Yang Lab

Qin Yang, PhD
Associate Professor of Radiation Oncology

Qin Yang, MD, PhD  research interests include somatic and cancer cell reprogramming, telomere recombination in tumorigenesis and the BRCA1-AKT pathway in breast cancer.

  • Somatic and cancer cell reprogramming:  The research projects are to understand mechanisms of somatic and cancer cell reprogramming, and to develop transgene-free reprogramming technology to efficiently generate “safe” cells for the reprogramming-based therapy.  His previous results showed that the p53 and cellular senescence are a crucial step for somatic cell reprogramming (Nature Communications, 2014; Cell Reports, 2014).  Genetic manipulations of the cellular senescence pathways efficiently induced somatic cell reprogramming. p53 mutations are involved in this reprogramming process. Furthermore, his lab screened a kinase inhibitor library and found that the kinase inhibitors contribute to cellular reprogramming, including somatic normal cell and cancer cell reprogramming.  Based on these results, he is developing two research directions: Reprogramming breast/brain cancers into normal cells and rescue of brain injury through neural cell regeneration.Telomere recombination in tumorigenesis: A substantial number of tumors (telomerase negative tumors) utilize the telomere recombination pathway to maintain their indefinite proliferation.  However, details of the molecular mechanism of this pathway are largely unknown.  He found new mechanisms of telomerase and telomere recombination in tumorigenesis (Cancer Res., 2007; Nature Cell Biology, 2009; Cell Cycle, 2009; Cell Cyle, 2014).  Currently, his lab is investigating how telomerase negative tumors are developed and the role of telomere associated proteins in this process.
  • The BRCA1-AKT pathway in breast cancer: BRCA1 is a key factor for development of breast cancers.  However, the reasons why BRCA1-deficiency leads to the development of cancer are not clearly understood.  He has proposed a new idea concerning that the oncogenic AKT pathway may be responsible for development of BRCA1-deficient cancers (Cancer Res. 2008; Oncogene. 2011; Oncogene, 2013, Oncotarget, 2014).  The goal of this project is to understand the mechanism of mTOR-FOXO3 conferring PARP inhibition resistance in BRCA1-deficient cancers, and to develop novel therapeutic strategies for BRCA1-deficient triple-negative breast cancer through targeting the mTOR-FOXO3 pathways together with or without PARP inhibition.

Contact

Faculty Bio

For more information about research opportunities in this laboratory, please contact Dr. Qin Yang (qyang@wustl.edu).

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