MiR-22-3p Expression is down-regulated in lung adenocarcinoma

Background: Our current study was performed with an attempt to detect the expression of microRNA-22-3p (miR-22-3p) in lung adenocarcinoma, as well as to analyze its role in clinical practice. In addition, its relationship with vascular endothelial growth factor (VEGF) and metastasis related indexes was focused. Material and Method: The trials in which 62 cases of lung adenocarcinoma were received to collect tumor tissue (study group) and normal lung tissue (control group) were eligible for this study. The expression of miR-22-3p in the two groups was detected through RT-PCR. Immunohistochemical method was used to detect the expression of VEGF and leukocyte differentiation antigen 31 (CD31) marked microvessel density (MVD) in lung adenocarcinoma. The expressions of matrix metalloproteinase-3 (MMP-3) and matrix metalloproteinase-7 (MMP-7) in lung adenocarcinoma were also detected through the use of Western Blot. Results: The present study revealed significant difference in the expression of miR-22-3p between the two groups. No significant difference in the expression of gender, age, neural invasion and the number of lesions were observed between groups. There was significant difference in the expression of miR-22-3p in the maximum diameter of tumor, pleural recidivism, vascular recidivism, lymph node metastasis and different TNM stages. Based on survival analysis, miR-22-3p was linked to survival time. Correlation analysis indicated that there was negative correlation between miR-22-3p and VEGF, miR-22-3p and MVD, miR-22-3p and MMP-3, and miR-22-3p and MMP-7 in lung adenocarcinoma. Conclusion: Our findings provide evidence that miR-22-3p is low expressed in lung adenocarcinoma tissues and the low expression of miR-22-3p is closely associated with clinicopathological characteristics and the prognosis. MiR-22-3p may be involved in the tumor progression of lung adenocarcinoma and may serve as a biomarker for the diagnosis and prognosis of lung adenocarcinoma.

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Erythropoietin Receptor is a Risk Factor for Prognosis: A Potential Biomarker in Lung Adenocarcinoma

10.21203/rs.3.rs-1211017/v1 ◽

2022 ◽

Author(s):

Ya-Jing Zhang ◽

Sen-Yu Wang ◽

Song-Tao Han ◽

Yao-Yao Huang ◽

Yang-Chun Feng

Keyword(s):

Lung Adenocarcinoma ◽

Gene Mutations ◽

Predictive Ability ◽

Erythropoietin Receptor ◽

Immunohistochemical Method ◽

Normal Lung ◽

Mrna Levels ◽

Protein Levels ◽

Potential Biomarker ◽

Epor Expression

Abstract Background: Lung cancer has the highest mortality rate of all cancers, and LUAD's survival rate is particularly poor. Erythropoietin receptor (EPOR) is a member of the cytokine class I receptor family and can be detected in cancers such as lung adenocarcinoma (LUAD), however, the expression levels and prognostic value of EPOR in LUAD are still unclear.Methods: Multiple bioinformatics databases such as TIMER, Kaplan-Meier Plotter and TCGA databases, immunohistochemical method, and clinicopathological data of 92 LUADpatients between January 2008 and June 2016 were used to explore the EPOR expression, gene mutations affecting EPOR expression, EPOR-interacting or coexpressed genes, potential biological functions and the correlation of EPOR expression with prognosis, immune microenvironment and so on.All statistical analyses were performed in the R version 4.1.1.Results: In this study, the EPOR mRNA expression in LUAD tissues was possibly downregulated compared with that in normal lung tissues, but the EPOR protein expression in LUAD tissues was higher than that in paired normal lung tissues. Mutations in five genes, DDX60L, LGR6, POTEB3, RIF1 and SOX5, resulted in downregulation of EPOR expression, mutations in 10 genes includingC1orf168, DBX2 and EIF5B, resulted in upregulation of EPOR expression. Erichment analyses showed that EPOR is involved in neural tissue ligand-receptor interactions, MAPK and PI3K/Akt signaling pathways and cancer pathways. The KM Plotter and PrognoScan databases consistently concluded that EPOR was associated with prognosis in LUAD patients. Our clinicopathological data showed that high EPOR expression was associated with poorer OS (29.5 vs 46 months) and had a good predictive ability for 5-year survival probability. Conclusions: EPOR expression might be downregulated at the mRNA levels and significantly upregulated at the protein levels in LUAD, which showed that the mRNA and protein levels of EPOR are inconsistent.The high expression of EPOR was associated with poor prognosis and is expected to be a potential new prognostic marker for LUAD.

