TP Tumor-Stroma Interactions Tumor and plasma proteomics insights into tumor stroma interactions 109 luminal human breast cancer specimens+plasma o high.

Slides:

Advertisements

Similar presentations

Triple-Negative Breast Cancer

Advertisements

What is it? Treatment options Prevention.  Disease  Cells grow and divide uncontrollably  No way to stop  Damage to body around them.

Systems biology in cancer research. What is systems biology? = Molecular physiology? “… physiology is the science of the mechanical, physical, and biochemical.

Figure S1. ID#1 Lipid Metabolism, Small Molecule Biochemistry, Drug Metabolism.

Figure 13.2 The Biology of Cancer (© Garland Science 2007) Hodgkins Lymphoma – A Cancer in Which 99% of the Tumor Cells Are Not Cancer Cells.

Dialogue Replaces Monologue:

Understanding and Optimizing Treatment of Triple Negative Breast Cancer Edith Peterson Mitchell, MD, FACP Clinical Professor of Medicine and Medical Oncology.

Metastatic Breast Cancer: One Size Does Not Fit All Clifford Hudis, M.D. Chief, Breast Cancer Medicine Service MSKCC.

Cancer A Disease of Mitosis.

Malignant Melanoma and CDKN2A

Tumor genetics Minna Thullberg

Results grade1 grade2 grade3 (1) Can we identify metabolites or metabolic pathways that are associated with breast cancer clinical parameters? Alex-CIS-GCTOF.

SC430 Molecular Cell Biology

Assessment of breast microcalcification with stereotactic guidance using the Spirotome Biopsy Needle. Comparison with other biopsy devices Dr Richard Harries.

Advanced Cancer Topics Journal Review 4/16/2009 AD.

1. Cancer and the cell cycle

Jo Anne Zujewski, MD Cancer Therapy Evaluation Program Division of Cancer Diagnosis and Treatment National Cancer Institute May 2011 Breast Cancer Biology.

BioTuesday BioTuesday 2010 Prediction BioSciences Founded in 2009 ‘theranostics’- drug/diagnostic combinations Oncology and Neuro/Cardiovascular.

P. falciparum Life Cycle & Pathogenesis of Malaria Miller et al., Nature  Molecular and genetic.

Computational biology of cancer cell pathways Modelling of cancer cell function and response to therapy.

Apostolos Zaravinos and Constantinos C Deltas Molecular Medicine Research Center and Laboratory of Molecular and Medical Genetics, Department of Biological.

Plasminogen-Activating Inhibitor-1 (PAI-1) High PAI-1 associated with: Obesity (especially visceral), possible fatty liver. 2,3,4 Inflammation and oxidative.

Primary Mets Node Patient 1Patient 2Patient 3 Primary Mets Node Patient 1Patient 2Patient 3 Primary Mets Node Patient 1Patient 2Patient 3 Primary Mets.

Epigenetic Control of Tamoxifen Resistant Breast Cancer Kristin Williams Arcaro Lab Thesis Resarch June 25, 2012 Kristin Williams Arcaro Lab Thesis Resarch.

Notes - Cancer and Cell Division

Craig D. Woodworth, Evan Michael, Laura Smith, and Matthias Nees. Department of Biology, Clarkson University, Potsdam, NY, USA, and Department of Pediatric.

Prognostic and Predictive Factors: Current Evidence for Individualized Therapy Predictive Molecular Markers: Hormone Receptor Status Presented by Kathleen.

Negative regulation of cell cycle by intracellular signals Checkpoint p53 detects DNA damage & activates p21 p21 inhibits cdk2-cyclinA Intracellular Regulation.

A B E F G C D NP460 vs HK1 (p

Animal models of breast and prostate cancer “Advances in targeting cancer pathways” by Cinbo delegates MEDITERRANEAN SCHOOL OF ONCOLOGY 08 April 2016,

Different microarray applications Rita Holdhus Introduction to microarrays September 2010 microarray.no Aim of lecture: To get some basic knowledge about.

Cell-based models of morphogenesis in normal and pathogenic development - Continued Maria Audi Byrne September 21 st 2007 Mathbiology and Statistics Seminar.

Comparison between Pathologic Characteristics of Her2 Negative and Positive Breast Cancer in a Single Cancer Center in Jordan DR Majdi A. Al Soudi, MD,

Figure 2. DNA methylation mediated MORT gene silencing is linked to luminal, receptor positive breast cancers. (A) MORT expression level plotted versus.

Intervista a Federico Cappuzzo

NF1 Low-Grade Glioma Synodos

Myeloma cell interaction with extracellular matrix (ECM) and accessory cells in the marrow. Myeloma cells require support from bone marrow stromal cells.

Lorena Bouzas Alfonsín Advanced Genetics

Controls the Cell Cycle

The student is expected to: 5A describe the stages of the cell cycle, including deoxyribonucleic acid (DNA) replication and mitosis, and the importance.

KEY CONCEPT Cell cycle regulation is necessary for healthy growth.

