all 15 studies exhibited a high risk of bias.Regarding applicability,two studies demonstrated a low risk,while 13 presented a high risk.(3)Regarding the TRIPOD reporting quality,the overall quality across the 15 studies was low.The primary reasons for this low compliance included the failure to report blinding,a lack of explanation for the sample size calculation method,lack of detailed description of missing data processing methods,and lack of information such as introduction to the model used.(4)Furthermore,the area under the receiver operating characteristic curve for the model ranged from 0.684 to 0.972,with the number of potential predictor variables varying from 15 to 28.(5)The results of meta-analysis showed that the postoperative recurrence rate of lumbar disc herniation patients treated with percutaneous endoscopic lumbar discectomy was 12％(95％CI=9.0％-15.0％),Modic changes(OR=6.72,95％CI=3.90-11.59),body mass index(OR=1.28,95％CI=1.10-1.49),work intensity(OR=3.22,95％CI=1.85-5.59),age(OR=2.28,95％CI=1.50-3.48),and smoking history(OR=2.65,95％CI=1.75-4.00)were independent influencing factors for postoperative recurrence of percutaneous endoscopic lumbar discectomy(all P＜0.05).CONCLUSION:The overall predictive performance of the recurrence risk prediction models after percutaneous endoscopic lumbar discectomy is satisfactory;however,the model exhibits a high overall risk of bias and applicability,coupled with low reporting quality.Additionally,there is a lack of prospective research and external validation.Future,risk prediction models should consider factors such as Modic changes,body mass index,work intensity,age,and smoking history as potential predictors.

Background: Influenza A virus (IAV) is a negative-sense RNA virus of the Orthomyxoviridae family and is the etiological agent of a highly contagious acute respiratory disease that can lead to acute lung injury. Objective: To elucidate the molecular mechanisms of IAV infection, an integrative research approach combining gene expression profiling, multinetwork analysis, and in vivo experimental validations was employed. Methods: First, a series of network-based analyses were performed, including protein-protein interaction network construction, weighted gene co-expression network analysis, and subsequent gene set enrichment analysis, to identify the major underlying mechanisms of IAV infection. Following gene expression analysis, core targets, both direct and indirect regulators, were screened. An IAV (H1N1) strain A/PR/8/34-induced acute lung injury mouse model was constructed for in vivo validations. Batch one included two groups to evaluate findings from the multi-network analysis: Mock (n = 10; 5 males and 5 females) and IAV (n = 10; 5 males and 5 females). Batch two included three groups to assess the role of toll-like receptor 3 (TLR3) in IAV infection: Mock (n = 6; 3 males and 3 females), IAV (n = 6; 3 males and 3 females), and TLR3 inhibitor (n = 6; 3 males and 3 females). Body weight was measured on days 0, 3, and 5 after infection. On day 5, lung tissues were collected to assess viral load and histopathological changes. Key targets were examined using enzyme-linked immunosorbent assay, Western blotting, and immunofluorescence staining, both in sera and lung tissues. Results: IAV infection was significantly associated with dysregulation of the immune-inflammation system, such as the LTR, nucle-otide-binding oligomerization domain-(NOD) like receptor, retinoic acid-inducible gene I-like receptor, and nuclear factor kappa-B signaling pathways. Gene set enrichment analysis further indicated that the TLR and necroptosis signaling pathways played crucial roles in the progression of IAV infection (TLR signaling pathway normalized enrichment score = 2.3941, P = 1.00 × 10 ⁻¹⁰; necroptosis normalized enrichment score = 1.9421, P = 6.21 × 10 ⁻⁷). Among the core targets, TLR3 and mixed lineage kinase domain-like protein (MLKL) may regulate gene expression at the transcriptional level (all P < 0.05). In vivo validation using an IAV (PR8) infected acute lung injury mouse model demonstrated increased viral load and lung index, alveolar structural damage, and inflammatory cell infiltration. Immunofluorescence staining exhibited large gaps in Lamin B1 staining and breaches in Emerin signals following IAV-PR8 infection. Expression levels of TLR3, p-receptor-interacting serine/threonine-protein kinase 3 (RIPK3)/RIPK3, and p-mixed lineage kinase domain-like protein (MLKL)/MLKL proteins in lung tissues, as well as proinflammatory factors and mediators in sera, were significantly elevated after IAV infection. Moreover, enhanced neutrophil infiltration (myeloperoxidase) and citrullinated histone H3 (a neutrophil extracellular trap-specific marker), both established indicators of neutrophil extracellular trap formation, were observed. Notably, treatment with a TLR3 inhibitor significantly ameliorated IAV-induced acute lung injury by regulating necroptosis-related targets. Conclusion: Our study provides network-based in vivo evidence that TLR3-receptor-interacting serine/threonine-protein kinase 3-MLKL-mediated necroptosis may underlie IAV-induced acute lung injury and could serve as a potential therapeutic target in severe influenza cases.

