Lili Wang
Columbia University, NY·Medicine & Clinical Research
Chronic lymphocytic leukemia (CLL) is a cancer of B cells, the immune cells that make antibodies. Some patients develop aggressive forms that current drugs cannot cure.
- Fields
Medicine & Clinical Research
Genetics
Microbiology & Immunology
- Topics
chronic lymphocytic leukemia
Richter's transformation
lymphoma
- Grants
- 2 known grants, through Nov 2029
What they work on
- 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.
- Define how the MGA/MYC/NME1 axis shapes the function of surrounding immune cells in RT, using the mouse model and patient samples from clinical trials of immunotherapy and CDK9 inhibitors.
- Test whether METTL3, an enzyme that adds m6A chemical tags to messenger RNA, is required for both the development and maintenance of CLL in mouse models.
- Dissect how METTL3 controls the RNA splicing network in CLL by identifying its m6A-modified target transcripts and the splicing factors it regulates.
- Evaluate METTL3 as a drug target in aggressive CLL, testing whether combining METTL3 inhibitors with blockers of RNA splicing regulators has a synergistic effect.
More about the research
In the worst case, Richter's transformation (RT), CLL turns into an aggressive lymphoma, and patients survive less than a year on average. Two projects ask what molecular changes make CLL aggressive and how those changes might be targeted. One looks at a growth-driving gene pathway and the surrounding immune cells in RT. The other looks at an RNA-modifying enzyme in aggressive CLL.
Why it matters
Patients with Richter's transformation live less than a year on average, and aggressive CLL remains incurable. This work could point to new treatment strategies. These include combining drugs that block the MYC pathway with immunotherapy, and drugs that block METTL3 together with RNA splicing regulators. Using samples from ongoing clinical trials ties these findings to how real patients respond.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Sunil Sudarshan
University of Alabama at Birmingham, AL·Biochemistry
Determine the molecular mechanism by which the oncometabolite L-2-hydroxyglutarate promotes the mRNA mark N6-methyladenosine (m6A) in renal cell carcinoma, and establish what this RNA hypermethylation does to gene expression.
Randall Davis
University of Alabama at Birmingham, AL·Microbiology & Immunology
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.
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.
The school
Columbia University: 89 labs on PI Pages, $1.4B a year on research, 625 research doctorates a year.
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