CarveMix: A simple data augmentation method for brain lesion segmentation.

Brain lesion segmentation provides a valuable tool for clinical diagnosis and research, and convolutional neural networks (CNNs) have achieved unprecedented success in the segmentation task. Data augmentation is a widely used strategy to improve the training of CNNs. In particular, data augmentation approaches that mix pairs of annotated training images have been developed. These methods are easy to implement and have achieved promising results in various image processing tasks. However, existing data augmentation approaches based on image mixing are not designed for brain lesions and may not perform well for brain lesion segmentation. Thus, the design of this type of simple data augmentation method for brain lesion segmentation is still an open problem. In this work, we propose a simple yet effective data augmentation approach, dubbed as CarveMix, for CNN-based brain lesion segmentation. Like other mixing-based methods, CarveMix stochastically combines two existing annotated images (annotated for brain lesions only) to obtain new labeled samples. To make our method more suitable for brain lesion segmentation, CarveMix is lesion-aware, where the image combination is performed with a focus on the lesions and preserves the lesion information. Specifically, from one annotated image we carve a region of interest (ROI) according to the lesion location and geometry with a variable ROI size. The carved ROI then replaces the corresponding voxels in a second annotated image to synthesize new labeled images for network training, and additional harmonization steps are applied for heterogeneous data where the two annotated images can originate from different sources. Besides, we further propose to model the mass effect that is unique to whole brain tumor segmentation during image mixing. To evaluate the proposed method, experiments were performed on multiple publicly available or private datasets, and the results show that our method improves the accuracy of brain lesion segmentation. The code of the proposed method is available at https://github.com/ZhangxinruBIT/CarveMix.git.

The Function and Mechanism of Long Non-Coding RNA RP11-23J9.4 in Thyroid Cancer.

INTRODUCTION: The objective of this research is to explore whether LncRNA RP11 23J9.4 can be used as a targeted marker for the treatment of thyroid cancer (TC), downregulation of LncRNA RP11 23J9.4 and X-ray radiation have synergistic inhibitory effect on TC. METHODS: The expression of LncRNA RP11 23J9.4 in papillary thyroid carcinoma (PTC) cell was downregulated by cell transfection, and its inhibitory effect on PTC cells was proved through proliferation, invasion experiment, apoptosis, and cell cycle analysis. The transfected cells were irradiated with 2 Gy X-ray. The above methods were also used to detect whether they had synergistic inhibitory effect on TC. The expression of Axin2 gene and protein were detected by real-time PCR, Western blotting, and immunohistochemistry. RESULTS: On the one hand, it is proved that downregulating the expression of LncRNA RP11 23J9.4 can inhibit the development of TC through Axin2. On the other hand, it is clear that downregulation of LncRNA RP11 23J9.4 and X-ray radiation have synergistic inhibitory effect on TC. CONCLUSIONS: LncRNA RP11 23J9.4 and X-ray have significant synergistic effect on TC. LncRNA RP11 23J9.4 can be used as a marker for TC targeted therapy.

Circadian pattern subtyping unveiling distinct immune landscapes in breast cancer patients for better immunotherapy.

BACKGROUND: While epidemiological studies have established a firm link between circadian disruption and tumorigenesis, the role and mechanism are not fully understood, complicating the design of therapeutic targets related to circadian rhythms (CR). Here, we aimed to explore the intertumoral heterogeneity of CR and elucidate its impact on the tumor microenvironment (TME), drug sensitivity, and immunotherapy. METHODS: Based on unsupervised clustering of 28 CR genes, two distinct CR subtypes (cluster-A and cluster-B) were identified in the TCGA cohort. We further constructed a circadian rhythm signature (CRS) based on the CR genes primarily responsible for clustering to quantify CR activity and to distinguish CR subtypes of individual patients from external datasets. CR subtypes were evaluated by TME characteristics, functional annotation, clinical features, and therapeutic response. RESULTS: The cluster-B (low-CRS) group was characterized by highly enriched immune-related pathways, high immune cell infiltration, and high anti-tumor immunity, while the cluster-A (high-CRS) group was associated with immunosuppression, synaptic transmission pathways, EMT activation, poor prognosis, and drug resistance. Immunohistochemistry (IHC) results demonstrated that high CD8+ T cell infiltration was associated with low-CR-protein expression. Importantly, patients with low CRS were more likely to benefit from immune checkpoint blockade (ICB) treatment, possibly due to their higher tumor mutation burden (TMB), increased immune checkpoint expression, and higher proportion of "hot" immunophenotype. CONCLUSION: In a nutshell, the cross talk in CR could reflect the TME immunoreactivity in breast cancer. Besides providing the first comprehensive pathway-level analysis of CR in breast cancer, this work highlights the potential clinical utility of CR for immunotherapy.

