CRYOSENSITIZERS: Ablation at the Edge

Similar documents
BL-8040: BEST-IN-CLASS CXCR4 ANTAGONIST FOR TREATMENT OF ONCOLOGICAL MALIGNANCIES. Overview and Mechanism of Action Dr.

Chapter 1 CELL INJURY CELL DEATH CELL ADAPTATIONS. M.G.Rajanandh, Dept. of Pharmacy Practice, SRM College of Pharmacy, SRM University.

Review of Hallmarks of Prostate Cancer (PCa) Nilgoon Zarei* Keywords: Prostate Cancer (PCa), Hallmarks of Cancer

Biopreservation Considerations for GMP Bioprocessing, Clinical Development, Supply Logistics, and Patient Delivery

Neoplasia 18 lecture 8. Dr Heyam Awad MD, FRCPath

C-Phycocyanin (C-PC) is a n«sjfc&c- waefc-jduble phycobiliprotein. pigment isolated from Spirulina platensis. This water- soluble protein pigment is

Transformation of Normal HMECs (Human Mammary Epithelial Cells) into Metastatic Breast Cancer Cells: Introduction - The Broad Picture:

Controlled Cryogenic Ablation Using Ultrasonic Sensing

Expressions of MVD, VEGF, Ki67 in Residual Prostate Cancer after Cryoablation

Deregulation of signal transduction and cell cycle in Cancer

Sensors & Transducers 2015 by IFSA Publishing, S. L.

Simplify the relations between genes and diseases into typed binary relations. PubMed BioText GoPubMed

Lecture 14 - The cell cycle and cell death

Introduction. Cancer Biology. Tumor-suppressor genes. Proto-oncogenes. DNA stability genes. Mechanisms of carcinogenesis.

ETIOLOGY AND PATHOGENESIS OF HYPOXIC-ISCHEMIC ENCEPHALOPATHY

Cryoablation Induces Necrosis and Apoptosis in Lung Adenocarcinoma in Mice

VIII Curso Internacional del PIRRECV. Some molecular mechanisms of cancer

CELL BIOLOGY - CLUTCH CH CANCER.

Molecular biology :- Cancer genetics lecture 11

Cell Injury MECHANISMS OF CELL INJURY

The Hallmarks of Cancer

Focus Application. Compound-Induced Cytotoxicity

CANCER THERAPEUTICS: A NOVEL APPROACH

Oncolytic Virotherapy: Targeting Cancer Stem Cells

New Developments in the Treatment of Colorectal Cancer. Jonathan Loree, MD, MS, FRCPC Department of Medical Oncology BC Cancer Vancouver Centre

CELL INJURY. Severity of Cell Injury

Focus Application. Compound-Induced Cytotoxicity

Corporate Medical Policy

Supplementary Figures

The Tumor Microenvironment

Basic tumor nomenclature

3D-Tissue Microsystems for Tumor Microenvironments Designs for Basic and Translational Research

Mechanisms of Cell Injury

34 Apoptosis Programmed cell death is vital to the health and development of multicellular organisms.

Mechanistic Toxicology

IL-24 AND ITS ROLE IN WOUND HEALING

Convergent and Divergent Mechanisms in Aging and Cancer

MOLECULAR CELL BIOLOGY

IVC History, Cancer Research

GMS 6644: Apoptosis. Introduction

shehab Moh Tarek ... ManarHajeer

IVC History, Cancer Research

- 1 - Cell types Monocytes THP-1 cells Macrophages. LPS Treatment time (Hour) IL-6 level (pg/ml)

Generation of post-germinal centre myeloma plasma B cell.

Cancer. Throughout the life of an individual, but particularly during development, every cell constantly faces decisions.

Biologics Effects of Targeted Therapeutics

Percutaneous cryoablation of lung tumors

Darwinian selection and Newtonian physics wrapped up in systems biology

TARGETED THERAPY FOR CHILDHOOD CANCERS

Mechanisms of Cell Injury: Loss of Calcium Homeostasis

Reperfusion Injury: How Can We Reduce It?

Mechanisms of Chemotherapeutic Drug Resistance An Overview

Tumor Microenvironment and Immune Suppression

Pathology of Inflammatory Breast Cancer (IBC) A rare tumor

Molecular and Cell Biology of Cancer. Code: ECTS Credits: 6. Degree Type Year Semester Biomedical Sciences OT 4 0

CHAPTER VII CONCLUDING REMARKS AND FUTURE DIRECTION. Androgen deprivation therapy is the most used treatment of de novo or recurrent

In vitro scratch assay: method for analysis of cell migration in vitro labeled fluorodeoxyglucose (FDG)

1. The metastatic cascade. 3. Pathologic features of metastasis. 4. Therapeutic ramifications. Which malignant cells will metastasize?

