scholarly journals Analysis of chronic inflammatory lesions of the colon for BMMF Rep antigen expression and CD68 macrophage interactions

2021 ◽  
Vol 118 (12) ◽  
pp. e2025830118
Author(s):  
Timo Bund ◽  
Ekaterina Nikitina ◽  
Deblina Chakraborty ◽  
Claudia Ernst ◽  
Karin Gunst ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Progenitor Cells ◽  
Chronic Inflammation ◽  
Antigen Expression ◽  
Rep Protein ◽  
Dna Mutations ◽  
Tumor Tissues ◽  
Cancer Tissues ◽  
Episomal Dna ◽  
Precancerous Tissue

Consumption of Eurasian bovine meat and milk has been associated with cancer development, in particular with colorectal cancer (CRC). In addition, zoonotic infectious agents from bovine products were proposed to cause colon cancer (zur Hausen et al., 2009). Bovine meat and milk factors (BMMF) are small episomal DNA molecules frequently isolated from bovine sera and milk products, and recently, also from colon cancer (de Villiers et al., 2019). BMMF are bioactive in human cells and were proposed to induce chronic inflammation in precancerous tissue leading to increased radical formation: for example, reactive oxygen and reactive nitrogen species and elevated levels of DNA mutations in replicating cells, such as cancer progenitor cells (zur Hausen et al., 2018). Mouse monoclonal antibodies against the replication (Rep) protein of H1MSB.1 (BMMF1) were used to analyze BMMF presence in different cohorts of CRC peritumor and tumor tissues and cancer-free individuals by immunohistochemistry and Western blot. BMMF DNA was isolated by laser microdissection from immunohistochemistry-positive tissue regions. We found BMMF Rep protein present specifically in close vicinity of CD68+ macrophages in the interstitial lamina propria adjacent to CRC tissues, suggesting the presence of local chronic inflammation. BMMF1 (modified H1MSB.1) DNA was isolated from the same tissue regions. Rep and CD68+ detection increased significantly in peritumor cancer tissues when compared to tissues of cancer-free individuals. This strengthens previous postulations that BMMF function as indirect carcinogens by inducing chronic inflammation and DNA damage in replicating cells, which represent progress to progenitor cells for adenoma (polyps) formation and cancer.

scholarly journals RNA-sequencing identified miR-3681 as a negative regulator in the proliferation and migration of cervical cancer cells via the posttranscriptional suppression of HGFR

RSC Advances ◽  
2019 ◽  
Vol 9 (39) ◽  
pp. 22376-22383 ◽  
Author(s):  
Fan Shi ◽  
Yingbing Zhang ◽  
Juan Wang ◽  
Jin Su ◽  
Zi Liu ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Cancer Cells ◽  
Rna Sequencing ◽  
Negative Regulator ◽  
Tumor Tissues ◽  
Differentially Expressed Mirnas ◽  
Cervical Cancer Cells ◽  
And Migration ◽  
Cancer Tissues ◽  
Proliferation And Migration

In this study, RNA-sequencing was used to investigate the differentially expressed miRNAs between cervical cancer tissues and matched adjacent non-tumor tissues.

The RAV12 Monoclonal Antibody Recognizes the N-Linked Glycotope RAAG12: Expression in Human Normal and Tumor Tissues

2009 ◽  
Vol 133 (9) ◽  
pp. 1403-1412
Author(s):  
Suzanne K. Coberly ◽  
Francine Z. Chen ◽  
Mark P. Armanini ◽  
Yan Chen ◽  
Peter F. Young ◽  
...  
Keyword(s):  
Monoclonal Antibody ◽  
Antigen Expression ◽  
Subcellular Location ◽  
Carbohydrate Antigen ◽  
Cytoplasmic Staining ◽  
Safety Issues ◽  
Normal Tissues ◽  
Tumor Tissues ◽  
Associated Proteins