Diagnostic accuracy of DNA-based SDC2 methylation test in colorectal cancer screening: a meta-analysis.

BACKGROUND: A growing body of research suggests that methylated genes can be used as early diagnostic markers for cancer. Some studies on methylated Syndecan 2 (SDC2) have shown that it has a great diagnostic ability in colorectal cancer. This meta-analysis was aimed to estimate the diagnostic performance of methylated SDC2 as a potential novel biomarker to screen for the colorectal cancer. METHODS: Two independent researchers conducted a comprehensive literature search to identify all relevant studies on SDC2 methylation for the diagnosis of colorectal cancer from inception to March 1, 2021. By using STATA and Revman software, the data were analyzed using a Bivariate mixed model. The quality of each study was also evaluated. RESULTS: A total of 12 studies comprised of 1574 colorectal cancer patients and 1945 healthy people were included in our meta-analysis. Bivariate analysis showed a pooled sensitivity of 0.81 [95% confidence interval (CI) 0.74-0.86], specificity of 0.95 (95% CI 0.93-0.96), positive likelihood ratio of 15.29 (95% CI 10.83-21.60), and negative likelihood ratio of 0.21 (95% CI 0.15-0.27). The diagnostic odds ratio and the area under the summary ROC curve for diagnosing colorectal cancer were 74.42 (95% CI45.44-121.89) and 0.96 (95% CI 0.94-0.97), respectively. For adenomas, the pooled sensitivity and specificity were 0.47 (95% CI 0.34-0.61) and 0.95 (95% CI 0.92-0.97), respectively. CONCLUSIONS: Our analysis revealed that methylated SDC2 could be considered as a potential novel biomarker to screen for colorectal cancer.

NCK1 promotes the angiogenesis of cervical squamous carcinoma via Rac1/PAK1/MMP2 signal pathway.

OBJECTIVE: The study was to explore the roles of Nck1 in the angiogenesis of cervical squamous cell carcinoma (CSCC). METHODS: mRNA and protein levels were evaluated with real-time quantitative PCR and immunohistochemisty/western blotting respectively. The cancer microvessel density (MVD) was assayed with CD34 endothelial labeling. Nck1 gene knock-in (SiHa-Nck1+) and knock-down (SiHa-Nck1-) were achieved by gene transfection and siRNA respectively. Protein level from cellular supernatant was measured with ELISA. Proliferation, migration and tube formation of the Human Umbilical Vein Endothelial cells (HUVECs) were evaluated by CCK-8 cell viability assay, transwell chamber assay and in vitro Matrigel tubulation assay respectively. RESULTS: Nck1 level gradually increased from normal cervical epithelia to high-grade CIN, overexpressed in CSCC and was associated with cancer MVD. The ability of proliferation, migration and tube formation of HUVECs was enhanced in SiHa-Nck1+-treated while decreased in SiHa-NcK1--treated cells compared to SiHa-control-treated cells. Mechanistically, RAC1-GTP, p-PAK1 and MMP2 were increased in SiHa-NCK1+ cells and pretreatment with the Rac1 inhibitor (NSC23766) significantly decreased their levels. Furthermore, inhibition of PAK1 reduced MMP2 level in SiHa-Nck1+ cells whereas the level of Rac1-GTP was unaltered. Also, inhibition of Rac1 or PAK1 impaired angiogenesis-inducing capacity of cancer cells. CONCLUSIONS: Nck1 promotes the angiogenesis-inducing capacity of CSCC via the Rac1/PAK1/MMP2 signal pathway.

[Kidney tumor segmentation in ultrasound images using adaptive sub-regional evolution level set models].