Molecular and Cell Biology of Cancer. Code: ECTS Credits: 6. Degree Type Year Semester Biomedical Sciences OT 4 0

VITAMIN E SUCCINATE: THE PREFERRED FORM OF VITAMIN E TO COMBAT BREAST, PROSTATE AND OTHER CANCERS

Molecular Biology of Cancer. Code: ECTS Credits: 6. Degree Type Year Semester

Cancer Cell Self Sufficiency in Growth Signals

Subject Index. Bcl-2, apoptosis regulation Bone marrow, polymorphonuclear neutrophil release 24, 26

Cardioblate CryoFlex Surgical Ablation System. Shaping Surgical Ablation.

Molecular Biology of Cancer. Code: ECTS Credits: 6. Degree Type Year Semester

Cancer and Gene Alterations - 1

Supplementary Material

DAX1, testes development role 7, 8 DFFRY, spermatogenesis role 49 DMRT genes, male sex differentiation role 15

MicroRNA expression profiling and functional analysis in prostate cancer. Marco Folini s.c. Ricerca Traslazionale DOSL

Healing and Repair. Dr. Nabila Hamdi MD, PhD

INDUCED HYPOTHERMIA. F. Ben Housel, M.D.

The Effect of Vascularization and Tissue Type on Cryosurgical Procedures. Reed Magleby Amanda Schallop Eric Shulman Joshua Sterling

In Vitro Studies of the Aurora-Kinase Inhibitor MLN8237 in Prostate Cancer Cell Lines

Part I. An Introduction to Cancer

Production of Exosomes in a Hollow Fiber Bioreactor

CONTRACTING ORGANIZATION: Oregon Health and Science University Portland, Oregon

Biobehavioral Pathways in Epithelial Ovarian Cancer

V 2/2015/EN PAIN MANAGEMENT

Multiparametric imaging in oncology

Drug Resistance: Oncology 520 March 27, 2012

Early Embryonic Development

Virchow s Hypothesis lymphorecticular infiltration of cancer reflected the origin of cancer at sites of inflammation

High Throughput Screening as a Research Tool. Robert Damoiseaux. Ph.D., Scientific Director Molecular Shared Screening Resources, UCLA

Chemical and Biochemical Mechanism Of Cell Injury.

Imaging ischemic strokes: Correlating radiological findings with the pathophysiological evolution of an infarct

The Hallmarks of Cancer

Thermal Physiology C H A P T E R. PowerPoint Lecture Slides prepared by Stephen Gehnrich, Salisbury University

Small-molecule activation of procaspase-3 to caspase-3 as a personalized anticancer strategy

Cancer Biology How a cell responds to DNA Damage

Contents. Preface XV Acknowledgments XXI List of Abbreviations XXIII About the Companion Website XXIX

Human induced pluripotent stem cell derived cardiomyocytes are a more relevant model for assessing drug-induced effects on mitochondrial function

Active surveillance: Shrinking the grey zone. Sommerakademi e Munich, June rd FOIUS Tel Aviv, July 2016

Melatonin and its Role in the Inhibition of Breast Cancer Ciara Nicol Ross Copyright 2014 by Ciara Ross and Koni Stone

UNIVERSITY OF MEDICINE AND PHARMACY CRAIOVA PhD SCHOOL. PhD THESIS

Objectives. Abbas Chapter 11: Immunological Tolerance. Question 1. Question 2. Question 3. Definitions

Cancer as a Metabolic Disease

Immunotherapy of Prostate Cancer

Mechanisms of Gene Regulation and Signal! Transduction in Hypoxia!

1.The metastatic cascade. 2.Pathologic features of metastasis. 3.Therapeutic ramifications

Transcription:

CRYOSENSITIZERS: Ablation at the Edge John G. Baust Institute of Biomedical Technology State University of New York Binghamton, NY USA JGBaust@binghamton.edu

Precision targeting Challenge Uncertain margin Responsiveness gradient

-15 o C 0 o C

Cryolesion Thermal variability within lesion Cooling rates Temperature Necrosis Apoptosis Multiple Modes of Cell Death Freeze Rupture Necrosis Apoptosis Freeze Rupture

Effect of Freezing on Viability of Prostate Cancer Cells In Vitro 100 90 80 % Viability 70 60 50 40 Clarke (2000) Hollister (1998) Bischoff (1997) Znati (1998) 30 20 10 0 - - - - - - - - - - - 0 10 20 30 40 50 60 70 80 90 100 110 Temperature (C)