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Hypodontia phenotype in patients with epithelial ovarian cancer

Radiology and Oncology ◽

10.2478/raon-2014-0034 ◽

2015 ◽

Vol 49 (1) ◽

pp. 65-70 ◽

Cited By ~ 2

Author(s):

Anita Fekonja ◽

Andrej Cretnik ◽

Danijel Zerdoner ◽

Iztok Takac

Keyword(s):

Ovarian Cancer ◽

Epithelial Ovarian Cancer ◽

Figo Stage ◽

Clinicopathological Characteristics ◽

Control Group ◽

Malignant Tumours ◽

Cancer Group ◽

Significant Difference ◽

The University ◽

And Control

Abstract Background. Ovarian cancer is usually diagnosed in an advanced stage and the present clinical and diagnostic molecular markers for early OC screening are insufficient. The aim of this study was to identify potential relationship between the hypodontia and epithelial ovarian cancer (EOC). Patients and methods. A retrospective study was conducted on 120 patients with EOC treated at the Department of Gynaecologic and Breast Oncology at the University Clinical Centre and 120 gynaecological healthy women (control group) of the same mean age. Women in both groups were reviewed for the presence of hypodontia and the patients with EOC also for clinicopathological characteristics of EOC according to hypodontia phenotype. Results. Hypodontia was diagnosed in 23 (19.2%) of patients with EOC and 8 (6.7%) controls (p = 0.004; odds ratio [OR] = 3.32; confidence interval [CI], 1.42-7.76). There was no statistically significant difference in patients with EOC with or without hypodontia regarding histological subtype (p = 0.220); they differed in regard to FIGO stage (p = 0.014; OR =3.26; CI, 1.23-8.64) and tumour differentiation grade (p = 0.042; OR = 3.1; CI, 1.01-9.53). Also, bilateral occurrence of EOC was more common than unilateral occurrence in women with hypodontia (p = 0.021; OR = 2.9; CI, 1.15-7.36). We also found statistically significant difference between the ovarian cancer group and control group in presence of other malignant tumours in subjects (p < 0.001). Conclusions. The results of the study suggest a statistical association between EOC and hypodontia phenotype. Hypodontia might serve as a risk factor for EOC detection.

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BCL3 and NSCLC: Are they related?

Journal of Clinical Oncology ◽

10.1200/jco.2013.31.15_suppl.e18507 ◽

2013 ◽

Vol 31 (15_suppl) ◽

pp. e18507-e18507

Author(s):

Fotinos-Ioannis D Dimitrakopoulos ◽

Anastasia E Kottorou ◽

Anna G Antonacopoulou ◽

Stella Marousi ◽

Ioulia Koukourikou ◽

...

Keyword(s):

Lung Tissue ◽

Immunohistochemical Analysis ◽

Stage Ii ◽

Disease Stage ◽

Normal Lung Tissue ◽

Maximum Diameter ◽

Normal Lung ◽

Histological Subtype ◽

Healthy Donors ◽

Significant Difference

e18507 Background: NFkB pathways have become objects of detailed research in the last years, although, little is known of the possible role of BCL3 in lung carcinogenesis. The aim of this study was to define the relation of the BCL3 single nucleotide polymorphism rs8100239 with NSCLC and its association with BCL3 protein expression. Methods: Using Tagger and Sysnps programs, we chose the rs8100239 polymorphism of BCL3.We used 294 blood and FFPE normal tissue specimens from patients with NSCLC and 280 blood specimens from healthy donors. DNA isolation was performed using the Qiagen DNA blood and the QIAamp DNΑ FFPE Tissue kits. Samples were genotyped using real-time PCR. Immunohistochemical analysis for BCL3 was performed on 90 FFPE specimens (80 tumors and 10 tumor-adjacent normal tissues) from NSCLC patients. Results: Approximately half of the healthy donors (45.5%) were AT heterozygotes, 36.6% were TT and 17.9% were AA homozygotes. The respective frequencies in patients were 43.8%, 33.1% and 23.1%. There was no statistically significant difference in allele frequencies between healthy controls and patients (p=0.297). However, patients of stage II carrying a T allele displayed two and five-year survival benefit compared to patients with AA genotype (p<0.001). Immunohistochemical analysis for BCL3 protein revealed a statistically significant difference between malignant and normal lung tissue (p<0.001). More specifically, BCL3 was detected in both the cytoplasm and nucleus in neoplastic tissues with strong intensity, whereas in non neoplastic tissue no immunostaining was noticed. BCL3 protein levels were not associated with the polymorphism. However, cytoplasmic expression of BCL3 was correlated with age (p=0.009), histological subtype (p=0.031) and disease stage (0.038). Furthermore, tumors with smaller diameter had higher BCL3 nuclear expression levels than larger tumors (p=0.009). Conclusions: Patients of stage II carrying a T allele had improved two and five-year survival. BCL3 expression is not correlated with rs8100239 status. However, it is related to histological subtype, stage and maximum diameter while it differs between malignant and normal lung tissue. This research has been co-financed by the EU and Greek national funds (Heracleitus II Program).

