Yang Poster 2015
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1) The document describes a Markov Chain model built to predict gene expression signatures associated with epithelial and mesenchymal cells based on data from 1165 breast cancer patients. 2) The model incorporates the known TGFB-induced EMT pathway and regulatory relationships between molecules to recursively predict expression likelihood. 3) Expression patterns are mapped to epithelial and mesenchymal cell types based on the expression level of the CDH1 gene, which plays a key role in cell phenotype and the initiation of EMT.
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1) DOT1L expression is associated with poorer survival and more aggressive phenotypes in breast cancer, particularly triple-negative and ER-negative subtypes.
2) Overexpression of DOT1L in MCF10A epithelial cells induces an epithelial-to-mesenchymal transition (EMT) as shown by changes in marker expression and morphology. Knockdown of DOT1L reverses these effects.
3) DOT1L promotes breast cancer cell invasion and migration in vitro, and lung metastasis in vivo in orthotopic xenograft mouse models. DOT1L may promote metastasis by facilitating EMT.Proteomics Exploration of Chronic Lymphocytic Leukemia_Crimson Publishers
Proteomics Exploration of Chronic Lymphocytic Leukemia_Crimson PublishersCrimsonpublishersCancer
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Chronic Lymphocytic Leukemia (CLL) is an adult heme malignancy characterized by the presence of mature-appearing CD5+ B cells in the blood, bone marrow, and secondary lymphoid organs [1]. In the United States, there will be an estimate of 20,720 new cases and 3,930 deaths according to the American Cancer Society statistics. Symptoms include swollen lymph nodes, frequent infections, and fatigue which negatively impacts the quality of life of people affected [1]. CLL is heterogeneous in its progression and clinical outcomes. Factors that contribute to the heterogeneity include the immunoglobulin heavy chain (IGHV) status and chromosomal aberrations [2,3]. There are two subtypes of CLL: Unmutated(U-CLL) and Mutated CLL(M-CLL). 40% and 60% of patients are diagnosed with unmutated and mutated CLL. U-CLL is characterized by the presence of CLL cells that have less than two percent of their IGHV mutated, whereas M-CLL cells have more than two percent mutated [4]. U-CLL is the more aggressive phenotype [2]. These cells have increased responsiveness to antigens that bind the B cell receptor (BCR) versus M-CLL cells [5]. M-CLL is the more indolent phenotype. Increased BCR signaling results in increased cell survival and proliferation [5].Natalia Cucu Simp 09
Natalia Cucu Simp 09Mihaiela Fazacas
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The document discusses epigenetic factors that contribute to imprinting diseases. It describes how epigenetic modifications like DNA and histone methylation establish parental imprints and regulate gene expression in a parent-of-origin specific manner. Alterations in these epigenetic marks can lead to imprinting disorders like Prader-Willi syndrome and Angelman syndrome, which are associated with changes in imprinted genes on chromosome 15. The authors investigate these diseases using methods like MS-PCR to analyze DNA methylation patterns.Tumor suppressor
Tumor suppressorfatmafars
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For downloading the presentation ,more presentations , infographics and blogs visit :
studyscienceblog.wordpress.comSilencing c-Myc translation as a therapeutic strategy through targeting PI3Kd...
Silencing c-Myc translation as a therapeutic strategy through targeting PI3Kd...Mark Lipstein
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This document summarizes a study examining the combination of a novel PI3Kδ inhibitor, TGR-1202, with the proteasome inhibitor carfilzomib for treating hematological malignancies. The study found that TGR-1202 synergizes strongly with carfilzomib in lymphoma, leukemia, and myeloma cell lines and primary cells by silencing c-Myc translation. This synergistic effect is driven by TGR-1202's unexpected additional activity of inhibiting CK1ε, which contributes to repressing phosphorylation of 4E-BP1 and lowering c-Myc protein levels. The results suggest that TGR-1202, as a dual PI3Kδ/CK1ε inhibitor, may haveSeminario biomol
Seminario biomolManuelaGaleano3
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This document summarizes a study that aimed to investigate the biological effects of HMGA2 on triple-negative breast cancer (TNBC) cells and the Hippo-YAP signaling pathway. The study used RNA interference with lentiviral vectors to silence the HMGA2 protein in TNBC cell lines. Immunofluorescence and confocal imaging were used to examine expression levels of epithelial-mesenchymal transition biomarkers and the Hippo-YAP pathway after HMGA2 silencing. Western blot was used to analyze HMGA2 levels in TNBC cell lines as well as levels of EMT markers and the hippo YAP pathway. An invasion assay using two chambers separated by a filter was also used to study TNBC cell invasionJCI0936541
JCI0936541Polina Goichberg
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1) The study found higher levels of MT1-MMP and lower levels of RECK, an MT1-MMP inhibitor, on circulating human CD34+ progenitor cells compared to those in bone marrow. MT1-MMP levels correlated with successful mobilization of CD34+ cells in healthy donors and patients receiving G-CSF treatment.