Freezing Response (15 min) of Human Prostate Cancer Cells (LNCaP) Treated with Double Freeze Cycle Percent Viability 100 75 50 25 0 Control -5 C -10 C -15 C -20 C -25 C -40 C Condition * * * Pre-Freeze Day 1 Day 3 Day 5 Day 7 Day 9 p< 0.005 Freezing Response (15 min) of Human Prostate Cancer Cells (PC-3) Treated with Double Freeze Cycle Percent Viability 100 75 50 25 * * * Pre-Freeze Day 1 Day 3 Day 5 Day 7 Day 9 0 Control -5 C -10 C -15 C -20 C -25 C -40 C Condition p< 0.005

Tissue-Engineered Prostate Model 1-Day Post Freeze PC-3 PC-3 LNCaP LNCaP

PC-3 Cell Recovery After Cryo, Chemo, and Combination 110 100 * 90 80 Percent Viable 70 60 50 40 2 Days 4 Days 6 Days 30 20 10 * * 0 Control 5-FU 2day 5-FU 4day -20 12hr prior 1 day prior 2 day prior 4 day prior P < 0.001

110 PC-3 Cell Recovery Following Exposure to Freezing (-15 0 C) Alone or in Combination with Cytotoxic Agents 100 90 80 % Viable 70 60 50 40 2 Days 5 Days 8 Days 11 Days 14 Days 30 20 10 0 Control Fre (-15) 5FU/Fre Tax/Fre Etop/Fre Cis/Fre FA/Fre

Comparison of Combinatorial Approaches to Cryosurgery -105 C -60 C -40 C -20 C -1 C Single Freeze -105 C -60 C -40 C -20 C -5 C Double Freeze Double Freeze/TRAIL Double Freeze/Taxotere

Factors Underlying Ablative Response Hypothermia Metabolic Uncoupling Energy Deprivation Waste Accumulation Ionic Imbalance ph Shifts (acidosis) Membrane Phase Transitions Cytoskeletal Disassembly Freezing Extracellular Ice Hyperosmolality Cell Volume Disruption Protein Denaturation Intracellular Ice Shearing Membrane Disruption Vascular Stasis Induction of Apoptosis Ischemia Hypoxia Nutrient deprivation Ionic imbalance Increased free radicals Energy deprivation Membrane alterations Biochemical alterations Induction of Necrosis All Events

Hallmarks of Cancer Proliferative Signaling Evade Growth Suppressors Resist Apoptosis Induce Angiogenesis Avoid Immune System Destruction Reprogram Cellular Energetics Enable Replicative Immortality (CSC) Recruit Non-cancerous Stromal Cell to Create Microenvironment Mobilization = Metastasis

120 Effects of VD3 and Freezing at -15 C (15 min) on Human Prostate Cancer Cell Lines LNCaP LP and PC-3 AR 100 Percent Viability 80 60 Pre-Freeze Day 1 Day 3 Day 5 Day 7 Day 9 40 20 0 Control 50nM FR171-15 C Only -15 C with 50nM FR171 LNCaP LP Condition Control 50nM FR171-15 C Only -15 C with 50nM FR171 PC-3 AR BJU Intl 2011

120 Effects of VD3 and Freezing at -15 C (15 min) on Human Prostate Cancer Cell Lines LNCaP HP and PC-3 100 Percent Viability 80 60 Pre-Freeze Day 1 Day 3 Day 5 Day 7 Day 9 40 20 0 Control 50nM FR 171-15 C Only -15 C with 50nM FR 171 Control 50nM FR 171-15 C Only -15 C with 50nM FR 171 LNCaP HP Condition PC-3 BJU Intl 2011

BJU Intl. 2011

Hallmarks of Cancer Proliferative Signaling loss of cell cycle control Evade Growth Suppressors - -p53 Resist Apoptosis - +Bcl-2, -p53 Induce Angiogenesis - +VEGF Avoid Immune System Destruction surface markers Reprogram Cellular Energetics - glycolysis Enable Replicative Immortality - CSC Recruit Non-cancerous Stromal Cells Create to Microenvironment tumor associated-endothelium Mobilization = Metastasis - - cell adhesion molecules

Hallmarks of Cancer VD3 + Cryo Induced Changes Proliferative Signaling restores of cell cycle control Evade Growth Suppressors - Resist Apoptosis - +bcl2, -p53 Induce Angiogenesis - +VEGF Avoid Immune System Destruction - Reprogram Cellular Energetics - Enable Replicative Immortality - CSC Recruit Non-cancerous Stromal Cell to Create Microenvironment - Mobilization = Metastasis - -cell adhesion molecules