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Expression level of ACE2 in lung adenocarcinoma.

Journal of Clinical Oncology ◽

10.1200/jco.2020.38.15_suppl.e21022 ◽

2020 ◽

Vol 38 (15_suppl) ◽

pp. e21022-e21022

Author(s):

Danni Liu ◽

Tianhao Mu ◽

Shifu Chen

Keyword(s):

Lung Adenocarcinoma ◽

Lung Tumor ◽

Expression Level ◽

Normal Lung ◽

Primary Lung Adenocarcinoma ◽

Significant Difference ◽

And Gender ◽

Novel Coronavirus ◽

Public Datasets ◽

Ethnicity And Gender

e21022 Background: 2019-nCoV, a novel coronavirus (2019-nCoV), has infected tens of thousands of people in Wuhan, Hubei Province, China. This new coronavirus has led to hundreds of deaths, and especially threatened people with underlying diseases. ACE2 was reported as the 2019-nCoV putative receptor. The expression abundance of ACE2 may cause different disease progressions. Here, we evaluated the expression profile of ACE2 from 283 samples in lung adenocarcinoma . Methods: 283 samples from the public datasets (GEO: GSE31210 and GEO: GSE2109) were grouped by tissue, ethnicity and gender. The data was normalized by the RMA algorithm. Student 's t-test was used to compare the expression of ACE2 in different groups . Results: The expression level of ACE2 of primary lung tumor was significantly higher than normal lung tissue ( p < 0.0001). ACE2 was significantly differential-expressed between Asian and Caucasian lung adenocarcinoma patients ( p < 0.0001). However, no significant difference of the expression of ACE2 was observed by gender ( p = 0.33). Conclusions: ACE2 was highly expressed in primary lung adenocarcinoma , compared with normal lung tissues. The expression level of ACE2 was higher in Asian lung adenocarcinoma patients than Caucasian’s. These conclusions imply that Asian people with lung adenocarcinoma may be more vulnerable to 2019-nCoV.

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A genetic variant in the promoter of lncRNA MALAT1 is related to susceptibility of ischemic stroke

10.21203/rs.2.19452/v1 ◽

2019 ◽

Author(s):

yan wang ◽

Xi-Xi Gu ◽

Hua-Tuo Huang ◽

Chun-Hong Liu ◽

Gui-Jiang Wei ◽

...

Keyword(s):