Objective To explore factors associated with early postoperative hormonal remission in patients with prolactinoma and to develop prediction models based on clinical and radiological features. Methods Data from 107 patients with prolactinoma who underwent transsphenoidal surgery at The First People’s Hospital of Huai’an, Nanjing Medical University between January 2020 and December 2024 was collected, included general clinical characteristics, preoperative laboratory indicators, and imaging features. Based on whether early postoperative prolactin (PRL) levels normalized, patients were divided into a remission group (n=76) and a non-remission group (n=31). Univariate logistic regression was used for preliminary evaluation of candidate variables, followed by LASSO regression for feature selection. Multiple machine learning models were constructed, including logistic regression, random forest, support vector machine, K-nearest neighbors, naive Bayes, decision tree, neural network, and gradient boosting decision tree (GBDT). All models were trained and evaluated using ten-fold cross-validation, with comprehensive assessment of model performance based on the area under the ROC curve (AUC), accuracy, sensitivity, specificity, precision, and F1 score. Results The maximum diameter of tumors in the non remission group was larger than that in the remission group (P=0.019), and the incidence of tumor stroke and preoperative PRL levels were significantly higher than those in the remission group (P＜0.001). Univariate analysis showed that sex, maximum tumor diameter, tumor stroke, and preoperative PRL levels were influencing factors for early postoperative hormone response in patients with prolactinoma (P＜0.05). The comparison results of machine learning models show that the neural network model performs the best (AUC=0.921) and has good clinical application value, followed by the GBDT model (AUC=0.893) and the support vector machine model (AUC=0.884). Other models also show certain predictive ability. Conclusions Sex, preoperative PRL levels, maximum tumor diameter, Hounsfield unit value, and tumor stroke are important factors affecting early hormone response after prolactinoma surgery. The machine learning model constructed based on the above variables has good predictive performance, and performs the best and has good clinical application value.

Objective To investigate the development, role, and regulatory mechanism of macrophage efferocytosis in the liver of hosts infected with Schistosoma japonicum. Methods The expression of efferocytosis-related gene like efferocytosis receptors, efferocytosis-related bridging molecules,“eat me” signal and “don’t eat me” signal was detected in the livers of patients and mice infected with S. japonicum in the Gene Expression Omnibus (GEO) database. Ten wild-type (WT) male mice (6 ~ 8 weeks old, weighing 20 ~ 25 g) were randomly divided into a Schistosoma japonicum infection (SJ) group and a normal control (NC) group, with 5 mice in each group. The efferocytosis of neutrophils and T cells by liver macrophages was detected in mice from SJ group and NC group using flow cytometry and immunofluorescence assay, respectively. The expression of efferocytosis-related Mer receptor tyrosine kinase (MerTK) and Axl receptor tyrosine kinase (Axl) proteins was determined in mouse liver tissues using Western blotting assay, and the proportion of MerTK⁺ macrophages and the average fluorescence intensity of macrophage MerTK were detected in mouse livers using flow cytometry. Changes in liver granulomas and fibrosis were observed in mice infected with S. japonicum following injection of efferocytosis inhibitors, and S. japonicum-infected mice without injection of efferocytosis inhibitors served as controls. Bone marrow-derived macrophages (BMDMs) were isolated from macrophage scavenger receptor class A (SR-A) conditional knockout (CKO) and wild-type (WT) mice, and changes in apoptotic neutrophils were detected in SR-A CKO mouse macrophages in vitro using flow cytometry. Then, BMDMs was divided into the WT mono-culture group, the WT and apoptotic