$1.9M Grant Awarded for Study on How Fat Cells Help Myeloma Cells Resist Treatment
A new research project aiming to better understand how fat cells help multiple myeloma cells resist treatment has won a $1.9 million grant from the National Cancer Institute of the National Institutes of Health.
The five-year funding was awarded to Michaela Reagan, PhD, a faculty scientist at the Maine Medical Center Research Institute (MMCRI), whose work has been focused on the communication between fat cells and multiple myeloma cells in the bone marrow.
The grant is a Method to Extend Research in Time (MERIT) Award, which is given to investigators who are in the first 10 years of their post-doctoral career. Reagan finished a post-doctoral fellowship at the Dana-Farber Cancer Institute in 2015 and joined MMCRI that same year.
“Michaela Reagan is a valuable asset to the state of Maine. She is making an important contribution to the science of blood and bone cancers,” Doug Sawyer, MD, PhD, chief academic officer of the Maine Medical Center, said in a press release. “This MERIT Award speaks to the quality of her work and the caliber of scientists we are able to recruit, mentor and support here at MMCRI and throughout the MaineHealth system.”
Myeloma is caused by an overgrowth of B cells, a type of white blood cell. Most commonly, this primarily affects the bone marrow, which is where B cells and other blood cells are made.
Although many treatments for myeloma have been developed, a continuing obstacle is the development of resistance — when myeloma cells adapt such that they are able to survive a particular treatment, rendering the therapy ineffective.
Treatment resistance is a complicated and multi-faceted process that involves both changes in the myeloma cells themselves, as well as in the surrounding healthy cells that are present in the niche where the tumor cells reside — referred to as the tumor microenvironment. In some cases, cancer cells will “co-opt” healthy cells to promote survival of cancer cells.
Understanding the processes by which myeloma cells resist treatments could help in the development of more effective treatment strategies.
“By figuring out how tumor cells evade cancer drugs, we are discovering their vulnerabilities and engineering novels ways to target the cancer,” Reagan said.
The new project will specifically focus on the role of fat cells — adipocytes — in treatment resistance, potentially providing an explanation as to why and how obesity worsens outcomes in myeloma and other cancer patients.
Previous research by Reagan and others has shown that, in the bone marrow, adipocytes directly support myeloma cells by increasing levels of a family of proteins called fatty acid-binding proteins. These proteins appear to give cancer cells protection against some anti-cancer medications.
The new project’s goal is to better understand how adipocytes make these resistance-related proteins. More broadly, the project is also aimed at finding other vulnerabilities in bone marrow-residing cancer cells.