Ischemic Stroke ◽

Lung Adenocarcinoma ◽

Protective Factor ◽

Genetic Variant ◽

Blood Lipid ◽

Control Group ◽

Lipid Levels ◽

Lncrna Malat1 ◽

Significant Difference ◽

Blood Lipid Levels

Abstract Metastasis-associated lung adenocarcinoma transcript-1 (MALAT1) was aberrantly expressed in diverse diseases including ischemic stroke (IS). This study aimed to investigate the association between MALAT1 polymorphism and IS risk. We performed the genotyping of rs600231, rs1194338, rs4102217 and rs591291 in the promoter of MALAT1 by SNPscan method. Quantitative PCR was used to determine the levels of MALAT1 relative expression. We found the rs1194338 C>A variant in MALAT1 promoter was associated with IS risk (AC vs. CC: adjusted OR = 0.623, 95% CI, 0.417-0.932, P = 0.021; AA vs. CC: adjusted OR = 0.474, 95% CI, 0.226-0.991, P = 0.047; AC/AA vs. CC: adjusted OR = 0.596, 95% CI, 0.406-0.874, P = 0.008; A vs. C adjusted OR = 0.658, 95% CI, 0.487-0.890, P = 0.007). The IS patients showed higher expression levels of MALAT1 compared with the control group ( P < 0.05), but patients with AC/AA genotypes of rs1194338 have no significant difference compared to CC genotype ( P > 0.05). In addition, no significant differences were observed in blood lipid levels among SNPs of MALAT1 ( P > 0.05). These results suggest that the rs1194338 AC/AA genotypes may be a protective factor for IS, which mechanism needs to be further explored.

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Aspirin Exerts Neuroprotective Effects by Reversing Lipopolysaccharide-Induced Secondary Brain Injury and Inhibiting Matrix Metalloproteinase-3 Gene Expression

Disease Markers ◽

10.1155/2021/3682034 ◽

2021 ◽

Vol 2021 ◽

pp. 1-10

Author(s):

Depeng Feng ◽

Dezhe Chen ◽

Tuanzhi Chen ◽

Xiaoqian Sun

Keyword(s):

Matrix Metalloproteinase ◽

Test Scores ◽

Neuroprotective Effect ◽

Brain Area ◽

Cerebral Injury ◽

Control Group ◽

Secondary Brain Injury ◽

Walking Test ◽

Matrix Metalloproteinase 3 ◽

Injured Brain

Objective. This study is aimed at exploring the possible neuroprotective mechanism of aspirin and the effect of bacterial endotoxin lipopolysaccharide (LPS) during cerebral ischaemia-reperfusion (CIRP) injury. Methods. We established three animal models: the CIRP, LPS, and CIRP+LPS models. Mortality, the injured brain area, and the beam walking test were used to estimate the degree of cerebral injury among the rats. Immunohistochemistry and immunofluorescence were used to detect activated microglia, matrix metalloproteinase-3 (MMP-3), and osteopontin (OPN). Results. The injured brain area and mortality were dramatically reduced ( p < 0.01 ), and the beam walking test scores were elevated ( p < 0.01 ) in the acetylsalicylic acid (ASA) group compared to the control group. The number of microglia-, MMP-3-, and OPN-positive cells also increased. Furthermore, the number of GSI-B4, OPN, and MMP-3 cells decreased in the ASA group compared to the control group. After LPS stimulation, the number of microglia reached a peak at 24 h; at 7 d, these cells disappeared. In the ASA group, the number of microglia was significantly smaller ( p < 0.05 ), especially at 24 h ( p < 0.01 ), compared to the LPS group. Moreover, the injured brain area and the mortality were dramatically increased and the beam walking test scores were reduced ( p < 0.01 ) after LPS simulation following CIRP. The degree of injury in the ASA group resembled that in the control group. However, the number of MMP-3-immunoreactive neurons or microglia was significantly larger than that of the control group ( p < 0.05 ). In the ASA group, the MMP-3 expression was also considerably decreased ( p < 0.05 ). Conclusions. After CIRP, microglia were rapidly activated and the expression of MMP-3 and OPN significantly increased. For rats injected with LPS at reperfusion, the injured brain area and mortality also dramatically increased and the neurologic impairment worsened. However, ASA exhibited a neuroprotective effect during CIRP injury. Furthermore, ASA can reverse LPS-induced cerebral injury and inhibit the inflammatory reaction after CIRP injury.

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Relationship of matrix metalloproteinase-3 -11715A/6A polymorphism (rs35068180) and dilated cardiomyopathy

Russian Journal of Cardiology ◽

10.15829/1560-4071-2020-3960 ◽

2020 ◽

Vol 25 (10) ◽

pp. 3960

Author(s):

S. Yu. Nikulina ◽

O. O. Kuznecova ◽

A. A. Chernova ◽

V. N. Maksimov

Keyword(s):