High-level TNFSF13 predict a good response to post-operative chemotherapy in patients with basal-like breast cancer: A systematic review 林惠鈺1,2 歸家豪1,3.

KEY CONCEPT Cell cycle regulation is necessary for healthy growth.

KEY CONCEPT Cell cycle regulation is necessary for healthy growth.

Cell Signaling.

The Multifaceted Role of the Intestinal Microbiota in Colon Cancer

KEY CONCEPT Cell cycle regulation is necessary for healthy growth.

BIOLOGY 12 Cancer.

KEY CONCEPT Cell cycle regulation is necessary for healthy growth.

KEY CONCEPT Cell cycle regulation is necessary for healthy growth.

Volume 66, Issue 2, Pages (February 2017)

Figure 1 Specificity of the various epidermal growth factor (EGF)

The Role of Tumor Stroma in Cancer Progression and Prognosis: Emphasis on Carcinoma-Associated Fibroblasts and Non-small Cell Lung Cancer Roy M. Bremnes,

KEY CONCEPT Cell cycle regulation is necessary for healthy growth.

KEY CONCEPT Cell cycle regulation is necessary for healthy growth.

Dietmar M.W. Zaiss, William C. Gause, Lisa C. Osborne, David Artis

KEY CONCEPT Cell cycle regulation is necessary for healthy growth.

KEY CONCEPT Cell cycle regulation is necessary for healthy growth.

Vicki Plaks, Niwen Kong, Zena Werb Cell Stem Cell

Kinome‐wide activity regulation derived from known substrates and 41 quantitative phosphoproteomic studies Kinome‐wide activity regulation derived from.

KEY CONCEPT Cell cycle regulation is necessary for healthy growth.

KEY CONCEPT Cell cycle regulation is necessary for healthy growth.

KEY CONCEPT Cell cycle regulation is necessary for healthy growth.

Optoacoustic Imaging and Gray-Scale US Features of Breast Cancers: Correlation with Molecular Subtypes Total external optoacoustic US feature scores of.

Tyrosine kinase inhibitors

KEY CONCEPT Cell cycle regulation is necessary for healthy growth.

Notch signaling from tumor cells: A new mechanism of angiogenesis

Dietmar M.W. Zaiss, William C. Gause, Lisa C. Osborne, David Artis

Connections between insulin/insulin-like growth factor 1 signaling and metabolic pathways in tumor cells. Connections between insulin/insulin-like growth.

UAB Nanostring Laboratory

Presentation transcript:

TP Tumor-Stroma Interactions Tumor and plasma proteomics insights into tumor stroma interactions 109 luminal human breast cancer specimens+plasma o high levels of Amphiregulin (AREG) in undissected tumor specimens o EGF not detectable in tumor specimens: Human plasma samples (healthy & diseased) show high but variable yields of HRG, BTC, EGF and many other ligands o Tumor VEGFA levels correlate with risk/grading o Tumor HGF shows inverse correlation with risk/grading o Stromal downregulation of Caveolin-1 correlates with risk VEGFA HGF

TP Tumor-Stroma Interactions Tumor and plasma proteomics insights into tumor stroma interactions 109 luminal human breast cancer specimens+plasma o Molecular impact of e.g. AREG and EGF on (A) downstream signaling, (B) transcription factor activation/expression and (C) induction/repression of miRs in model systems of human breast cancer o Systems biology of crosstalk between InsulinR/IGFR and EGFR signals, integration of cytokine signaling o What initiates the downregulation of Caveolin-1 in stroma cells (CAF)? o Proteome profiling of other molecular subtypes of human breast cancer (HER2 pos., TN, basal)

Inflammatory cytokines IL-1, IL6, IL-8, TNFα, TGFβ, VEGFA, … Growth factors AREG, EGF, HGF, IGF-1… WP2 Modeling of ligand-specific signaling (e.g. EGF vs. AREG), integration of insulin and cytokine signaling Readout: (1) mRNA/Illumina (2) RPPA (3) TF enrichment for RPPA (nuclei)  identify cooperative effects between signaling nodes, molecular subtype-specific  validation of crosstalk effects in co-culture models „kinase dynamics involved in transcription factor activation and feedback controls of signaling systems“ WP3 data-driven development of „tumor stroma“ treatment concepts  validation in co-culture models  validation in human tumors (IHC, RPPA) WP1 Cytokine, proteome, & GF profiles of human breast cancer specimens → identify targets for WP2 Basal, HER2+, triple negative breast cancer TP Tumor-Stroma Interactions DNA damage cell cycle Hedgehog TGFb/SMAD PI3K/PTEN cell adhesion apoptosis NOTCH JAK/STAT metabolic transformation WNT RAS/RAF 12 core pathways involved in cancer fatty tissue blood vessels WP4 validate „tumor stroma“ treatment concepts in mouse models → analyse mouse tumors, mouse plasma proteomics → explant tumors/cell culture, measure cytokines, growth factors