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Systemic Effects of Metastatic Cancer

WEBINAR

Only

Systemic Effects of Metastatic Cancer

Wednesday, October 21 - Thursday, October 22, 2020 EDT

Webinar

Presented By

The New York Academy of Sciences

 

Metastatic cancer exerts systemic effects on the entire body. Its influence on the immune system and distant organs leads to pre-metastatic niche formation and metastasis, alongside vascular and metabolic changes, lung failure, loss of bone density, muscle wasting and cachexia, as well as neuropathies. These effects not only promote tumor progression, but they are deleterious to patient quality of life and survival.

The myriad effects induced by metastasis present several new therapeutic targets, and successful blockade of cancer’s systemic influence may have several beneficial outcomes: it could interfere with disease progression, and it could enhance patient quality of life and longevity. In addition, systemic alterations may serve as sentinels of cancer spread, and therefore provide a novel panel of biomarkers for early detection of metastasis. This symposium aims to deepen our understanding of the complex results of systemic metastatic disease, and inspire the development of effective therapeutic strategies to prevent and treat the systemic outcomes of cancer metastasis.

Registration

Member
$60
Nonmember Academia, Faculty, etc.
$130
Nonmember Corporate, Other
$170
Nonmember Not for Profit
$130
Nonmember Student, Undergrad, Grad, Fellow
$90
Member Student, Post-Doc, Fellow
$30
Member
$30
Nonmember Academia, Faculty, etc.
$65
Nonmember Corporate, Other
$85
Nonmember Not for Profit
$65
Nonmember Student, Undergrad, Grad, Fellow
$45
Member Student, Post-Doc, Fellow
$15
Member
$30
Nonmember Academia, Faculty, etc.
$65
Nonmember Corporate, Other
$85
Nonmember Not for Profit
$65
Nonmember Student, Undergrad, Grad, Fellow
$45
Member Student, Post-Doc, Fellow
$15
Deadline:
0
days
left

Scientific Organizing Committee

Swarnali Acharyya, PhD
Swarnali Acharyya, PhD

Columbia University

David Lyden, MD, PhD
David Lyden, MD, PhD

Weill Cornell Medicine

George Miller
George Miller, MD

NYU School of Medicine

Alexia Zaromytidou, PhD
Alexia Zaromytidou, PhD

Nature Cancer

Sonya Dougal
Sonya Dougal, PhD

New York Academy of Sciences

Kari Fischer, PhD
Kari Fischer, PhD

New York Academy of Sciences

Keynote Speakers

Kornelia Polyak
Kornelia Polyak, MD, PhD

Dana-Farber Cancer Institute

Gregg Semenza
Gregg Semenza, MD, PhD

Johns Hopkins University School of Medicine

Speakers

Swarnali Acharyya, PhD
Swarnali Acharyya, PhD

Columbia University

Michael Angelo
Michael Angelo, MD, PhD

Stanford University

Susan Bullman, PhD
Susan Bullman, PhD

Fred Hutchinson Cancer Research Center

Brunhilde Felding, PhD
Brunhilde Felding, PhD

Scripps Research

Silvia Formenti
Silvia Formenti, MD

Weill Cornell Medicine

Paul Frenette
Paul Frenette, MD

Albert Einstein College of Medicine

Cyrus Ghajar
Cyrus Ghajar, PhD

Fred Hutchinson Cancer Research Center

Tim Greten
Tim Greten, MD

National Cancer Institute

Theresa Guise
Theresa Guise, MD

Indiana University School of Medicine

Lee Jones
Lee Jones, PhD

Memorial Sloan Kettering Cancer Center

Rosandra N. Kaplan, MD
Rosandra N. Kaplan, MD

National Cancer Institute

George Miller
George Miller, MD

NYU School of Medicine

Andy J. Minn, MD, PhD
Andy J. Minn, MD, PhD

University of Pennsylvania

Carla Prado, PhD, RD
Carla Prado, PhD, RD

University of Alberta

Patricia Steeg
Patricia Steeg, PhD

National Cancer Institute

Matthew Vander Heiden
Matthew Vander Heiden, MD, PhD

Massachusetts Institute of Technology

Program Supporters

This event is supported by a grant from Genentech, a member of the Roche Group.

Wednesday

October 21, 2020

10:30 AM

Introduction and Welcome Remarks

Speakers

David Lyden, MD, PhD
Weill Cornell Medicine
Kari Fischer, PhD
New York Academy of Sciences

Session 1: Tumor-Induced Systemic Effects

10:45 AM

Cancer-Associated Fibroblast Exosomes and IFN-Response Signaling

Speaker

Andy J. Minn, MD, PhD
University of Pennsylvania
11:15 AM

Induction of the Pre-Metastatic Niche

Speaker

Rosandra N. Kaplan, MD
National Cancer Institute
11:45 AM

Networking Break

11:55 AM

Why is Skeletal Muscle Anti-Metastatic?