Matrix Metalloproteinase ◽

Unknown Etiology ◽

Control Group ◽

General Direction ◽

Matrix Metalloproteinase 3 ◽

Arterial Walls ◽

Idiopathic Cardiomyopathy ◽

The Mean ◽

Relationship Of ◽

The Relationship

Aim. To study the relationship of matrix metalloproteinase-3 (MMP3) genetic polymorphism and dilated ischemic cardiomyopathy (DCM), as well as idiopathic cardiomyopathy (ICM) of unknown etiology.Material and methods. A total of 221 patients with DCM and ICM were examined (mean age, 55,30±9,69 years). The group of ischemic DCM consisted of 111 people (99 men (89,2%) and 12 women (10,8%)). The mean age of DCM subjects was 51,73±9,74 years (male subgroup, 51,00±8,96 years; female subgroup, 57,75±3,71 years). The ICM group consisted of 110 people (100 men (91,5%) and 10 women (8.5%)). The mean age of ICM subjects was 58,68±8.38 years (male subgroup, 58,29±8.,6 years; female subgroup, 62,90±6,29 years). The control group of subjects (n=121) consisted of healthy people without cardiovascular diseases (mean age, 53,6±4,8 years). All patients of the experimental group underwent routine diagnostic tests, as well as coronary angiography. In case of suspected myocarditis, cardiac magnetic resonance imaging was performed. All patients underwent polymerase chain reaction to determine the MMP3-11715A/6A polymorphism (rs35068180).Results. In patients with cardiomyopathy, regardless of the disease origin, significant differences were verified in comparison with the control group. Allele 6A (65,8% vs 59,3%, p=0,044) and genotype 6A/6A (42,1% vs 32,6%, p=0,099) were found significantly more frequently in patients with cardiomyopathy than in the control group. In addition, despite various etiological factors, the pathogenetic involvement of MMP3 is likely to have a general direction.Conclusion. In all patients with cardiomyopathy, the prevalence of MMP3 gene A allele was shown. Due to decrease in the transcription activity in homozygous 6A allele, the stromelysin level in arterial walls also decreases. This promotes the activation of procollagenase-1, the deposition of extracellular matrix and cardiac remodeling

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Effect of early body cavity continuous circulation hyperthermia perfusion chemotherapy combined with systemic chemotherapy (and nursing) on survival rate and serum tumor markers in patients with advanced gastric cancer

European Journal of Inflammation ◽

10.1177/2058739220942339 ◽

2020 ◽

Vol 18 ◽

pp. 205873922094233

Author(s):

Xia Liu ◽

Miao Tang

Keyword(s):

Survival Rate ◽

Matrix Metalloproteinase ◽

Tumor Markers ◽

Systemic Chemotherapy ◽

Matrix Metalloproteinase 2 ◽

Control Group ◽

Study Group ◽

Term Survival ◽

Serum Tumor Markers ◽

Significant Difference

This study was designed to investigate the effects of early coelom continued circulatory hyperthermic perfusion chemotherapy combined with systemic chemotherapy on the survival and serum tumor markers. A total of 128 patients with advanced gastric carcinoma who have received surgical treatments were selected and were randomly divided into study group (receiving early circulatory intraperitoneal hyperthermic perfusion chemotherapy combined with systemic chemotherapy postoperatively) and control group (receiving chemotherapy alone postoperatively), with 64 cases in each. Comparison of serum tumor markers (CA724, CA242), vascular endothelial growth factor (VEGF), matrix metalloproteinase-2 (MMP-2), matrix metalloproteinase-9 (MMP-9), immune function indexes (CD3+, CD4+, CD8+), and 5-year survival rate was assessed. Before treatment, there was no significant difference in the serum tumor markers (CA724 and CA242) as well as the serum VEGF, MMP-2, and MMP-9 levels among the two groups ( P > 0.05). However, the above parameters in the study group were significantly lower than control group 8 weeks after the treatment ( P < 0.05). Before treatment, there was no significant difference in CD3+, CD4+, CD8+ and CD4+/CD8+ between the two groups ( P > 0.05). Eight weeks after the treatment, the CD3+, CD4+ and CD4+/CD8+ in the study group were significantly higher than those in the control group ( P < 0.05), while the CD8+ levels was significantly lower than the latter group ( P < 0.05). The 2-year recurrence rate in the study group was lower than the control group ( P < 0.05). Furthermore, survival rates (1-year, 3-year and 5-year) of the study group were all higher than control group ( P < 0.05). Early circulatory hyperthermia perfusion chemotherapy combined with systemic chemotherapy contributed to the decrease in the serum tumor markers (CA724, CA242) as well as the serum VEGF, MMP-2, and MMP-9 levels, improved the immune functions. This therapeutic regimen prolonged the long-term survival conditions of the patients as well as proved the safety and effectiveness.