Hallmarks of Cancer VD3 + Cryo Induced Changes Proliferative Signaling restores of cell cycle control Evade Growth Suppressors restores p27, p53 Resist Apoptosis - +bcl2, -p53 Induce Angiogenesis - +VEGF Avoid Immune System Destruction - Reprogram Cellular Energetics - Enable Replicative Immortality - CSC Recruit Non-cancerous Stromal Cell to Create Microenvironment - Mobilization = Metastasis - -cell adhesion molecules

Hallmarks of Cancer VD3 + Cryo Induced Changes Proliferative Signaling restores of cell cycle control Evade Growth Suppressors restores p27, p53 Resist Apoptosis inhibits Bcl-2 Induce Angiogenesis - +VEGF Avoid Immune System Destruction - Reprogram Cellular Energetics - Enable Replicative Immortality - CSC Recruit Non-cancerous Stromal Cell to Create Microenvironment - Mobilization = Metastasis - -cell adhesion molecules

Hallmarks of Cancer VD3 + Cryo Induced Changes Proliferative Signaling restores of cell cycle control Evade Growth Suppressors restores p27, p53 Resist Apoptosis inhibits Bcl-2 Induce Angiogenesis inhibits VEGF transcription Avoid Immune System Destruction - Reprogram Cellular Energetics - Enable Replicative Immortality - CSC Recruit Non-cancerous Stromal Cell to Create Microenvironment - Mobilization = Metastasis - -cell adhesion molecules

Hallmarks of Cancer VD3 + Cryo Induced Changes Proliferative Signaling restores of cell cycle control Evade Growth Suppressors restores p27, p53 Resist Apoptosis inhibits Bcl-2 Induce Angiogenesis inhibits VEGF transcription Avoid Immune System Destruction -? Reprogram Cellular Energetics uncouples metabolism Enable Replicative Immortality - CSC Recruit Non-cancerous Stromal Cell to Create Microenvironment - Mobilization = Metastasis - -cell adhesion molecules

Hallmarks of Cancer VD3 + Cryo Induced Changes Proliferative Signaling restores of cell cycle control Evade Growth Suppressors restores p27, p53 Resist Apoptosis inhibits Bcl-2 Induce Angiogenesis inhibits VEGF transcription Avoid Immune System Destruction -? Reprogram Cellular Energetics uncouples metabolism Enable Replicative Immortality - ablates CSC (?) Recruit Non-cancerous Stromal Cell to Create Microenvironment - Mobilization = Metastasis - -cell adhesion molecules

Hallmarks of Cancer VD3 + Cryo Induced Changes Proliferative Signaling restores of cell cycle control Evade Growth Suppressors restores p27, p53 Resist Apoptosis inhibits Bcl-2 Induce Angiogenesis inhibits VEGF transcription Avoid Immune System Destruction -? Reprogram Cellular Energetics uncouples metabolism Enable Replicative Immortality - ablates CSC (?) Recruit Non-cancerous Stromal Cell to Create Microenvironment ablates stromal cells Mobilization = Metastasis - -cell adhesion molecules

Hallmarks of Cancer VD3 + Cryo Induced Changes Proliferative Signaling restores of cell cycle control Evade Growth Suppressors restores p27, p53 Resist Apoptosis inhibits Bcl-2 Induce Angiogenesis inhibits VEGF transcription Avoid Immune System Destruction -? Reprogram Cellular Energetics uncouples metabolism Enable Replicative Immortality - ablates CSC (?) Recruit Non-cancerous Stromal Cell to Create Microenvironment ablates stromal cells Mobilization = Metastasis - ++cell adhesion molecules

Vitamin D3 Increases Cryoablation Efficacy Key Findings VD3 pre-treatment pulse (2 days) followed by freezing (in vitro and in vivo) resulted in Total cell ablation without of re-growth for both androgen-sensitive (AS) and androgen-insensitive (AI) prostate cancers. Increased levels of both necrotic and apoptotic cell death cascades. Increased caspase activity and duration in AI cells more significantly than was observed for AS cells. Elevated caspase-9 activity in the AI cells indicates that vitamin D3 treatment prior to freezing was able to increase mitochondrial mediated apoptotic cascades to levels comparable with freeze-sensitive AS cells. Single Pulse Vitamin D3 exposure offers a promising neo-adjunctive cryosensitization strategy.

Cryosurgical Technology (boat) Cryoablation: Self Taught