Kidney tumor is one of the diseases threatening human health. Ultrasound is widely applied in kidney tumor diagnosis due to its high popularization, low price and no radiation. Accurate segmentation of kidney tumor is the basis of precise treatment. Kidney tumors often grow in the middle of cortex, so that segmentation is easy disturbed by nearby organs. Besides, ultrasound images own low contrast and large speckle, leading to difficult segmentation. This paper proposed a novel kidney tumor segmentation method in ultrasound images using adaptive sub-regional evolution level set models (ASLSM). Regions of interest are firstly divided into subareas. Secondly, object function is designed by integrating inside and outside energy and gradient, in which the ratio of these two parts are adjusted adaptively. Thirdly, ASLSM adapts convolution radius and curvature according to centroid principle and similarity inside and outside zero level set. Hausdorff distance (HD) of (8.75 ± 4.21) mm, mean absolute distance (MAD) of (3.26 ± 1.69) mm, dice-coefficient (DICE) of 0.93 ± 0.03 were obtained in the experiment. Compared with traditional ultrasound segmentation method, ASLSM is more accurate in kidney tumor segmentation. ASLSM may offer convenience for doctor to locate and diagnose kidney tumor in the future.

The anti-inflammatory effect of BML-111 on COPD may be mediated by regulating NLRP3 inflammasome activation and ROS production.

The aim of this study is to investigate whether the lipoxin receptor agonist BML-111 exerts a protective effect against inflammation in a mouse model of chronic obstructive pulmonary disease (COPD) by regulating NLRP3 inflammasome activation and reactive oxygen species (ROS) production. In this study, mice were randomly divided into the following five groups: control group (Control), COPD model group (Model), BML-111 low-dose group (Low-BML), BML-111 high-dose group (High-BML) and Dexamethasone group (Dex). NLRP3 involvement and oxidative stress were evaluated. Differential cell counts in the BALF were calculated to obtain a reliable enumeration of each cell type, and the levels of TGF-ß, TNF-α, IL-1ß, and IL-10 in BALF were evaluated using ELISA. We found that the white blood cell and lymphocyte numbers in the BALF were significantly lower in the High-BML group than in the Model group. ELISA of the BALF showed that BML-111 reduced TGF-ß and IL-1ß levels to some extent. HE staining showed various degrees of reduction in inflammatory cell infiltration in the bronchopulmonary tissue and blood vessels of the Low-BML, High-BML and Dex groups. Measurement of oxidative stress showed that SOD activity was significantly upregulated and that the increase in MDA content was prevented in the High-BML and Dex groups. According to the Western blotting analysis, the levels of NLRP3, Cleaved-IL-1ß and Cleaved-caspase-1 were decreased and Nrf-2 was increased to various extents in the Low-BML, High-BML and Dex groups. Based on these findings, BML-111 may prevent NLRP3 inflammasome activation and inhibit ROS production via upregulation of Nrf-2, thereby exerting an anti-inflammatory effect on COPD model mice.

Astrocyte elevated gene-1 promotes progression of cervical squamous cell carcinoma by inducing epithelial-mesenchymal transition via Wnt signaling.

OBJECTIVE: The aim of this study was to investigate the association of astrocyte elevated gene-1 (AEG-1) with epithelial-mesenchymal transition of cervical squamous cell carcinoma (CSCC) and the underlying mechanisms. METHODS: The expression of proteins was determined by immunohistochemistry in tissues. Overexpression and knockdown of AEG-1 in SiHa cells were achieved by stable AEG-1 gene transfection (SiHa-AEG-1+) and AEG-1-siRNA (SiHa-AEG-1-), respectively. The cellular levels of messenger RNA and proteins were assessed with reverse transcription polymerase chain reaction and Western blotting, respectively. The cell invasion capacity was assessed by the chamber invasion assay. RESULTS: AEG-1 was overexpressed in clinical CSCC and associated with lymph node metastasis, parametrial involvement, stromal invasion, and vascular invasion. A high level of vimentin and a low level of E-cadherin were also detected in the cancer tissues. AEG-1 expression was positively correlated with vimentin expression and negatively with E-cadherin expression in CSCC tissues. In addition, high level of AEG-1 was related to unfavorable prognosis of CSCC. On a cellular level, overexpression of AEG-1 was found to lead to an up-regulation of vimentin and a down-regulation of E-cadherin on messenger RNA and protein level in SiHa cells, whereas AEG-1 knockdown led to a contrary result. Meanwhile, the nuclear levels of NF-κB p65 and ß-catenin were also increased in SiHa-AEG-1+, whereas their nuclear levels were decreased in SiHa-AEG-1-. Inhibition of Wnt signaling significantly reduced vimentin level and enhanced E-cadherin level in SiHa-AEG+, but inhibition of NF-κB signaling did not. SiHa-AEG-1+ and SiHa-AEG- showed an enhanced and a decreased invasive capacity, respectively. The enhanced invasiveness of SiHa-AEG-1+ was weakened by inhibition of Wnt signaling. CONCLUSIONS: AEG-1 was associated with the progression of CSCC by promoting epithelial-mesenchymal transition via Wnt signaling pathway.