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Does Matrix Metalloproteinase-3 Polymorphism Play a Role in Age-Related Macular Degeneration in Patients With Myocardial Infarction?

Medicina ◽

10.3390/medicina48080060 ◽

2012 ◽

Vol 48 (8) ◽

pp. 60 ◽

Cited By ~ 1

Author(s):

Rasa Liutkevičienė ◽

Diana Žaliaduonytė-Pekšienė ◽

Dalia Žaliūnienė ◽

Olivija Gustienė ◽

Vytautas Jašinskas ◽

...

Keyword(s):

Myocardial Infarction ◽

Gene Polymorphism ◽

Matrix Metalloproteinase ◽

Macular Degeneration ◽

Early Stage ◽

Gene Promoter ◽

Age Related Macular Degeneration ◽

Control Group ◽

Matrix Metalloproteinase 3 ◽

Age Related

Objective. The aim of our study was to determine if the genotype of the matrix metalloproteinase- 3 (MMP-3) gene might carry the risk of age-related macular degeneration (ARMD) in patients with myocardial infarction. Material and Methods. A total of 499 patients with an acute myocardial infarction or with a history of myocardial infarction were enrolled into the study. They were subdivided into 2 groups: 273 patients with ARMD and 226 patients without ARMD. The control group comprised 560 persons from a random sample of the Lithuanian population. DNA was analyzed using real-time polymerase chain reaction to genotype polymorphism 5A/6A at a position –1171 of the MMP-3 gene promoter. Results. Of the 499 patients with myocardial infarction, 47% had early-stage ARMD. The patients with ARMD were older than the patients in the group without ARMD (62.1±10.8 vs. 59.6±11.1, P<0.01). The analysis of MMP-3 gene polymorphism did not reveal any differences in the distribution of 5A/5A, 5A/6A, and 6A/6A genotypes between the ARMD group, non-ARMD group, and the control group (24.2%, 52.5%, and 23.3% in the ARMD group; 28.7%, 51.9%, and 19.4% in non-ARMD group; and 25.7%, 49.3% and 25.0%, in the control group, respectively). Conclusions. MMP-3 gene polymorphism had no predominant effect on the development of ARMD in patients with myocardial infarction.

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Serum matrix metalloproteinases and tympanosclerosis

The Journal of Laryngology & Otology ◽

10.1017/s002221511000201x ◽

2010 ◽

Vol 125 (2) ◽

pp. 142-146 ◽

Cited By ~ 2

Author(s):

H Aslan ◽

M Sinan Başoğlu ◽

B Şentürk ◽

C Özbay ◽

H Katilmiş ◽

...

Keyword(s):

Matrix Metalloproteinases ◽

Matrix Metalloproteinase ◽

Otitis Media ◽

Disease Process ◽

Chronic Otitis Media ◽

Control Group ◽

Success Rates ◽

Tissue Inhibitor ◽

Matrix Metalloproteinase 1 ◽

Significant Difference

AbstractAim:To investigate levels of matrix metalloproteinases 2 and 9, and of their tissue inhibitor (i.e. tissue inhibitor matrix metalloproteinase 1), in the serum of patients with tympanosclerosis.Materials and method:We included 40 patients (age range 13–63 years) who had undergone surgery in the ENT department of İzmir Atatürk Training and Research Hospital between 2002 and 2007. Twenty had uncomplicated chronic otitis media and 20 had tympanosclerosis. We also included as the control group 20 individuals with no history of previous otic complaints or systemic or infectious disease. Serum levels of serum matrix metalloproteinases 2 and 9 and of tissue inhibitor matrix metalloproteinase 1 were measured in all subjects and compared.Result:Significantly higher levels of serum matrix metalloproteinases 2 and 9 were found in the tympanosclerosis group, compared with the chronic otitis media and control groups. There was no statistically significant difference in tissue inhibitor matrix metalloproteinase 1 level between the three groups.Conclusion:Tympanosclerosis surgery has poor success rates, since the pathological process is still active. We suggest that high levels of matrix metalloproteinases may play a role in the continuation of the disease process.

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