2) Treatment with G-CSF further increased MT1-MMP and decreased RECK expression on human and mouse hematopoietic cells in a PI3K/Akt-dependent manner. Blocking MT1-MMP impaired chemotaxis and homing of mobilized human CD34+ progenitors.
3) Mobilization of human progenTumor Immunology
Tumor ImmunologyABED ALRAHMAN DAKKAK
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A presentation descripes tumors,pathogensis,devlopment,antigenes and genes.
how host responds to them and how tumors evade immunity with latest lines of therapy and prevention.
facaulity of pharmacy.Damascus university.master of libaratory diagnossis. immunology.
Baraa ALomar and feras debanEmt and ecm 2013
Emt and ecm 2013Elsa von Licy
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The document provides information about epithelial-mesenchymal transition (EMT) and its role in development, disease, and signaling pathways. It discusses:
1) The differences between epithelial and mesenchymal cell markers and properties. 2) How EMT converts epithelial cells into mesenchymal cells through disrupting cell adhesion and interactions with the extracellular matrix. 3) The transient and context-specific nature of EMT. 4) The role of EMT in embryogenesis, cancer progression and metastasis, and fibrosis. 5) Signaling pathways and factors that activate and suppress EMT such as TGF-β, Wnt, Notch, hypoxia, and inflammation. 6) How EMT generates cancer stem-like cells andCancer epigenetics
Cancer epigeneticsArad Boustan
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The epigenetic regulation of DNA-templated processes has been intensely studied over the last 15
years. DNA methylation, histone modification, nucleosome remodeling, and RNA-mediated targeting regulate many biological processes that are fundamental to the genesis of cancer. Here, we
present the basic principles behind these epigenetic pathways and highlight the evidence suggesting that their misregulation can culminate in cancer. This information, along with the promising clinical and preclinical results seen with epigenetic drugs against chromatin regulators, signifies that it
is time to embrace the central role of epigenetics in cancer.Genetics of childhood solid tumors
Genetics of childhood solid tumorsBSMMU
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Genetic changes play an important role in the development of childhood tumors. There are three main categories of genes affected: proto-oncogenes, tumor suppressor genes, and DNA repair genes. Mutations in tumor suppressor genes like RB1 and TP53 can lead to cancers due to a loss of control of cell proliferation. Activation of proto-oncogenes also contributes to childhood cancers like leukemias and solid tumors. Molecular diagnostic techniques can identify genetic alterations that provide prognostic and therapeutic insights for managing childhood cancers.Therapeutic strategies that target the cellular transformation process for ca...
Therapeutic strategies that target the cellular transformation process for ca...JiaYiiChong
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SCT60103 GTC Group 1 Presentation
Strategies are focussed more in cancer treatment rather than preventionSTaRS Poster Final
STaRS Poster FinalLeandro Fernandez
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1) Human pulmonary artery endothelial cells were treated with normal TGF-β or nano-encapsulated TGF-β to analyze gene expression related to TGF-β and NF-κB signaling pathways.
2) The nano-encapsulated TGF-β decreased expression of genes in the NF-κB pathway and fibronectin, while increasing expression of Smad3 in the TGF-β pathway, compared to normal TGF-β.
3) This suggests that nano-encapsulated TGF-β may attenuate the NF-κB activation pathway and improve TGF-β’s therapeutic potential for treating pulmonary hypertension and sickle cell disease.Duzkale_2011_CLL biomarker LDOC1
Duzkale_2011_CLL biomarker LDOC1Hatice Duzkale, MD, MPH, PhD, FACMG
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This document summarizes a study investigating the expression and prognostic significance of the LDOC1 gene in chronic lymphocytic leukemia (CLL) and normal B cells. The key findings are:
1) LDOC1 mRNA expression is significantly lower in CLL cases with mutated immunoglobulin variable region genes compared to unmutated cases.