Diagnosis and Treatment of Keloid: Method Summary and Effect Evaluation.

Keloid is a prevalent skin disorder characterized by the abnormal growth of keloid tissue, which usually occurs following wound healing or surgical incisions. It typically progresses through several stages: the inflammatory stage, the proliferative stage, collagen remodeling, and ultimately the formation of keloid. This review aims to summarize the diagnostic and therapeutic methods for keloid, and evaluate their effectiveness. The diagnosis of keloid is usually based on medical history and clinical manifestations such as pain, itching, erythema, and induration. Other commonly used diagnostic methods include tissue biopsy and ultrasound examination. Various treatment options for keloid exist, including physical therapy, medication, surgical treatment, and radiation therapy. Physical therapy includes pressure therapy, laser therapy, such as silicone sheets, elastic bandages, and laser irradiation. Medication treatment mainly involves the application of topical medications or intralesional injections, such as topical corticosteroids, 5-fluorouracil, and others. Radiation therapy can be administered using applicators and superficial radiation therapy, among other methods. The treatment outcomes of keloid vary from person to person and recurrence is common. Therefore, a comprehensive treatment approach may be the most effective strategy. Individualized treatment plans should consider factors such as the patient's age, gender, medical history, and the severity of the condition. In conclusion, the diagnosis and treatment of keloid require consideration of multiple factors and the implementation of individualized treatment plans. Future research should focus on identifying the molecular mechanisms underlying the occurrence and progression of keloid in order to develop more effective treatment methods.

PD-1 inhibitor causes pathological injury to multiple organs in a Lewis lung cancer mouse model.

Recently, immunotherapy has become one of the most promising strategies in the treatment of malignant tumors. However, nonspecific immune activation may lead to immunotherapy-related adverse effects (irAEs). IrAEs involve almost all organs and may be life-threatening. However, current research on irAEs is scarce, and knowledge regarding histopathology is insufficient. In the present study, after Lewis lung cancer mouse model formation, the experimental group mice were intraperitoneally injected with a programmed cell death protein 1 (PD-1) inhibitor. Hematoxylin and eosin (H&E) staining, immunohistochemistry (IHC), and Masson's trichrome staining were used to evaluate the pathological characteristics of the heart, lungs, spleen, intestines, kidneys, and liver. Echocardiography was used to evaluate heart function. The results showed that one or more inflammatory cells were positively expressed in each organ in the PD-1 inhibitor group. Compared to the control group, Masson's trichrome staining showedincreased fibrosis of the heart, spleen, and kidney in the PD-1 inhibitor group, and echocardiography also showed impaired cardiac function in the PD-1 inhibitor group. Thus, the PD-1 inhibitor-induced inflammatory response may beimplicated in the impairment of multiple murine organs. This is the first study to describe the pathological changes in multiple organs caused by PD-1 inhibitors in a holistic form.

99mTc-MDP 3-Phase Bone Imaging in 3 Cases of Pigmented Villonodular Synovitis.

ABSTRACT: Pigmented villonodular synovitis (PVNS) is a rare proliferative synovial benign disorder, which is characterized by villonodular hyperplasia of joints, tendon sheath, and synovium; invasion of adjacent tissue; and sometimes visible hemosiderin deposition. Studies regarding bone scan findings of PVNS were relatively limited. Here, we report our findings on 99mTc-MDP 3-phase bone scan with SPECT/CT images on delayed phase in 3 patients with joint PVNS.

Knowledge transfer between brain lesion segmentation tasks with increased model capacity.

Convolutional neural networks (CNNs) have become an increasingly popular tool for brain lesion segmentation in recent years due to its accuracy and efficiency. However, CNN-based brain lesion segmentation generally requires a large amount of annotated training data, which can be costly for medical imaging. In many scenarios, only a few annotations of brain lesions are available. One common strategy to address the issue of limited annotated data is to transfer knowledge from a different yet relevant source task, where training data is abundant, to the target task of interest. Typically, a model can be pretrained for the source task, and then fine-tuned with the scarce training data associated with the target task. However, classic fine-tuning tends to make small modifications to the pretrained model, which could hinder its adaptation to the target task. Fine-tuning with increased model capacity has been shown to alleviate this negative impact in image classification problems. In this work, we extend the strategy of fine-tuning with increased model capacity to the problem of brain lesion segmentation, and then develop an advanced version that is better suitable for segmentation problems. First, we propose a vanilla strategy of increasing the capacity, where, like in the classification problem, the width of the network is augmented during fine-tuning. Second, because unlike image classification, in segmentation problems each voxel is associated with a labeling result, we further develop a spatially adaptive augmentation strategy during fine-tuning. Specifically, in addition to the vanilla width augmentation, we incorporate a module that computes a spatial map of the contribution of the information given by width augmentation in the final segmentation. For demonstration, the proposed method was applied to ischemic stroke lesion segmentation, where a model pretrained for brain tumor segmentation was fine-tuned, and the experimental results indicate the benefit of our method.

