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Web Desc
Role of Inflammation in Oncogenesis
joint with Molecular and Cellular Biology of Immune Escape in Cancer
Organizer(s): Nina Bhardwaj and Giorgio Trinchieri
Date: February 07 - 12, 2010
Location: Keystone Resort, Keystone, CO, USA
Sponsored by Celgene Corporation, Hoffmann-La Roche, Inc. and Pfizer Global Research & Development
Summary of Meeting:
Cancer is characterized by accelerated and uncontrolled growth, dysregulation of apoptosis, invasion and metastasis. While genetic and epigenetic mechanisms may underlie transformation, the tumor microenvironment promotes the neoplastic process. Chronic inflammation and infection, in particular, are linked to the development of cancer. Examples include the association between inflammatory bowel disease and colon cancer, Helicobacter pylori infection with gastric cancer and HPV with cervical cancer. Recent studies have linked the innate immune system, through production of inflammatory cytokines, with cancer progression. Factors such as TNF alpha, IL-6, and TGF beta, produced by macrophages and dendritic cells amongst other cells, enhance tumor growth, invasion, metastasis, and angiogenesis, while simultaneously impairing anti-tumor immune mechanisms. There have been several advances in our understanding of the influences of inflammation on tumorigenesis. However, critical elements of the involved inflammatory pathways that modulate tumor progression still remain to be identified. The complex interrelationship between inflammatory vs. immune suppressive cytokines and their effects on the neoplastic process remain to be defined. The association between DNA damage and inflammation and the link between pathogen associated molecular patterns (PAMPs) and novel pattern recognition molecules (TLRs and NOD like receptors) in driving tumor development require further characterization. How cancer associated inflammation might actively dysregulate the innate immune system, in particular of dendritic cell, NK and NKT cell anti-tumor function, is also an area of interest and intense speculation. This meeting will focus specifically on mechanisms of inflammation-induced carcinogenesis, and will bring together investigators with diverse interests and expertise - immunology, signal transduction, cancer biology and therapeutics. It is anticipated that the pairing with the concurrent Keystone Symposia meeting on Immune Escape in Cancer will attract a large body of scientists who share a common interest in cancer pathogenesis, inflammation and mechanisms underlying immune evasion. The goal of the meeting is to enhance discussion, foster collaborations, report on new paradigms, and ultimately to develop approaches that will modulate inflammation-associated tumor progression.
Scholarship Deadline: October 7 2009
Discounted Abstract Deadline: October 7 2009
Abstract Deadline: November 6 2009
Discounted Registration Deadline: December 7 2009
We gratefully acknowledge additional support for this conference from:
Celgene CorporationCephalonHoffmann-La Roche, Inc.Pfizer Global Research & Development
We gratefully acknowledge additional in-kind support for this conference from those foregoing speaker expense reimbursements:

Genentech, Inc.
We gratefully acknowledge the generous grant for this conference provided by:

National Cancer Institute (NCI)
Grant No. 1R13CA144225-01
We appreciate the organizations that provide Keystone Symposia with additional support, such as marketing and advertising:

Click here to view more of these organizations
Special thanks to the following for their support of Keystone Symposia initiatives to increase participation at this meeting by scientists from underrepresented backgrounds:

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