2) LDOC1 is expressed in normal peripheral blood B cell subsets, suggesting it may play a role in normal B cell development.
3) High LDOC1 expression in CLL correlates with poor prognostic biomarkers and overall survival.
4) LDOC1 mRNA level is an excellent predictor of overall survival in untreated CLL patients.Project proposal from venkatesh (bt)
Project proposal from venkatesh (bt)venkatesh naik
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This document presents a study plan to investigate molecular markers and toll-like receptor expression in myelodysplastic syndrome (MDS) patients in Assam, India. The study aims to measure mutation levels of genes like TET2, SAXL1, RUNX1, RAS, and TP53 in MDS patients and determine expression of toll-like receptors TLR1-10 at mRNA and protein levels. The methodology involves collecting blood samples from MDS patients, extracting RNA and protein, and using techniques like qRT-PCR, ELISA, western blotting, and flow cytometry for analysis. The expected significance is that the study may help explore gene expression and mutation patterns in MDS patients in Assam and support approaches for treatingMolecular target therapy_in_colorectal_cancer[1]![Molecular target therapy_in_colorectal_cancer[1]](https://cdn.slidesharecdn.com/ss_thumbnails/moleculartargettherapyincolorectalcancer1-171117132543-thumbnail.jpg?width=560&fit=bounds)
Molecular target therapy_in_colorectal_cancer[1]HebatAllah Bakri
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i would be so grateful if this presentation adds to your knowlege
and i welcome any comments. thanks in advance Genetic Markers in AML
Genetic Markers in AMLFerdie Fatiga
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Genetic markers such as cytogenetic abnormalities, mutations, and gene expression levels can help classify acute myeloid leukemia (AML) patients into prognostic groups. Three significant genetic markers mentioned are FLT3 mutations, NPM1 mutations, and CEBPA mutations. FLT3 internal tandem duplications and tyrosine kinase domain mutations confer a poor prognosis. NPM1 mutations are favorable when isolated, but unfavorable when combined with FLT3 mutations. CEBPA mutations, especially biallelic mutations, are an independent favorable prognostic factor associated with longer remission duration and overall survival.Yang Poster 2015
- 1. Prediction of Gene Signatures in TGFB-induced Breast Cancer Metastasis by Markov Chain Model Yang Cong, Shenyi Chen, Stephen T.C. Wong Department of Systems Medicine and Bioengineering, Houston Methodist Research Institute, 6670 Berter Ave, Houston, TX 77030 Abstract Introduction TGFB-EMT pathway CDH1 transcription factor selection Expression Signature Prediction Results Acknowledgements •NCI Center for Modeling Cancer Development U54 Ca149196 Metastasis is a major cause of patient death in breast cancer. Epithelial-mesenchymal transition (EMT) plays the initiation role in the metastasis cascade. Based on gene profiling data of 1165 breast cancer patients in TCGA, we built a statistical Markov Chain model to predict gene signatures of epithelial and mesenchymal cells. Based on the literature integrated TGFB-induced EMT pathway, we extracted the regulatory mechanism among molecules. We used a recursive algorithm to predict the likelihood of expression signatures and further mapped the prediction with known epithelial and mesenchymal expression patterns. A molecule is regulated by its regulators, and the change of its expression level only depends on the observed expression of all its regulators The loss of the epithelial adhesion molecule E-cadherin (CDH1) is considered as a fundamental event in EMT and an early step in cancer metastasis. EMT can be induced by several growth factors, such as TGFB1, hepatocyte growth factor, and platelet-derived growth factor PDGF. Also EMT can be induced by any one of the following transcription factors alone, such as SNAI1, SNAI2, TWIST1, FOXC1, FOXC2, ZEB1 and ZEB2. A central target of these transcription factors listed above is the repression of E-cadherin gene CDH1. The expression level of CDH1 plays a key role in the cell phenotype. The inhibition of CDH1 expression is the starter of EMT process. Epithelial cells have a high expression level of CDH1, meanwhile mesenchymal cells have a low expression. Hence, we map the expression patterns with cell types based on the expression level of CDH1. Data Processing