Volatile organic compounds as a potential screening tool for neoplasm of the digestive system: a meta-analysis.

This meta-analysis was aimed to estimate the diagnostic performance of volatile organic compounds (VOCs) as a potential novel tool to screen for the neoplasm of the digestive system. An integrated literature search was performed by two independent investigators to identify all relevant studies investigating VOCs in diagnosing neoplasm of the digestive system from inception to 7th December 2020. STATA and Revman software were used for data analysis. The methodological quality of each study was assessed using the Quality Assessment of Diagnostic Accuracy Studies tool. A bivariate mixed model was used and meta-regression and subgroup analysis were performed to identify possible sources of heterogeneity. A total of 36 studies comprised of 1712 cases of neoplasm and 3215 controls were included in our meta-analysis. Bivariate analysis showed a pooled sensitivity of 0.87 (95% confidence interval (CI) 0.83-0.90), specificity of 0.86 (95% CI 0.82-0.89), a positive likelihood ratio of 6.18 (95% CI 4.68-8.17), and a negative likelihood ratio of 0.15 (95% CI 0.12-0.20). The diagnostic odds ratio and the area under the summary ROC curve for diagnosing neoplasm of the digestive system were 40.61 (95% CI 24.77-66.57) and 0.93 (95% CI 0.90-0.95), respectively. Our analyses revealed that VOCs analysis could be considered as a potential novel tool to screen for malignant diseases of the digestive system.

Inhibition of mTORC1 signaling protects kidney from irradiation-induced toxicity via accelerating recovery of renal stem-like cells.

BACKGROUND: Irradiation-induced kidney damage is inevitable during radiotherapeutic practice, which limits effective radiotherapy doses on tumor treatment. In the present study, the role of mTOR complex 1 (mTORC1) signaling was investigated in irradiation-induced renal injuries. METHODS: Mice were exposed to 8.0-Gy X-ray of total body irradiation and subsequently treated with rapamycin. Changes of renal morphology were assessed by hematoxylin and eosin staining. Expression of pS6 and CD133 was detected via immunostaining. Cellular apoptosis and proliferation were measured by TUNEL, caspase-3 and BrdU staining. Activation of mTORC1, TGF-ß and NF-κB signaling pathways was determined through western blot analysis. RESULTS: Our data displayed that irradiation disrupted the structures of renal corpuscles and tubules and decreased the density of CD133+ renal stem-like cells, which were related with increasing cellular apoptosis and decreasing cell proliferation post exposure. Activation of mTORC1, TGF-ß and NF-κB signaling pathways was determined in irradiated renal tissues, which were inhibited by rapamycin treatment. Application of rapamycin after irradiation decreased cellular apoptosis and increased autophagy and cell proliferation in renal tissues. The density of CD133+ renal stem-like cells was significantly increased in irradiated kidneys after rapamycin treatment. The morphology of irradiated renal corpuscles and tubules was gradually recovered upon rapamycin treatment. CONCLUSIONS: These findings indicate that inhibition of mTORC1 signaling by rapamycin ameliorates irradiation-induced renal toxicity mediated by decreasing cellular apoptosis and increasing CD133+ renal stem-like cells.

[Expressions of STAT3, p-STAT3 and E-cadherin in colorectal cancer and clinical implications].

