NAME: Feng Bai

POSITION TITLE: Professor, Department of Pathology, Shenzhen University School of Medicine

OFFICE PHONE: 0755-26937526; EMAIL: baifeng@szu.edu.cn 　

EDUCATION/TRAINING　

A.Personal Statement

  I graduated from Lanzhou Medical College, China and received a bachelor’s degree in Medicine (M.D. equivalent) in 1988 and a Master’s degree in Pathology in 1994.  I spent 7 years training in the field of human pathology at Lanzhou Medical College followed by 5 years of training in mouse pathology at Kyushu University, Japan. Over the course of 18 years, I have acquired working experience in the pathology of genetically engineered mouse model systems.  While working as a postdoctoral fellow and a research associate in Dr. Yue Xiong’s lab at UNC-CH, I characterized more than 30 different mouse mutants for various CDK inhibitor genes and tumor suppressors as well as demonstrated their functions in controlling stem/progenitor cells and tumorigenesis of multiple tissues.  In 2003, I received a postdoctoral fellowship award from the Prostate Cancer Research Program of the United States Department of Defense.  In 2009, I discovered that p18INK4c is a downstream target of GATA3 and restrains mammary luminal progenitor cell proliferation and tumorigenesis. Since moving to the University of Miami as an associate scientist in 2011, I discovered that heterozygous germline deletion of Brca1 alters the fate of mammary luminal cells and transforms them into basal-like breast cancers.  I also discovered that BRCA1 suppresses epithelial-to-mesenchymal transition and stem cell dedifferentiation during mammary gland and tumor development. I demonstrated that p19^ink4d controls pituitary anterior lobe cell proliferation. More recently, I discovered that estrogen promotes estrogen receptor negative BRCA1 deficient tumor metastasis.  In collaboration with Dr. Yanbin Zhang, we discovered that FANCA promotes DNA double strand break repair by catalyzing sing-strand annealing and strand exchange. In Dec. 2018, I moved to China and became a full professor at the Shenzhen University School of Basic Medical Science.

1.    Pei XH*, Bai F*, Smith MD, Usary J, Fan C, Pai SY, Ho IC, Perou CM, Xiong Y. (2009) CDK inhibitor p18^INK4c is a downstream target of GATA3 and controls mammary luminal progenitor cell proliferation and tumorigenesis  Cancer Cell. 15:389-401. *equal contribution.

2.  Bai F, Smith MD, Chan HL, Pei XH. (2013) Germline mutation of Brca1 alters the fate of mammary luminal cells and causes luminal-to-basal mammary tumor transformation. Oncogene. 32:2715-2725. Featured Article.

3. Bai F, Chan HL, Scott A, Smith MD, Fan C, Herschkowitz JI, Perou, CM, Livingstone AS, Robbins DJ, Capobianco AJ, Pei XH. (2014) BRCA1 suppresses epithelial-to-mesenchymal transition and stem cell dedifferentiation during mammary and tumor development. Cancer Res. 74:6161-6172.

B.Positions and Honors

Positions and Employment

1988- 1990  Research Associate, Department of Pathology, Lanzhou Medical College, Lanzhou, China.  

1994- 1995  Assistant Professor, Department of Pathology, Lanzhou Medical College. Lanzhou, China.

1995- 1996  Visiting Scholar, Research Institute for Diseases of the Chest, Kyushu University. Fukuoka,Japan.  

1996- 2000  Graduate Student, Research Institute for Diseases of the Chest, Kyushu University, Fukuoka, Japan. Advisor: Dr. Nobuyuki Hara

2000-2006  Postdoctoral Fellow in the lab of Dr. Yue Xiong, Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill,NC, USA

2006-2010  Research Associate in the lab of Dr. Yue Xiong, Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill,NC, USA

2011-2018  Associate Scientist, Molecular Oncology Program, DeWitt Daughtry Family Department of Surgery, Sylvester Comprehensive Cancer Center,University of Miami, FL, USA

2018-Present  Professor, School of Basic Medical Sciences, Shenzhen University,China

Other Experience and Professional Memberships

Teaching Experience

1988 - 1995 Department of Pathology (for medical students), Lanzhou Medical College, China.

Clinical Experience

1989 - 1995  Lanzhou Medical College,China Routine pathological diagnosis for patient samples from the affiliated hospitals of Lanzhou Medical College, China.

Professional Memberships

1988-1994 Member, Chinese Society of Pathology

1995-2000 Member, Japanese Society of Lung Cancer

Honors

1996              Research Award, Kyushu University. Japan

1998              Foreign Graduate Student Scholarship. Japan

2003     Department of Defense (DOD): Postdoctoral Traineeship Award, USA

C.Contributions to Science

1. Investigation of the role of INK4 family of cell cycle inhibitors in endocrine tumorigenesis and hearing loss. 

   I discovered that the function of p18^Inkc in suppressing endocrine tumor development is fully dependent on Cdk4 and p18^Inkc collaborates with Men1 to suppress endocrine tumorigenesis.  I also discovered that p19^Ink4d is the major cell cycle inhibitor gene that controls pituitary anterior lobe cell proliferation and tumorigenesis.  We demonstrated that the function of p19 in suppressing pituitary cell proliferation is independent of Cdk4, and that loss of Cdk4 rescues p19^INK4d deficiency induced hearing loss.