Abstract Context.—RAAG12 is a primate-restricted N-linked carbohydrate antigen present on multiple membrane-associated proteins. RAAG12 is recognized by the RAV12 monoclonal antibody. RAV12 binds to RAAG12-expressing gastrointestinal adenocarcinomas, modifies growth factor-mediated signaling, induces oncotic cell death in vitro, and has antitumor activity toward gastrointestinal tumor xenografts. Objective.—To determine the expression pattern of RAAG12 in normal and tumor tissue to identify indications for clinical study and potential safety issues. Design.—Immunohistochemistry of 36 normal human tissues and a broad range of tumor tissues to profile RAAG12 expression. Results.—More than 90% of colon, gastric, and pancreatic adenocarcinomas expressed RAAG12, and expression was uniform in most samples. Expression of RAAG12 at lower frequency and/or uniformity was observed in other cancers, including esophageal, ovarian, liver, breast, and prostate carcinomas and adenocarcinomas. Similar RAAG12 expression was observed between primary and metastatic colon adenocarcinomas. No staining was seen on cardiovascular, endocrine, neuromuscular, hematopoietic, or nervous system tissue from non–tumor-bearing individuals. RAAG12 was expressed on mucosal and glandular/ductal epithelium. The gastrointestinal tract mucosa and pancreatic/biliary ducts displayed the most uniform reactivity. RAAG12 exhibited differential subcellular localization in these normal, compared with tumor, tissues. Normal polarized epithelia primarily displayed apical membrane and cytoplasmic staining, whereas tumors exhibited whole membrane staining that increased with decreasing differentiation. Conclusions.—High expression of RAAG12 on tumors of gastrointestinal origin suggests these cancers are appropriate targets for RAV12 therapy. Differential subcellular location of RAAG12 on normal epithelia may limit accessibility of RAV12 to the subset of normal tissues that exhibit antigen expression.

Abstract 190: Epigenetic Modifications of Pro-inflammatory Gene Expression in Macrophages by a Demethylase Enzyme, JMJD3, May Promote Chronic Inflammation in Type 2 Diabetic (T2D) Wounds

2013 ◽  
Vol 33 (suppl_1) ◽  
Author(s):  
Katherine A Gallagher ◽  
Amrita Joshi ◽  
William Carson ◽  
Dawn Coleman ◽  
Peter Henke ◽  
...  
Keyword(s):  
Gene Expression ◽  
Progenitor Cells ◽  
Chronic Inflammation ◽  
Histone Methylation ◽  
Gene Promoter ◽  
Epigenetic Modifications ◽  
Macrophage Phenotype ◽  
M1 Macrophage ◽  
Type 2 Diabetic

Introduction Type 2 diabetic(T2D) wounds are characterized by chronic inflammation, maintained by an exaggerated M1(pro-inflammatory) macrophage phenotype response. We seek to define a link between epigenetic modifications of bone marrow(BM) cells in T2D and dysregulated macrophages in wounds. We hypothesized that a chromatin modifying demethylase enzyme, JMJD3, is responsible for the decrease in H3K27me3 repressive methylation at the IL-12 gene promoter and thus drives an M1 macrophage phenotype in T2D wounds. Methods BM/adipose tissue(AT)/wounds were harvested from 30 diet-induced obese mice(DIO)(MG= 350g/DL) and 30 matched(WT) controls. For chromatin immunoprecipitation(ChIP) analysis, cells were isolated via ferromagnetic columns(CD34+,CD11b+). ChIP to detect histone methylation at the promoter regions of JMJD3 and IL-12(key M1 macrophage gene) was performed and RNA analysis was done with standard primers. Results JMJD3 mRNA in the BM is significantly increased in the DIO versus WT. ChIP showed increased H3K4me3(gene expression mark) in CD34+ progenitor cells and a corresponding decrease in H3K27me3(repressive mark) in monocytes at the promoter region of JMJD3. These changes correspond with the decrease in H3K27me3 seen at the IL-12 promoter in macrophages(CD11b+) from AT/T2D wounds. Conclusions Epigenetic changes initiated by JMJD3 in BM progenitor cells result in changes in histone methylation at the IL-12 promoter favoring an M1 phenotype in macrophages and thus contributes to the chronic inflammation seen in T2D wounds and AT. Whether manipulation of epigenetic enzymes could reduce chronic inflammation in T2D wounds requires further work.

scholarly journals Mucus and adiponectin deficiency: role in chronic inflammation-induced colon cancer

2013 ◽  
Vol 28 (9) ◽  
pp. 1267-1279 ◽  
Author(s):  
Arpit Saxena ◽  
Manjeshwar Shrinath Baliga ◽  
Venkatesh Ponemone ◽  
Kamaljeet Kaur ◽  
Bianca Larsen ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Chronic Inflammation

scholarly journals Cytogenetic differences in blood and cancer tissue samples of the same patient group

