The CANCAN team is supported through the Cancer Grand Challenges initiative. Learn more here

Our Team

 

Our vision is to develop mechanistically informed treatments for cancer cachexia to improve the quality of life and life expectancy for patients. Solving the cancer cachexia challenge is of great value because cancer cachexia reduces survival and quality of life for many patients with advanced cancer.

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Our Team

 

Our vision is to develop mechanistically informed treatments for cancer cachexia to improve the quality of life and life expectancy for patients. Solving the cancer cachexia challenge is of great value because cancer cachexia reduces survival and quality of life for many patients with advanced cancer.

;

Program Overview

CANCAN brings together clinical and basic science thought leaders in cancer biology, metabolism, nutrition, immunology, endocrinology, neurobiology, epidemiology, and behavior. We will team up highly accomplished thought leaders with vibrant young investigators to combine deep knowledge with the newest innovative concepts and state-of-the-art technology, models, and statistical approaches. By functioning as a “virtual institute” with aligned goals, we will overcome the typical barriers that slow therapeutic development including identifying and validating robust targets. Together, we will share resources, data, and expertise while inviting new exceptional investigators into this stagnant field.  Ultimately, it will be the quality of our team members that will ensure we meet our overall goal of determining the causes of and providing treatments for cancer cachexia.

 

Team CANCAN will address the causes of cancer cachexia by addressing 4 main hypotheses:

 

  1. We hypothesize that cancer cachexia results from a systemic metabolic imbalance driven by tumor-intrinsic factors and neuroendocrine dysregulation. Potential causes include tumor-secreted factors and induction of an inflammatory response that directly or indirectly alters the metabolism of host tissues to feed tumor metabolism, increase wasteful energy expenditure and promote anorexia.

 

  1. We hypothesize that targeting the metabolic imbalance itself or the upstream mediators will alleviate cancer cachexia. These include tumor-intrinsic factors, inflammatory cytokines, endocrine hormones, microbiome species, and anorexic factors. It is also highly likely that one factor will not underlie all of cancer cachexia.

 

  1. We hypothesize that there are multiple cancer cachexia phenotypes with distinct etiologies. We will unbiasedly define cancer cachexia subtypes and link them to specific causes and treatments to better inform clinical care and pre-clinical modeling.

 

  1. We hypothesize that there will be no single remedy for cancer cachexia, and that combinations of agents delivered to well-defined patient populations will be required. Only our multidisciplinary team can address this issue.

Meet the team

A Global Team

Rutgers The State University of NJ/CINJ
Weill Medical College of Cornell University
Cold Spring Harbor Laboratory
Harvard Medical School
Kaiser Foundation Research Institute (Kaiser Permanente)
Pennington Biomedical Research Center (Louisiana State University)
Harvard T.H Chan School of Public Health
Salk Institute for Biomedical Studies
The University of Rochester
The The Scotland Institute of Cancer Research
University College London
The University of Cambridge MRC Institiute of Metabolic Science Metabolic Research Laboratories
The University of Cambridge/Cancer Research U.K (Biffi Group)
The University of Glasgow
Princeton University
CANCAN
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