Yang Yang-Hartwich
Yale University, CT·Genetics
Most women who die of ovarian cancer die because the disease has spread, not because of the original tumor. Up to 70% of ovarian cancers are high-grade serous carcinoma (HGSC), a type that usually starts not in the ovary but in the fallopian tube, in the secretory cells lining it.
- Fields
Genetics
Biology
Medicine & Clinical Research
- Topics
ovarian cancer
high-grade serous carcinoma
fallopian tube
- Grants
- 1 known grant, through Apr 2027
What they work on
- Define how NR2F2, a gene-regulating nuclear receptor, controls the migration and adhesion of ovarian cancer cells that drive spread through the peritoneal cavity.
- Map the expression and activation of NR2F2 across stages of tumor development, from precursor lesions in the oviduct to metastatic tumors, in the Ovgp1-iCreER BPRN mouse model of high-grade serous carcinoma.
- Test whether inhibiting NR2F2 blocks metastasis of high-grade serous carcinoma and determine the underlying mechanism, using tumor organoids and in vivo models.
- Characterize the fallopian-tube-derived tumor-initiating cells found by single-cell RNA sequencing, and relate their gene signature to patient prognosis using TCGA human tumor data.
More about the research
Mutations such as those in BRCA and p53, genes that normally help repair DNA and restrain damaged cells, turn these lining cells into early precancerous lesions. Cells then scatter through the abdominal cavity before any ovarian tumor is visible, which is why only about 15% of patients are caught at the more curable stage I. Very little is known about how those scattered deposits form, and that gap is the focus of this work.
Why it matters
Metastatic high-grade serous ovarian cancer is usually found late and has few effective treatments. By pinpointing the cells and the NR2F2 signaling pathway that let fallopian-tube-derived tumors spread through the abdomen, this work could reveal new drug targets for blocking spread or preventing recurrence, and its link between a tumor-initiating-cell gene signature and poor patient outcomes could help identify women at higher risk.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Analisa DiFeo
University of Michigan, MI·Medicine & Clinical Research
Determine how loss of the microRNA miR-181a affects immune cell infiltration and interferon signaling in patient-derived ovarian tumor organoids, with and without a STING agonist or anti-PD-L1 immunotherapy.
Mazhar Adli
Northwestern University, IL·Genetics
Create human cell models of uterine fibroids by using CRISPR to engineer specific MED12 mutations, and determine how these mutations drive tumor formation.
Yuxuan Miao
University of Chicago, IL·Microbiology & Immunology
Use in vivo CRISPR screens and stem cell interactome sensors in mouse skin to find how epithelial stem cells remodel nearby immune cells into a temporary protective niche after wounding.
The school
Yale University: 73 labs on PI Pages, $1.5B a year on research, 438 research doctorates a year.
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