2020 ◽  
Vol 4 (1) ◽  
pp. 01-03
Author(s):  
Osman Demirhan ◽  
Deniz Taştemir Korkmaz ◽  
Nesrin Çetinel
Keyword(s):  
Malignant Disease ◽  
Chromosomal Abnormalities ◽  
Cancer Tissue ◽  
Tissue Samples ◽  
Genetic Changes ◽  
Tumor Tissues ◽  
Cancer Tissues ◽  
Gene Expression Alterations ◽  
Breast Tissues ◽  
Improved Methods

Breast cancer (BC) is the most prevalent malignant disease in females worldwide. Genomic instability in tumor tissue has been associated with tumor progression. These genetic changes may take a variety of forms, including numerical and structural chromosomal abnormalities (CAs), epigenetic changes, and gene expression alterations. Many tumor tissues are made up of genetically different cell populations, and the study of the causes and consequences of this heterogeneity play a central role in cancer research. In this study, CAs in blood and cancer tissues of patients with sporadic BC were examined. Our findings shows that the increase in numerical sex aneuploidy in BC tissues is significantly higher than in blood tissue. These aneuploidy increases in cancer tissues seem to be compatible with the development and increase of cancer, and can play a role in the pathogenesis of cancers. These changes are consistent with early and long-standing exposure to carcinogens, especially estrogens. These findings should clarify our understanding of breast carcinogenesis in breast tissues and promote development of improved methods for risk assessment and BC prevention in women.

scholarly journals Upgraded Spatial Gray Level Dependence Matrices for Textural Analysis in Colon Cancer Tissues

2018 ◽  
Vol 7 (2.20) ◽  
pp. 291 ◽  
Author(s):  
B Saroja ◽  
A Selwin Mich Priyadharson
Keyword(s):  
Colon Cancer ◽  
Texture Feature ◽  
Image Data ◽  
Texture Features ◽  
Gray Level ◽  
Colon Tissue ◽  
Data Set ◽  
Histopathological Image ◽  
Cancer Biopsy ◽  
Cancer Tissues

Colon or Bowel or Colorectal Cancer (CRC) is commonly determined by diagnosing a sample of colon tissue and further analysed by medical imaging. The colon tissue classification method count on specific changes between texture features extracted from benign and malignant regions. The variations in the image acquisition methods effects the colon tissue analysis. In this paper, an Upgraded Spatial Gray Level Dependence Matrices (U-SGLDM) is emphasized to extract textural features. The licensed image set of all applicable types of tissues within colon cancer are used for experimentation. Several texture feature sets are extracted to show the significant differences among the eight colon cancer biopsy images in the image data set. The fractal dimension-Hurst Coefficient is added to U-SGLDM for long range assessment. The Prominence of the analysis evoked in the representation of histopathological image structure over longer periods.  

scholarly journals Expression of Ia antigens on myeloid progenitor cells in chronic myeloid leukemia: direct analysis using partially purified colony- forming cells

Blood ◽  
1985 ◽  
Vol 65 (2) ◽  
pp. 414-422
Author(s):  
SA Cannistra ◽  
JF Daley ◽  
P Larcom ◽  
JD Griffin
Keyword(s):  
Cell Cycle ◽  
Chronic Myeloid Leukemia ◽  
Progenitor Cells ◽  
Myeloid Leukemia ◽  
Antigen Expression ◽  
Colony Stimulating Factors ◽  
Myeloid Progenitor ◽  
Hla Dr ◽  
Ia Antigens ◽  
Myeloid Progenitor Cells

