Elke Pogge von Strandmann, Silke Reinartz, Uwe Wager, Rolf Müller 

Slides:



Advertisements
Similar presentations
Epidermal growth factor receptor tyrosine kinase inhibitors as initial therapy for non- small cell lung cancer: Focus on epidermal growth factor receptor.
Advertisements

Advances in Molecular Biology of Lung Disease
Figure 1. Resistance mechanism against first generation epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKI). (A) Mutations in the EGFR.
Mechanism of Action of Colchicine in the Treatment of Gout
Kusumawadee Utispan, Sittichai Koontongkaew 
Relapsed/Refractory Multiple Myeloma: Defining Refractory Disease and Identifying Strategies to Overcome Resistance  David S. Siegel  Seminars in Hematology 
Myeloma cell interaction with extracellular matrix (ECM) and accessory cells in the marrow. Myeloma cells require support from bone marrow stromal cells.
Colorectal Cancer Stem Cells: From the Crypt to the Clinic
Molecular targeted therapies in hepatocellular carcinoma: From pre-clinical models to clinical trials  Pippa Newell, Augusto Villanueva, Josep M. Llovet 
Immunologic pathomechanism of Hodgkin's lymphoma
Figure 4 The mechanistic link between the epithelial-to-mesenchymal
Inflammation and Colon Cancer
Prevention of ischemia-reperfusion injury in cardiac surgery: Therapeutic strategies targeting signaling pathways  Kay Maeda, MD, PhD, Marc Ruel, MD,
Treatment of Glioma in the 21st Century: An Exciting Decade of Postsurgical Treatment Advances in the Molecular Era  Joon H. Uhm, MD, Alyx B. Porter,
Potential pathways directly linking obesity with cancer.
Liver regeneration Journal of Hepatology
Biochemical and physiological effects from exhaust emissions
Oncology Meets Immunology: The Cancer-Immunity Cycle
NOD-like and Toll-like receptors or inflammasomes contribute to kidney disease in a canonical and a non-canonical manner  Hans-Joachim Anders, Maciej.
Germaine Wong, Jeremy R. Chapman, Jonathan C. Craig 
Jean-Charles Nault, Jessica Zucman-Rossi  Journal of Hepatology 
Immunologic pathomechanism of Hodgkin's lymphoma
Genetic Modifiers of the Breast Tumor Microenvironment
Do Diabetes Drugs Modify the Risk of Pancreatic Cancer?
Data Triumph at C Cancer Cell
Management of advanced renal cancer
Nat. Rev. Gastroenterol. Hepatol. doi: /nrgastro
Colorectal Cancer Stem Cells: From the Crypt to the Clinic
Personalizing Therapy for Colorectal Cancer
Targeting ROS1 with Anaplastic Lymphoma Kinase Inhibitors: A Promising Therapeutic Strategy for a Newly Defined Molecular Subset of Non–Small-Cell Lung.
Elke Pogge von Strandmann, Silke Reinartz, Uwe Wager, Rolf Müller 
Biochemical and physiological effects from exhaust emissions
Personalizing Therapy for Colorectal Cancer
R. Balfour Sartor, MD  Clinical Gastroenterology and Hepatology 
Rapamycin in transplantation: A review of the evidence
Tyrosine Kinase Inhibitors in Clinical Practice: Patient Selection
A Radical Role for p38 MAPK in Tumor Initiation
Volume 66, Issue 2, Pages (February 2017)
Macrophages and Therapeutic Resistance in Cancer
Development of PI3K/AKT/mTOR Pathway Inhibitors and Their Application in Personalized Therapy for Non–Small-Cell Lung Cancer  Vassiliki Papadimitrakopoulou,
Unraveling the Pros and Cons of Interferon-γ Gene Regulation
Bhagelu Ram Achyut, Li Yang  Gastroenterology 
Craig H Selzman, MD, Stephanie A Miller, MD, Alden H Harken, MD 
Macrophages and Therapeutic Resistance in Cancer
Volume 22, Issue 6, Pages (December 2012)
Inhibition of mammalian target of rapamycin: Two goals with one shot?
Tumoral presence of human cytomegalovirus is associated with shorter disease-free survival in elderly patients with colorectal cancer and higher levels.
Michael G. Katz, MD, PhD, Anthony S. Fargnoli, PhD, Andrew P
Volume 70, Issue 7, Pages (October 2006)
Gregory B. Vanden Heuvel  Kidney International 
Targeting Cancer Stemness in the Clinic: From Hype to Hope
Valder R Arruda, Patricia Favaro, Jonathan D Finn  Molecular Therapy 
Primary Double-Strike Therapy for Cancers to Overcome EGFR Kinase Inhibitor Resistance: Proposal from the Bench  Kenichi Suda, MD, PhD, Paul A. Bunn,
Learning from PD-1 Resistance: New Combination Strategies
Nanna Fyhrquist, Sampsa Matikainen, Antti Lauerma 
Volume 21, Issue 8, Pages (August 2013)
Yan Feng, MD, Praveena S. Thiagarajan, PhD, Patrick C. Ma, MD 
Azucena Ramos, Michael T. Hemann  Cell 
Azucena Ramos, Michael T. Hemann  Cell 
Benjamin Solomon, MBBS, PhD, Richard B. Pearson, PhD 
Figure 4 Bile-acid-induced TGR5 signalling pathways in macrophages
Intratumoral hypoxia, radiation resistance, and HIF-1
Learning from PD-1 Resistance: New Combination Strategies
Jinhua Tang, Na Liu, Shougang Zhuang  Kidney International 
Nat. Rev. Urol. doi: /nrurol
Primary immunodeficiencies: A rapidly evolving story
Sundararaman Swaminathan, Matthew D. Griffin  Kidney International 
Volume 10, Issue 3, Pages (September 2006)
Illustration of cancer cells and tumor microenvironment–deregulated miRNA target networks leading to tumor growth and progression. Illustration of cancer.
Something in the Air: Hyperoxic Conditioning of the Tumor Microenvironment for Enhanced Immunotherapy  Robert D. Leone, Maureen R. Horton, Jonathan D.
Presentation transcript:

Tumor–Host Cell Interactions in Ovarian Cancer: Pathways to Therapy Failure  Elke Pogge von Strandmann, Silke Reinartz, Uwe Wager, Rolf Müller  Trends in Cancer  Volume 3, Issue 2, Pages 137-148 (February 2017) DOI: 10.1016/j.trecan.2016.12.005 Copyright © 2017 The Authors Terms and Conditions

Figure 1 Key Figure: Schematic Representation of Signaling Pathways in the Ovarian Cancer Microenvironment Impinging on the Response of Tumor Cells to Chemotherapeutic Drugs. (A) Clinically successful first-line chemotherapy (most patients) with few surviving tumor cells. (B) Disease progression during or shortly after chemotherapy due to genetically determined inherent resistance (small fraction of patients). (C) Cancer recurrence in initially responsive patients within 3 years (most patients) with two possible consequences (D and E). (D) Multiple cycles of tumor reduction and regrowth in relapsed patients due to transient resistance presumably controlled by microenvironmental cues. (E) Acquisition of a state of stable resistance largely driven by genetic alterations. Abbreviations: CAA, cancer-associated adipocyte; CAF, cancer-associated fibroblast; CD8+, cytotoxic T cell; Cys, cysteine; ECM, extracellular matrix; EGF, epidermal growth factor; EMT, epithelial–mesenchymal transition; GSH, glutathione; IFNγ, interferon-γ; IL-x, interleukin-x; L1-CAM, L1 cell adhesion molecule; MET, mesenchymal–epithelial transition; miR, microRNA; mTOR, mammalian (or mechanistic) target of rapamycin; NFκB, nuclear factor-κB; NK, natural killer cell; PI3K, phosphoinositide 3-kinase; PKB, protein kinase B; ROS, reactive oxygen species; STAT, signal transducers and activators of transcription; SYK, spleen tyrosine kinase; TAM, tumor-associated macrophage; TGFβ: growth transforming growth factor β; TNFα, tumor necrosis factor-α; Tu, tumor cell. Genes and proteins are named according to the HUGO gene nomenclature. References are quoted in the main text. Trends in Cancer 2017 3, 137-148DOI: (10.1016/j.trecan.2016.12.005) Copyright © 2017 The Authors Terms and Conditions

Figure I Model Illustrating Different Mechanisms of Ovarian Carcinoma Chemoresistance. CTX, cyclophosphamide (chemotherapy). Trends in Cancer 2017 3, 137-148DOI: (10.1016/j.trecan.2016.12.005) Copyright © 2017 The Authors Terms and Conditions