Cancer cells are surrounded by immune cells, blood vessels, chemical signals and a support matrix—collectively, the tumor microenvironment. Most microenvironments help tumors grow and metastasize, but some can restrict tumors. My lab studies how to target the bad microenvironments and support the good ones to combat cancer.
Mikala Egeblad and colleagues study cancer and, in particular, the microenvironment in which the cancer cells arise and live. Solid tumors are abnormally organized tissues that contain not only cancer cells, but also various other stromal cell types and an extracellular matrix, and these latter components constitute the microenvironment. Communications between the different components of the tumor influence its growth, its response to therapy, and its ability to metastasize. Among the tumor-associated stromal cells, the lab’s main focus is on myeloid-derived immune cells, a diverse group of cells that can enhance angiogenesis and metastasis and suppress the cytotoxic immune response against tumors. Egeblad is interested in how different types of myeloid cells are recruited to tumors and how their behaviors—for example, their physical interactions with cancer cells and other immune cells—influence cancer progression, including metastasis. The Egeblad lab studies the importance of the myeloid cells using mouse models of breast and pancreatic cancer and real-time imaging of cells in tumors in live mice. This enables them to follow the behaviors of and the interactions between cancer and myeloid cells in tumors during progression or treatment. This technique was instrumental when the lab showed that cancer drug therapy can be boosted by altering components of the tumor microenvironments, specifically reducing either matrix metalloproteinases (enzymes secreted by myeloid cells) or chemokine receptors (signal receptors on myeloid cells). Most recently, the Egeblad lab has showed that when a specific type of myeloid cell, called neutrophil, is activated during inflammation it can awaken sleeping cancer to cause cancer recurrence. The neutrophils do so by forming so-called neutrophil extracellular traps, structures of extracellular DNA and these alter the extracellular matrix surrounding the sleeping cancer cells to provide a wake-up signal.
Mikala Egeblad wins Marks Foundation ASPIRE Award
December 20, 2019
Associate Professor Mikala Egeblad received the ASPIRE award to fund research understanding the relationship between stress and metastasis.
Partnership raises funds for women in science
October 4, 2019
Partnership raises more than $200,000 to support women in science.
Event: Women’s Partnership for Science Lecture and Luncheon
August 8, 2019
Begun in 2002, CSHL’s annual Women’s Partnership for Science lectures and luncheons promote and support women pursuing careers in biomedical research.
CSHL celebrates 20 years of graduate school at 2019 commencement
May 20, 2019
The Watson School of Biological Sciences held its 16th commencement, with seven researchers graduating with doctoral degrees.
Watson School 2019 Ph.D.s
May 19, 2019
Seven students were awarded Ph.D. degrees from Watson School this May. Here, they reflect on their time at the Laboratory as they look to the future.
Three Strohm Sisters funds ongoing cancer research
December 19, 2018
The Three Strohm Sisters Family Foundation donated $5,000 to Associate Professor Mikala Egeblad’s for her continued research.
Katie Oppo fund donates $75k to ovarian cancer research
December 11, 2018
The Katie Oppo Research Fund gave $75,000 to Mikala Egeblad's lab for ovarian cancer research.
Big bold dreamers
December 10, 2018
Dreamers drive discoveries. CSHL honors its many scientists making big impacts in their respective fields.
How a sleeping cancer awakens and metastasizes
September 27, 2018
Chronic inflammation can reawaken dormant cancer cells and spur metastasis. It may be preventable
Metastasis & immunity
June 25, 2018
How immune cells can help cancer spread, or stop it in its tracks—A free Public Lecture featuring Mikala Egeblad, Ph.D. and Sylvia Adams, M.D.