The regulation of Ia (HLA-DR) antigen expression on myeloid progenitor cells may be closely related to the control of myelopoiesis in both normal individuals and chronic myeloid leukemia (CML) patients. In an effort to study directly the expression and behavior of Ia surface molecules on myeloid progenitor cells, we used an immunologic purification technique to enrich these cells approximately 100-fold from the peripheral blood of CML patients. The majority of cells in this blast population expressed HLA-DR antigens. Thirty percent to 40% of cells could form a granulocyte or monocyte colony in agar, and these cells tended to express the highest levels of HLA-DR. The number of HLA- DR molecules per cell increased about twofold as the cells tranversed the cell cycle from G0/G1 to G2/M. This was true for unstimulated cells or cells exposed to colony-stimulating factors. Some of this increase was related to a corresponding increase in cell size and is also seen with other cell surface antigens such as beta-2-microglobulin. Ia antigen expression was not modified by culture with colony-stimulating factors, fetal calf serum, or serum-free, prostaglandin-free medium for periods of up to 24 hours. These results demonstrate that Ia antigens are expressed on the myeloid progenitor cells of CML, are increased in the S and G2/M phases of the cell cycle, and are stable under most in vitro culture conditions for at least 24 hours of culture.

scholarly journals Angioplasticity in asthma

2009 ◽  
Vol 37 (4) ◽  
pp. 805-810 ◽  
Author(s):  
Kewal Asosingh ◽  
Serpil C. Erzurum
Keyword(s):  
Bone Marrow ◽  
Progenitor Cells ◽  
Chronic Inflammation ◽  
Endothelial Progenitor Cells ◽  
Blood Supply ◽  
Present Knowledge ◽  
Current View ◽  
Vascular Remodelling ◽  
Bone Marrow Derived Cells ◽  
Supply Systems

Plasticity of the lung vasculature is intrinsically more complex than other organs due to the presence of two blood supply systems under different arterial pressures, the pulmonary and bronchial arterial systems. The bronchial and pulmonary circulations may both contribute to vascular remodelling in lungs after injury or inflammation. Vascular remodelling in the airway is a long recognized component in asthma. Growing numbers of reports suggest that a pro-angiogenic milieu is not a consequence of, but rather dictates the chronic inflammation of asthma. The fairly recent discovery of EPCs (endothelial progenitor cells) has enabled us to study the bone-marrow-derived cells that regulate lung vascular plasticity in asthma. This mini review provides a concise synopsis of our present knowledge about vascular plasticity in adult lungs, summarizes our current view of angioplasticity in asthma and highlights yet unresolved areas of potential interest.

scholarly journals Screening of Differentiation-Specific Molecular Biomarkers for Colon Cancer

2018 ◽  
Vol 46 (6) ◽  
pp. 2543-2550 ◽  
Author(s):  
Lu Qi ◽  
Yanqing Ding
Keyword(s):  
Gene Expression ◽  
Colon Cancer ◽  
Molecular Markers ◽  
Cancer Cells ◽  
Cancer Patients ◽  
Roc Curve ◽  
Expression Profiles ◽  
Tissue Specific ◽  
Specificity And Sensitivity ◽  
Cancer Tissues

Background/Aims: Owing to the lack of effective molecular markers to evaluate colon cancer differentiation grade, screening of effective molecular markers for the diagnosis and treatment of colon cancer is of great significance. This study is a screening study for molecular markers related to the differentiation of colon using the tissue-specific genes of colon. Methods: This study compared the expression profiles of colon cancer at various differentiation grades and screened the down-regulated genes associated with decreased differentiation. IL22RA1 gene was derived from the intersection of obtained gene and colon tissue-specific genes. We used DriverDB and The Human Protein Atlas to analyze the expression level of IL22RA1 in various tissue cells, also used Kaplan-Meier method to analyze the correlation between IL22RA1 and the survival of colon cancer patients, and then used the ROC curve to analyze the specificity and sensitivity of IL22RA1 diagnosis of differentiated colon cancer. Results: We found that IL22RA1 gene expression was progressively down-regulated in high-differentiated, moderate-differentiated, low-differentiated, and undifferentiated colon cancer tissues. Both RNA and protein levels of IL22RA1 were higher in colon tissues and colon cancer tissues than in other normal and cancer tissues. Comparison of IL22RA1 expression in different cancer cells found that IL22RA1 expression was significantly higher in CACO-2 colon cancer cells than in other cancer cells. Survival analysis showed that IL22RA1 gene expression was positively correlated with the overall survival rate of colon cancer patients (P=0.0224). ROC curve analysis revealed that IL22RA1 expression had good specificity and sensitivity to stage II colon cancer. Conclusion: These findings suggest that IL22RA1 serves as a specific molecular marker for the differentiation of colon cancer.

Sign in / Sign up

Export Citation Format

Share Document