Randall Davis
University of Alabama at Birmingham, AL·Microbiology & Immunology
B cells are immune cells that make antibodies. When they grow out of control they cause most non-Hodgkin's lymphomas, including chronic lymphocytic leukemia (CLL), the most common leukemia in Western countries.
- Fields
Microbiology & Immunology
Medicine & Clinical Research
- Topics
B cells
B lymphocytes
Fc receptor-like
- Grants
- 1 known grant, through Jan 2031
What they work on
- Determine how FCRL1, a B cell surface receptor overproduced in leukemia, influences B cell responses in human and mouse disease models of chronic lymphocytic leukemia and immune tolerance.
- Dissect the tyrosine-based signaling mechanisms by which FCRL1 adjusts B cell receptor signals, testing why its effect on B cell activation depends on context.
- Investigate conserved roles for FCRL1 in living animals using new physiological models, to link its signaling to B cell cancer and autoimmunity.
More about the research
These cancers depend on signals from the B cell receptor (BCR), the surface protein that recognizes targets. Current treatments target surface proteins such as CD19 and CD20 or block BCR signaling, but patients can become resistant over time. Better options require knowing how B cells tune BCR signals at rest and when activated, and what goes wrong in disease.
Why it matters
Understanding FCRL1 could reveal new ways to treat B cell leukemias and lymphomas such as CLL, especially where patients have become resistant to current antibody, cell-based or small-molecule therapies. It could also inform therapies for autoimmune diseases driven by B cells. Because FCRL1 is overproduced on many B cell cancers and tracks with aggression, it may serve as a therapeutic target.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Markus Müschen
Yale University, CT·Microbiology & Immunology
Test whether persistent PI3K signaling, a growth pathway, forces B-ALL, CLL and mantle cell lymphoma cells to grow too large and run out of ATP, triggering energy crisis and central-tolerance elimination.
Susheela Tridandapani
Ohio State University, OH·Microbiology & Immunology
Determine how stimulating NOD2, an intracellular bacterial-fragment sensor, reshapes monocytes and CLL nurse-like macrophages, including loss of the inhibitory phosphatase SHIP1 and receptor CD31 and gain of the activating Fc receptor FcγRI.
Lili Wang
Columbia University, NY·Medicine & Clinical Research
Determine how the MGA/MYC/NME1 pathway, a growth program switched on when the gene Mga is silenced, changes tumor-cell properties during the CLL-to-Richter's transformation, using the lab's mouse RT model.
The school
University of Alabama at Birmingham: 45 labs on PI Pages, $866M a year on research, 166 research doctorates a year.
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