neutrophils co-culture group, the SR-A CKO mono-culture group, and the SR-A CKO and neutrophils co-culture group, and the expression of MerTK and Axl was quantified in vitro using Western blotting and real-time quantitative PCR (RT-qPCR) assays during neutrophil efferocytosis. The efferocytosis of neutrophils and T cells by mouse liver macrophages was detected in the SR-A CKO SJ group and the WT SJ group using flow cytometry and immunofluorescence assay, and the expression of MerTK and Axl proteins was determined in mouse liver tissues in both groups using Western blotting. In addition, the proportion of MerTK⁺ macrophages and the average fluorescence intensity of macrophage MerTK were detected in mouse livers in both groups using flow cytometry. Results Data from the GEO database showed that the expression of some efferocytosis receptors and efferocytosis-related bridging molecules, and “eat me” and “don’t eat me” signals all appeared a tendency towards a rise in livers of patients and mice in the SJ group relative to the NC group, suggesting that S. japonicum infection-induced liver diseases may be associated with efferocytosis. Flow cytometry detected higher proportions of Ly6G⁺ cells [(13.13 ± 0.45)% vs. (6.48 ± 0.25)%; t = 22.30, P < 0.05] and CD3⁺ cells [(7.60 ± 0.33)% vs. (3.30 ± 0.42)%; t = 13.98, P < 0.05] in mouse liver macrophages in the SJ group than in the NJ group, and the expression of MerTK protein [(2.30 ± 0.14) vs. (1.14 ± 0.46); t = 4.19, P < 0.05], the mean fluorescence intensity of macrophages [(160.67 ± 15.28) vs. (94.50 ± 19.61); t = 4.81, P < 0.05], and the proportion of MerTK⁺ macrophages [(20.78 ± 4.17)% vs. (6.85 ± 0.39)%; t = 6.57, P < 0.05] were significantly higher in mouse liver tissues in the SJ group than in the NC group. The Axl expression was lower in mouse liver tissues in the SJ group than in the NC group [(1.25 ± 0.08) vs. (1.93 ± 0.37); t = 2.79, P < 0.05], and the area of granulomas around single eggs [(9.18 ± 1.81) × 10⁴μm² vs. (5.24 ± 1.35) × 10⁴ μm²; t = 3.03, P < 0.05] and proportion of collagen fibers [(25.27 ± 3.99)% vs. (15.14 ± 4.02)%; t = 3.10, P < 0.05] were significantly greater in livers of S. japonicum-infected mice with injection of efferocytosis inhibitors than in mice without injection of efferocytosis inhibitors. The in vitro efferocytosis efficiency of BMDMs [(32.83 ± 3.17)% vs. (45.43 ± 2.34)%; t = 5.54, P < 0.05], and the proportions of Ly6G⁺ [(9.37 ± 0.48)% vs. (13.13 ± 0.72)%; t = 7.50, P < 0.05] and CD3⁺ cells [(4.95 ± 0.17)% vs. (7.64 ± 0.50)%; t = 8.87, P < 0.05] in liver macrophages post-infection with S. japonicum were significantly lower in SR-A CKO mice than in WT mice, and the expression of MerTK protein [(0.65 ± 0.25) vs. (1.96 ± 0.69); t = 3.10, P < 0.05], the average fluorescence intensity of macrophages [(138.33 ± 8.39) vs. (160.67 ± 15.28); t = 3.03, P < 0.05] and the proportion of MerTK⁺ macrophages [(13.17 ± 5.01)% vs. (22.63 ± 2.06)%; t = 3.56, P < 0.05] were significantly lower in mouse liver tissues in the SR-A CKO SJ group than in the WT group. Western blotting detected no significant difference in the Axl protein expression in mouse liver tissues between the SR-A CKO SJ group and the WT SJ group [(0.48 ± 0.07) vs. (0.68 ± 0.30); t = 1.09, P > 0.05]. There were significant differences in the relative MerTK mRNA and protein expression during efferocytosis of BMDMs among the WT monoculture group, the WT and apoptotic neutrophils co-culture group, the SR-A CKO mono-culture group, and the SR-A CKO and neutrophils co-culture group (F = 9.41 and 40.68, both P values < 0.05). In addition, there was a significant difference in the relative Axl mRNA expression during efferocytosis of BMDMs among the four groups (F = 13.62, P < 0.05); however, no significant difference was seen in the relative Axl protein expression (F = 1.27, P > 0.05). Conclusions Efferocytosis of liver macrophages is seen in mice infected with S. japonicum and inhibits liver fibrosis. SR-A may up-regulate the efficiency of macrophage efferocytosis through regulating the expression of efferocytosis receptors.