OBJECTIVE: To investigate the correlation of expressions of STAT3 and p-STAT3 with epithelial mesenchymal transition(EMT)-associated protein E-cadherin in colorectal cancer, and to examine the association of above expressions with tumor invasion and metastasis of colorectal cancer. METHODS: Immunohistochemistry assay ElivisionTM plus was used to detect the expressions of STAT3, p-STAT3 and E-cadherin protein in colorectal cancer tissue samples of 50 cases and their corresponding adjacent non-tumor tissues. Association of these protein expressions with tumor invasion and metastasis was analyzed with χ(2) test. Correlation of STAT3 and p-STAT3 with E-cadherin was analyzed with Spearman method. RESULTS: Positive expression rates of STAT3, p-STAT3 and E-cadherin protein in colorectal cancer tissues were 72%(36/50), 76%(38/50) and 26%(13/50), which were significantly higher compared to adjacent normal intestinal mucosa tissues [24%(12/50), 26%(13/50) and 68%(34/50), all P<0.05]. STAT3, p-STAT3 and E-cadherin expressions were associated with tumor differentiation, tumor invasion depth, tumor size, lymph node metastasis, TNM staging (all P<0.05). In colorectal cancer tissues, STAT3 protein expression was positively correlated with p-STAT3 expression. STAT3 and p-STAT3 expressions in colorectal cancer tissues were negatively correlated with E-cadherin expression(P<0.05). CONCLUSION: STAT3 and p-STAT3 may be involved in tumor EMT through inhibition of E-cadherin expression, leading to the development of colorectal cancer.

[Gastroscopic and pathological characteristics of patients with or without schistosomiasis in Poyang Lake area].

OBJECTIVES: To understand the gastroscopic and pathological characteristics of patients with miasis in Poyang Lake area, and to explore the relationship between schistosomiasis and pathological changes of gastric mucosa. METHODS: Volunteers with or without schistosomiasis were recruited and divided into a case group and a control group. All the objects were examined by electronic gastroscopy and pathological examinations. RESULTS: Two hundred and fifty-three volunteers diagnosed with chronic or advanced schistosomiasis in the case group showed different degrees of gastric mucosal changes, including 7 cases with schistosomal eggs deposited beneath the gastric mucosa (with an incidence of 2.77%) , 33 cases with dysplastic hyperplasia and intestinal metaplasia (with an incidence of precancerous lesion of 13.04%), and 1 case with gastric cancer. While in the 200 volunteers without schistosomiasis in the control group, the results showed milder gastric mucosal changes, 33 cases were detected with dysplastic hyperplasia and intestinal metaplasia (with an incidence of 7.50%), and 1 case was diagnosed gastric cancer. The difference between the incidences of precancerous lesion in the two groups had no statistic significance (P > 0.05). CONCLUSIONS: The incidence and extent of gastric mucosal changes in schistosomiasis patients are higher and more serious than those in non-schistosomiasis patients, and gastrointestinal schistosomiasis is not related to gastric cancer.

Expression of MMP9 and CD147 in invasive squamous cell carcinoma of the uterine cervix and their implication.

Matrix metalloproteinase 9 (MMP9) and CD147 play a role in invasion and metastasis of many types of human malignancies. The correlation of the expression of MMP9 and CD147 with invasion and metastasis of invasive squamous cell carcinoma (SCC) of the uterine cervix has not been examined. In the present study, RT-PCR assay was used to detect the expression level of MMP9 mRNA semiquantitatively, and immunohistochemical stain was adapted to evaluate the score of CD147 on the cell membrane or in the cytoplasm of tumor cells of 65 cases of invasive squamous cell carcinoma of the uterine cervix and 21 cases of chronic cervitis tissues. MMP9 and CD147 expression in correlation with invasion, metastasis, and differentiation of invasive SCC of the uterine cervix was analyzed statistically. We found that MMP9 and CD147 expression was elevated significantly in tumor tissue compared to the control (cervical epithelium of chronic cervitis) (P<0.01). In the comparison of MMP9 and CD147 expression in 47 cases with lymph node metastasis and 18 cases without lymph node metastasis, there was a significantly higher expression of MMP9 and CD147 in the group with lymph node metastasis (P<0.05 for MMP9, P<0.01 for CD147). MMP9 expression was significantly higher in 24 cases of poor differentiation than in 41 cases of moderate differentiation (P<0.05). No difference was found in CD147 expression between poor and moderate differentiation (P>0.05). No significant difference in MMP9 and CD147 expression levels was obtained between 26 cases of FIGO stage I tumors and 39 cases of stage II tumors (P>0.05 for MMP9, P>0.05 CD147). There was no correlation between MMP9 or CD147 expression levels and the resected tumor size (P>0.05). The positive correlation (r=0.568, P<0.001) of MMP9 expression and CD147 score was seen in the tumor tissues of 65 cases. The data in this study show that MMP9 and CD147 expression are correlated with invasion, metastasis of squamous cell carcinoma of the uterine cervix, and that MMP9 expression is correlated with poor differentiation of invasive squamous cell carcinoma of the uterine cervix.