Natural History, Response to Treatment

Slides:



Advertisements
Similar presentations
Zeroing in on Non-Small Cell Lung Cancer: Integrating Targeted Therapies into Practice.
Advertisements

Transcriptional profiling I – microarrays and proteomics
Evaluating cell lines as tumor models by comparison of genomic profiles Domcke, S. et al. Nat. Commun 4:2126.
Metastatic Breast Cancer: One Size Does Not Fit All Clifford Hudis, M.D. Chief, Breast Cancer Medicine Service MSKCC.
Immune dysfunction & its consequences
Stress Regulation of Tumor Biology Robert T. Croyle, PhD Director Division of Cancer Control and Population Sciences Concept Presentation NCI Board of.
Jo Anne Zujewski, MD Cancer Therapy Evaluation Program Division of Cancer Diagnosis and Treatment National Cancer Institute May 2011 Breast Cancer Biology.
Clinical Division of Oncology Department of Medicine I Medical University of Vienna, Austria Cancer Biology.
Gene Therapy AP Biology Unit 2 + What is Gene Therapy? A way to treat or cure diseases by inserting the “correct” DNA into the cell. Most promising for.
The Cancer Systems Biology Consortium (CSBC)
Michael Birrer Ian McNeish New Developments in Biology and Targets of Epithelial Ovarian Cancer.
Computational biology of cancer cell pathways Modelling of cancer cell function and response to therapy.
Moein Farshchian Ph.D Candidate of Cell and Molecular Biology.
Control of Gene Expression
Breast Cancer and BRCA2. 1 million women worldwide diagnosed. 1 out of 12 women in Western Europe and the United States 30% mortality rate Highest cause.
Recombinant DNA What is the basis of recombinant DNA technology? How does one “clone” a gene? How are genetically modified organisms (GMOs) created? Illustration.
OMICS International welcomes submissions that are original and technically so as to serve both the developing world and developed countries in the best.
New Proposals for Lung Cancer Staging Akif Turna, MD, PhD, FETCS Yedikule Teaching Hospital for Chest Diseases and Thoracic Surgery, Istanbul, Turkey.
Progress in Cancer Therapy Following Developments in Biopharma
INTERPRETING GENETIC MUTATIONAL DATA FOR CLINICAL ONCOLOGY Ben Ho Park, M.D., Ph.D. Associate Professor of Oncology Johns Hopkins University May 2014.
Cell Therapy in CV Disease: Newest Evidence. 2 Induction of pluripotent stem cells from human fibroblasts Study Source of fibroblasts Transcription factors.
Cancer The biological formation of cancer and treatments for the disease.
Tumor Heterogeneity: From biological concepts to computational methods Bo Li, PhD Dana Farber Cancer Institute Harvard Statistics Department.
Figure Molecular Biology of the Cell (© Garland Science 2008)
Figure 14-1 Molecular Biology of the Cell (© Garland Science 2008)
Bristol-Myers Squibb is actively conducting translational medicine research to further our understanding of cancer biology and to identify which patient.
Ari Brooks, MD Cancer Surgeon, Big Data End User
Research, 2016, Vol. 4, No. 1, doi: /jfnr-4-1-6
NF1 Low-Grade Glioma Synodos
Biomedical Therapies Foundation Standard 1: Academic Foundation
Snail-overexpressing cancer cells modulates tumor-associated macrophages through promoting M2 polarization and suppressing inflammasome activation Speaker:
Volume 71, Issue 2, Pages (February 2017)
Figure 1 Cellular processes involved in cancer development
Figure 1 Radiation-induced effects on tumour cells
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,
Nat. Rev. Clin. Oncol. doi: /nrclinonc
Correlation of log-transformed signal intensity from two Affymetrix microarray hybridizations using platelet RNA. Plotted are those probesets with an average.
KEY CONCEPT Entire genomes are sequenced, studied, and compared.
Regulating the Cell Cycle
KEY CONCEPT Entire genomes are sequenced, studied, and compared.
Gene Therapy: Past, Present, and Future
Megan E. Daly, MD, Arta M. Monjazeb, MD, PhD, Karen Kelly, MD 
KEY CONCEPT Entire genomes are sequenced, studied, and compared.
Nat. Rev. Urol. doi: /nrurol
Nat. Rev. Rheumatol. doi: /nrrheum
Diagnostic approaches to measure the impact of cancer therapies on clonal evolution. Diagnostic approaches to measure the impact of cancer therapies on.
Preclinical Accelerators of Precision Medicine Todd R. Golub, M.D.
Expression profiles of GAS virulence factors during planktonic and biofilm growth. Expression profiles of GAS virulence factors during planktonic and biofilm.
Primary Double-Strike Therapy for Cancers to Overcome EGFR Kinase Inhibitor Resistance: Proposal from the Bench  Kenichi Suda, MD, PhD, Paul A. Bunn,
Holger Lawall, MD, Peter Bramlage, MD, PhD, Berthold Amann, MD 
KEY CONCEPT Entire genomes are sequenced, studied, and compared.
Intratumoral hypoxia, radiation resistance, and HIF-1
Mechanism of PD-1/PD-L1 pathway-induced immunosuppression within the tumour microenvironment. Mechanism of PD-1/PD-L1 pathway-induced immunosuppression.
Fig. 5 Hypoxic tumors from obese mice associate with increased production of IL-6 by adipocytes and myeloid cells. Hypoxic tumors from obese mice associate.
Fig. 2. Clinically actionable somatic genomic alterations in various tumor types. Clinically actionable somatic genomic alterations in various tumor types.
Distribution of immune checkpoint in tumor cells and immune microenvironment. CTLA-4, cytotoxic T lymphocyte antigen-4; MHC, major histocompatibility complex;
KEY CONCEPT Entire genomes are sequenced, studied, and compared.
Signalling pathways and involved entities that are unravelling experimental therapeutic targets for TNBC. Depicted molecular landscape of TNBC confers.
Sensitivity analysis of cellular responses to perturbation of the DNA damage response signaling in the presence of chemotherapies. Sensitivity analysis.
Geographic colocalization of PD-L1+ tumor cells with infiltrating immune cells in MCC. The predominant pattern of tumor cell PD-L1 expression is at the.
Fig. 5 n-HA regulates gene expressions related to tumor suppression, calcium homeostasis, and immune response. n-HA regulates gene expressions related.
Overview of important signalling pathways in angiogenesis and antiangiogenic agents. Overview of important signalling pathways in angiogenesis and antiangiogenic.
Clinical outcomes resulting from inhibition of tumor-intrinsic and myeloid NF-κB activation in melanoma chemotherapy. Clinical outcomes resulting from.
(A) Lymph node priming phase: recognition of major histocompatibility complex (MHC) by T-cell receptor (TCR), coactivating CD 28/B7 pathway activation.
Illustration of cancer cells and tumor microenvironment–deregulated miRNA target networks leading to tumor growth and progression. Illustration of cancer.
Human cancer immunotherapy strategies targeting B7-H3 A, blockade of B7-H3 with blocking mAbs neutralizes inhibitory signaling in its unidentified receptor(s)
Fig. 1. Schematic description of whole-exome or targeted next-generation sequencing analyses. Schematic description of whole-exome or targeted next-generation.
Biomarkers in Early-Stage Non–Small-Cell Lung Cancer: Current Concepts and Future Directions  Mauricio Burotto, MD, Anish Thomas, MD, Deepa Subramaniam,
Immunological effects of anticancer therapy.
Fig. 8 Immune correlates of protection.
Presentation transcript:

Natural History, Response to Treatment Morphology, Anatomy Natural History, Response to Treatment

Natural History, Response to Treatment Gene expression, Proteomics, etc Morphology, Anatomy Natural History, Response to Treatment

Cell of Origin Genomic Changes Natural History, Response to Treatment Shat et al, Nature 2012 Gene expression, Proteomics, etc Morphology, Anatomy Natural History, Response to Treatment

Tumor Microenvironment Cell of Origin Genomic Changes Tumor Microenvironment Fibroblasts Macrophages Lymphocytes Endothelial cells Shat et al, Nature 2012 Gene expression, Proteomics, etc Morphology, Anatomy Natural History, Response to Treatment

Tumor Microenvironment Host Factors Cell of Origin Genomic Changes Tumor Microenvironment Host Factors Fibroblasts Macrophages Lymphocytes Endothelial cells Shat et al, Nature 2012 Gene expression, Proteomics, etc Morphology, Anatomy Natural History, Response to Treatment

Precision Oncology Cell of Origin Genomic Changes Tumor Microenvironment Host Factors Fibroblasts Macrophages Lymphocytes Endothelial cells Shat et al, Nature 2012 Gene expression, Proteomics, etc Morphology, Anatomy Natural History, Response to Treatment Chemotherapy (DNA repair/checkpoint/cell death) Biological therapy (growth signaling pathways) Immune Therapy (tumor/host factors)

Precision Oncology Cell of Origin Genomic Changes Tumor Microenvironment Host Factors Fibroblasts Macrophages Lymphocytes Endothelial cells Shat et al, Nature 2012 Gene expression, Proteomics, etc Morphology, Anatomy Histology guided clincial trials Natural History, Response to Treatment Chemotherapy (DNA repair/checkpoint/cell death) Biological therapy (growth signaling pathways) Immune Therapy (tumor/host factors)

Precision Oncology Cell of Origin Genomic Changes Tumor Microenvironment Host Factors Fibroblasts Macrophages Lymphocytes Endothelial cells Shat et al, Nature 2012 Gene expression, Proteomics, etc Morphology, Anatomy BIG DATA?? Genomically informed Clinical trials Histology guided clincial trials Natural History, Response to Treatment Chemotherapy (DNA repair/checkpoint/cell death) Biological therapy (growth signaling pathways) Immune Therapy (tumor/host factors)

Precision Oncology Cell of Origin Genomic Changes Tumor Microenvironment Host Factors Fibroblasts Macrophages Lymphocytes Endothelial cells Shat et al, Nature 2012 Gene expression, Proteomics, etc Morphology, Anatomy BIG DATA?? Genomically informed Clinical trials Histology guided clincial trials Natural History, Response to Treatment Chemotherapy (DNA repair/checkpoint/cell death) Biological therapy (growth signaling pathways) Immune Therapy (tumor/host factors) Shridar Ganesan, MD, Phd Assoc. Dir. Transl. Science Chief, Sec. Molecular Oncology Rutgers -CINJ