OBJECTIVE: To investigate the effectiveness and safety of simultaneous bilateral total knee athroplasty (SB-TKA) for the treatment of patients aged 65 years and younger with bilateral knee osteoarthritis (KOA) by comparing with patients undergoing unilateral total knee arthroplasty (U-TKA). METHODS: A clinical data of patients, who underwent primary TKA for KOA and met the selection criteria between June 2019 and July 2023, was retrospectively analyzed, including 181 patients in the U-TKA group and 52 patients in the SB-TKA group. The baseline data of age, gender, disease duration, body mass index, and preoperative hemoglobin (Hb), knee range of motion (ROM), Oxford knee score (OKS), and visual analogue scale (VAS) score for pain were compared between the two groups, with no significant difference ( P>0.05). The operation time, postoperative hospital stay, and all complications related to knee arthroplasty were recorded. Hb was measured at 2 days after operation and the difference between pre- and post-operation was calculated. The knee function and pain were evaluated by using ROM, OKS score, and VAS score and compared between the two groups. RESULTS: The operation time and postoperative hospital stay duration were significantly shorter in the U-TKA group than in the SB-TKA group ( P<0.05). The difference of Hb was significantly lower in the U-TKA group ( P<0.05). All patients were followed up 12-61 months (mean, 37.2 months). There was no significant difference in follow-up time between the two groups ( P>0.05). At last follow-up, the ROM, OKS score, and VAS score of both groups were better than the preoperative ones, and the differences were significant ( P<0.05); there were significant differences between the two groups in the ROM and OKS score ( P<0.05), while no significant difference was found in the VAS score ( P>0.05). Mild complications were observed in 31 cases (17.13%) and severe complications in 3 cases (1.66%) in the U-TKA group, while mild complications were observed in 14 cases (26.92%) in the SB-TKA group, and no severe complication occurred. There was no significant difference in the incidences of mild and severe complications between the two groups ( P>0.05). CONCLUSION In patients aged 65 years and younger with bilateral KOA, knee function and mobility can significantly improved when treated by SB-TKA. While patients had lower postoperative knee mobility and function scores compared with U-TKA, there was no significant difference in pain scores or overall incidence of complication. Strict patient selection and scientific perioperative management are important to achieve good effectiveness after operation in patients with SB-TKA.
Humans ; Arthroplasty, Replacement, Knee/adverse effects* ; Male ; Female ; Retrospective Studies ; Osteoarthritis, Knee/physiopathology* ; Range of Motion, Articular ; Treatment Outcome ; Middle Aged ; Operative Time ; Length of Stay ; Knee Joint/physiopathology* ; Pain Measurement ; Postoperative Complications/epidemiology* ; Aged

Dysfunction of anti-tumor immune responses is crucial for cancer progression. Immune checkpoint blockade (ICB), which can potentiate T cell responses, is an effective strategy for the normalization of host anti-tumor immunity. In recent years, immune checkpoints, expressed on both tumor cells and immune cells, have been identified; some of them have exhibited potential druggability and have been approved by the US Food and Drug Administration (FDA) for clinical treatment. However, limited responses and immune-related adverse events (irAEs) cannot be ignored. This review outlines the development and applications of ICBs, potential strategies for overcoming resistance, and future directions for ICB-based cancer immunotherapy.
Humans ; Immune Checkpoint Inhibitors/therapeutic use* ; Neoplasms/drug therapy* ; Immunotherapy/methods* ; Animals

Ischemic stroke (IS) is a globally life-threatening disease. Presently, few therapeutic medicines are available for treating IS, and rt-PA is the only drug approved by the US Food and Drug Administration (FDA) in the US. In fact, many agents showing excellent neuroprotection but no blood flow-improving activity in animals have not achieved ideal clinical efficacy, while thrombolytic drugs only improving blood flow without neuroprotection have limited their wider application. To address these challenges and meet the huge unmet clinical need, we have designed and identified a novel compound AAPB with dual effects of neuroprotection and cerebral blood flow improvement. AAPB significantly reduced cerebral infarction and neural function deficit in tMCAO rats, pMCAO rats, and IS rhesus monkeys, as well as displayed exceptional safety profiles and excellent pharmacokinetic properties in rats and dogs. AAPB has now entered phase I of clinical trials fighting IS in China.

