Li Yang, Ph.D.
- Center for Cancer Research
- National Cancer Institute
- Building 37, Room 3134C
- Bethesda,, MD 20892-4255
Dr. Yang’s research program focuses on the mechanisms underlying tumor-host interplay in cancer metastatic progression. Dr. Yang has contributed to the identification of the immune and inflammatory mediators in the anti- and pro-tumor functional switch of TGF-β, the epigenetic regulation of TGF-β signaling, mechanisms of myeloid cell recruitment in the tumor microenvironment, as well as myeloid TGF-β signaling in cancer immune surveillance and in inflammatory stroke.
As the head of the Tumor Microenvironment and Metastasis Section, Dr. Yang is particularly interested in how tumor suppressors modulate the host immune environment, and the epigenetic mechanisms responsible for tumor cell plasticity and metastatic colonization.
Areas of Expertise
Metastatic spread accounts for most cancer-associated deaths in patients, but treatment options are limited. How cancer cells acquire the competence to colonize distant organs is poorly understood. The goal of my research team is to identify the cause-effect mediators that link the genomic/epigenetic alterations and tumor microenvironment and options for therapeutic intervention. We collaborate with basic research laboratories as well as clinicians and epidemiologists.
We have several focused research areas:
Roles of tumor suppressors (TSs) in metastatic progression: TSs are powerful transcriptional and signaling regulators that negatively modulate cell proliferation and survival. As such, TSs counteract the growth promoting activity of oncogenes mainly through cell autonomous mechanisms. It is not clear whether TSs play a direct role in metastatic colonization. Our studies demonstrate that tumor suppressors are often silenced during metastatic progression through epigenetic mechanisms (e.g., promoter hypermethylation and histone modification). TS deregulation promotes the acquisition of plasticity and the ability of tumor cells to adapt to hostile tissue microenvironments, thus facilitating metastatic spread. We use integrated genome-wide genetic and epigenetic approaches to investigate the role of TSs during metastatic progression and the underlying mechanisms involving host inflammatory and immune responses.
Epithelial and myeloid TGF-β in cancer metastasis: TGF-β is a powerful metastasis promoter in later stages of cancer progression; however, it mediates growth inhibition in early stages. The factors mediating the functional change of TGF-β are largely unknown, which poses significant challenges to our understanding of TGF-β cancer biology and to the successful application of TGF-β-targeted therapy. We use focused genetic models in which TGF-β signaling is inactivated in specific cell types in the tumor and microenvironment, including host myeloid cells or stromal fibroblasts, to discover molecular mediators and pathways important in tumor-stroma crosstalk.
Immune microenvironment regulation of tumor dormancy: the ability of residual tumor cells to persist in a dormant state can occur during metastatic progression and/or following extended periods of clinical remission that may last decades. The mechanisms for tumor dormancy induction or tumor cell reactivation remain unclear. We are currently using in vitro and in vivo molecular imaging, single-cell RNA sequencing, and mouse models of breast cancer to investigate the molecular and cellular mechanisms mediated by the immune microenvironment in tumor dormancy.
Please contact Dr. Li Yang for information regarding the availability of postdoctoral and graduate fellowship positions in the lab. Graduate students may apply through the Graduate Partnership Program that sponsors doctoral students at NIH through partnerships with various universities, including the University of Maryland and Johns Hopkins University, and others as well.
Apoptosis-induced nuclear expulsion in tumor cells drives S100a4-mediated metastatic outgrowth through the RAGE pathway
Induction of DNMT3B by PGE2 and IL6 at Distant Metastatic Sites Promotes Epigenetic Modification and Breast Cancer Colonization
miR-130a and miR-145 reprogram Gr-1+CD11b+ myeloid cells and inhibit tumor metastasis through improved host immunity
TGF-β signaling in myeloid cells is required for tumor metastasis
Roles of tumor suppressors in regulating tumor-associated inflammation
Li Yang, Ph.D.
Dr. Li Yang is a Senior Investigator at the National Cancer Institute. She received her Ph.D. in the Department of Cancer Biology at Vanderbilt University, under the mentorship of Dr. David Carbone. Her dissertation research focused on COX-2 pathway in tumor progression, immune suppression, and the contribution of host myeloid cells to tumor blood vessel formation. She investigated TGF-β regulation of inflammation and tumor microenvironment during her postdoc research with Dr. Harold Moses. She joined NCI in 2009 and was tenured in 2016. Her research program is devoted to understanding the molecular mechanisms underlying tumor-stroma interaction during metastatic process.
Dr. Yang is a recipient of the Federal Technology Transfer Award, co-recipient of FLEX Program Awards for Principal Investigators, CCR, NCI, as well as U.S.-China Biomedical Collaborative Research Grant award.
|Position||Degree Required||Contact Name||Contact Email|
|Post-doctoral Fellow - Mechanisms of immune microenvironment, tumor dormancy||Ph.D. or equivalent||Li Yangfirstname.lastname@example.org|
Apoptotic cell death promotes metastasis of surviving neighbors
Our publication "Apoptosis-induced nuclear expulsion in tumor cells drives S100a4-mediated metastatic outgrowth through the RAGE pathway" was recently featured on the cover of Nature Cancer.
Justin Gray, a graduate student in the NIH-Johns Hopkins GPP, awarded his Ph.D.
Justin completed his doctoral research in the Yang lab (July 2017 - June 2022) and is now working at BioNTech.