a. Pei XH, Bai F, Tsutsui T, Kiyokawa H, Xiong Y. (2004)  Genetic evidence for functional dependency of p18^Ink4c on Cdk4.  Mol Cell Biol. 24, 6653-6664.

b. Bai F*, Pei XH*, Nishikawa T, Smith MD, Xiong Y. (2007) p18Ink4c, but not p27Kip1, collaborates with Men1 to suppress neuroendocrine organ tumors. Mol Cell Biol. 27, 1495-1504. *equal contribution.

c. Bai F, Chan HL, Smith MD, Kiyokawa H, Pei XH.  (2014) p19^Ink4d is a tumor suppressor and controls pituitary anterior lobe cell proliferation. Mol Cell Biol. 34:2121-2134. (Cover article).

d. Ma Q*, Grati M*,Bai F*,PeiJ,Pei XH,Liu X. Rescue from early onset hearing loss in a mouse  model lacking the cyclin-dependent kinase inhibitor p19Ink4d. Cell Death & Disease.  2016;10;7:e2131. *equal contribution

2. Investigation of the physiological function of INK4 genes.

   I discovered that p18^Inkc is a haploinsufficient   tumor suppressor.  I also discovered that p18Ink4c collaborates with Men1 to constrain lung stem cell expansion and suppress non-small-cell lung cancers, and with Pten to constrain a positive regulatory loop between cell growth and cell cycle control. I demonstrated that p16^INK4a loss rescues functional decline of Brca1-deficient mammary stem cells.

a. Bai F, Pei XH, Godfrey VL, Xiong Y. (2003) Haploinsufficiency of p18^INK4c sensitizes mice to carcinogen-induced tumorigenesis. Mol Cell Biol. 23, 1269-1277.

b. Bai F*, Pei XH*, Pandolfi PP, Xiong Y. (2006) p18 Ink4c and Pten constrain a positive regulatory loop between cell growth and cell cycle control. Mol Cell Biol. 26, 4564-4576. *equal contribution. 

c. Pei XH*, Bai F*, Smith MD, Xiong Y. (2007) p18Ink4c collaborates with Men1 to constrain lung stem cell expansion and suppress non-small-cell lung cancers. Cancer Res. 67, 3162-3170. *equal contribution.

d. . Scott A, Bai F*, Chan HL, Liu S, Slingerland JM, Robbins DJ, Capobianco AJ, Pei XH*. p16INK4a loss rescues functional decline of Brcac1-deficient mammary stem cells. Cell Cycle. 2017;6:759-764. *Corresponding Author.

3.  Investigation of the function of Brca1 and FANCA genes.

   I discovered that estrogen promotes estrogen receptor negative BRCA1-deficient tumor initiation and progression.  Through collaboration with Dr. Yanbin Zhang, we demonstrated that FANCA promotes DNA double strand break repair by catalyzing single-strand annealing and strand exchange.

a.   Wang C, Bai F*, Zhang L, Li E, Pei XH. Estrogen promotes estrogen receptor negative BRCA1-deficient tumor initiation and progression. Breast Cancer Research. 2018; 74:1-17. *Corresponding Author.

b.  Benitez A, Liu W, Palovcak A, Wang G, Moon J, An K, Kim A, Zheng K, Zhang Y, Bai F, Mazin AV, Pei XH, Yuan F,Zhang Y. (2018) FANCA  promotes DNA double strand break repair by catalyzing single-strand annealing and strand exchange. Mol Cell. 2018;71(4):621-628.

Complete List of Published Work in NCBI (a total of 36 peer-reviewed publications)

D.Additional Information: Research Support and/or Scholastic Performance 

Current Support:

 1. Title: Suppression of prostate cancer by PTEN and P18^INK4C

PI:     Bai F

Agency:  DOD Prostate Cancer Research Program Award (W81XWH-04-1-0011)

Amount: $100,000(¥685,000)

Period:   1/1/2003–1/1/2005

2.  Title: BRCA1 controls mammary stem/progenitor differentiation and proliferation, epithelial-mesenchymal transition and tumorigenesis

CI:      Bai F

Agency: DOD Breast Cancer Research Program (BCRP) 

Type: Idea Award  (W81XWH-10-1-0302)

Amount:  $554,491(¥3,800,000)

Period: 4/15/2010–12/31/2012

3.  Title: Function of Brca1 in maintaining mammary luminal cell fate and suppressing epithelial to mesenchymal transition and tumorigenesis.

CI:       Bai F

Agency: Sylvester Braman Family Breast Cancer Institute, University of Miami

Type:      Developmental Grant

Amount: $50,000 (¥343,000)

Period:  9/1/2011–8/31/2013

4.  Title: Genetic analysis of the role of GATA3 in breast tumorigenesis.

CI:    Bai F

Agency:  Flight Attendant Medical Research Institute (FAMRI)

Amount:  $50,000(¥343,000)

Period:   07/01/2014– 6/30/15

5.  Title: The role of Brca1 in suppressing dedifferentiation in breast tumorigenesis

CI:    Bai F

Agency: American cancer society institutional research grant

Type:   Pilot project grant

Amount:  $45,000(¥309,000)

Period:   10/1/2013–9/30/15