BACKGROUND: Chronic kidney disease (CKD) is associated with common pathophysiological processes, such as inflammation and fibrosis, in both the heart and the kidney. However, the underlying molecular mechanisms that drive these processes are not yet fully understood. Therefore, this study focused on the molecular mechanism of heart and kidney injury in CKD. METHODS: We generated an microRNA (miR)-26a knockout (KO) mouse model to investigate the role of miR-26a in angiotensin (Ang)-II-induced cardiac and renal injury. We performed Ang-II modeling in wild type (WT) mice and miR-26a KO mice, with six mice in each group. In addition, Ang-II-treated AC16 cells and HK2 cells were used as in vitro models of cardiac and renal injury in the context of CKD. Histological staining, immunohistochemistry, quantitative real-time polymerase chain reaction (PCR), and Western blotting were applied to study the regulation of miR-26a on Ang-II-induced cardiac and renal injury. Immunofluorescence reporter assays were used to detect downstream genes of miR-26a, and immunoprecipitation was employed to identify the interacting protein of LIM and senescent cell antigen-like domain 1 (LIMS1). We also used an adeno-associated virus (AAV) to supplement LIMS1 and explored the specific regulatory mechanism of miR-26a on Ang-II-induced cardiac and renal injury. Dunnett's multiple comparison and t -test were used to analyze the data. RESULTS: Compared with the control mice, miR-26a expression was significantly downregulated in both the kidney and the heart after Ang-II infusion. Our study identified LIMS1 as a novel target gene of miR-26a in both heart and kidney tissues. Downregulation of miR-26a activated the LIMS1/integrin-linked kinase (ILK) signaling pathway in the heart and kidney, which represents a common molecular mechanism underlying inflammation and fibrosis in heart and kidney tissues during CKD. Furthermore, knockout of miR-26a worsened inflammation and fibrosis in the heart and kidney by inhibiting the LIMS1/ILK signaling pathway; on the contrary, supplementation with exogenous miR-26a reversed all these changes. CONCLUSIONS Our findings suggest that miR-26a could be a promising therapeutic target for the treatment of cardiorenal injury in CKD. This is attributed to its ability to regulate the LIMS1/ILK signaling pathway, which represents a common molecular mechanism in both heart and kidney tissues.
Animals ; MicroRNAs/metabolism* ; Angiotensin II/toxicity* ; Mice ; Renal Insufficiency, Chronic/chemically induced* ; Mice, Knockout ; Disease Models, Animal ; Male ; Signal Transduction/genetics* ; LIM Domain Proteins/genetics* ; Mice, Inbred C57BL ; Cell Line ; Humans

BACKGROUND: Several studies have demonstrated the occurrence of secondary tumors as a rare but significant complication of chimeric antigen receptor T (CAR-T) cell therapy, underscoring the need for a detailed investigation. Given the limited variety of secondary tumor types reported to date, a comprehensive characterization of the various secondary tumors arising after CAR-T therapy is essential to understand the associated risks and to define the role of the immune microenvironment in malignant transformation. This study aims to characterize the immune microenvironment of a newly identified secondary tumor post-CAR-T therapy, to clarify its pathogenesis and potential therapeutic targets. METHODS: In this study, the bone marrow (BM) samples were collected by aspiration from the primary and secondary tumors before and after CD19 CAR-T treatment. The CD45 + BM cells were enriched with human CD45 microbeads. The CD45 + cells were then sent for 10× genomics single-cell RNA sequencing (scRNA-seq) to identify cell populations. The Cell Ranger pipeline and CellChat were used for detailed analysis. RESULTS: In this study, a rare type of secondary chronic myelomonocytic leukemia (CMML) were reported in a patient with diffuse large B-cell lymphoma (DLBCL) who had previously received CD19 CAR-T therapy. The scRNA-seq analysis revealed increased inflammatory cytokines, chemokines, and an immunosuppressive state of monocytes/macrophages, which may impair cytotoxic activity in both T and natural killer (NK) cells in secondary CMML before treatment. In contrast, their cytotoxicity was restored in secondary CMML after treatment. CONCLUSIONS This finding delineates a previously unrecognized type of secondary tumor, CMML, after CAR-T therapy and provide a framework for defining the immune microenvironment of secondary tumor occurrence after CAR-T therapy. In addition, the results provide a rationale for targeting macrophages to improve treatment strategies for CMML treatment.
Humans ; Lymphoma, Large B-Cell, Diffuse/therapy* ; Tumor Microenvironment/genetics* ; Antigens, CD19/metabolism* ; Leukemia, Myelomonocytic, Chronic/genetics* ; Immunotherapy, Adoptive/adverse effects* ; Male ; Single-Cell Analysis/methods* ; Female ; Sequence Analysis, RNA/methods* ; Receptors, Chimeric Antigen ; Middle Aged