Speaker

Cyrus Ghajar, PhD
Fred Hutch
12:25 PM

Platelet Function in Metastasis

Speaker

Brunhilde Felding, PhD
Scripps Research

Session 2: Early Career Spotlight - Short Talks

12:55 PM

4 x 10 minute talks from selected abstracts

1:35 PM

Networking Break

Session 3: Immune and Microbiota Dysregulation

2:00 PM

How the Liver Specific Environment Controls Growth of Primary Tumors and Metastasis to the Liver

Speaker

Tim Greten, MD
National Cancer Institute
2:30 PM

Diversity of Tumor Microenvironment and Immunotherapeutic Response in Primary vs Metastatic Disease

Speaker

George Miller, MD
New York University
3:00 PM

Persistence of Tumor Associated Microbiota in Metastases

Speaker

Susan Bullman, PhD
Fred Hutch
3:30 PM

Networking Break

3:45 PM

Focal Radiotherapy to Convert the Tumor into an In Situ Vaccine

Speaker

Silvia Formenti, PhD
Weill Cornell Medicine
4:15 PM

Keynote: Hypoxia-Inducible Factors Promote Evasion of Anti-Tumor Immunity

Speaker

Gregg Semenza, MD, PhD
Johns Hopkins University
5:00 PM

Closing Remarks & Day 1 Adjourns

Thursday

October 22, 2020

10:45 AM

Welcome Back

Speaker

Kari Fischer, PhD
New York Academy of Sciences

Session 4: Multi-Organ Pathologies

10:50 AM

Influence of Metabolism on Metastasis

Speaker

Matthew Vander Heiden, MD, PhD
Massachusetts Institute of Technology
11:20 AM

Triggers of Muscle Wasting in Metastatic Cancers

Speaker

Swarnali Acharyya, PhD
Columbia University
11:50 AM

Networking Break

12:00 PM

Cancer, Bone and Beyond: An Integrated View of the Bone Microenvironment

Speaker

Theresa Guise, MD
Indiana University School of Medicine
12:30 PM

Neural Regulation of Hematopoietic Stem Cells and Cancer Cells

Speaker

Paul Frenette, MD
Albert Einstein College of Medicine
1:00 PM

Virtual Poster Session

Session 5: Imaging, Diagnosis, and Treatment

2:00 PM

High Dimensional Spatial Mapping of Immune Cell Populations in Solid Human Tumors

Speaker

Michael Angelo, MD, PhD
Stanford University
2:30 PM

Targeted Nutrition Interventions to Prevent & Manage Low Muscle Mass in Cancer

Speaker

Carla Prado, PhD, RD
University of Alberta
3:00 PM

Exercise and Cancer

Speaker

Lee Jones, PhD
Memorial Sloan Kettering Cancer Center
3:30 PM

Networking Break

3:45 PM

Brain Metastases of Breast Cancer

Speaker

Patricia Steeg, PhD
National Cancer Institute
4:15 PM

Keynote: Non-Cell-Autonomous Drivers of Breast Tumor Progression

Speaker

Kornelia Polyak, MD, PhD
Dana-Farber Cancer Institute

Most breast tumors display a high degree of intratumor heterogeneity, with many distinct subpopulations of cancer cells present. Elevated diversity within a tumor increases the chance for cellular adaptation, as individual clones may react differently to changes in the tumor microenvironment. Thus, treatment of heterogeneous tumors may lead to selection of a resistant clone, its expansion and tumor progression. However, the fitness of cancer cells depends not only on their intrinsic properties, but could also be affected through interactions between different subpopulations. These interactions could be the reason for maintenance of minor clones along the major population. Therefore, intratumor heterogeneity may have functional relevance in tumor progression and colonization of metastatic sites. To emulate clonal interactions, we used the previously developed polyclonal breast cancer model of MDA-MB-468 cell line expressing soluble factors, IL-11 and FIGF.The IL-11 and FIGF clones, when present as minor population, support the growth of other clones in vivo. Moreover, polyclonal tumor with minor driving clone population arehighly metastatic. Thus, we hypothesized that clonal interactions could not only drive tumor growth, but could also play an important role in metastasis.We have found that polyclonal tumors lead to polyclonal metastases, composed of mixture of neutral and driver clones. To investigate the mechanisms of clonal interactions driving polyclonal metastasis, we performed RNA profiling of subpopulations and stroma from polyclonal tumors. Our results suggest that this cooperation is indirect and that driver clones promote metastasis by altering the tumor microenvironment. We have also found that minor driver clones affect the immune cells within primary tumor, circulating blood and metastatic site. These systemic changes significantly influence the metastatic progression. We are currently testing whether a treatment targeting this indirect clonal interaction mechanism could prevent polyclonal metastatic spread.Our study shows that the interaction between minor clones and other cancer cells could drive tumor growth and metastasis. Moreover, our results suggest that clonal cooperation in metastatic progression may be indirect and involve modulation of immune microenvironment of the primary tumor and distant organs.

5:00 PM

Closing Remarks & Conference Concludes