? I have abroad background in both clinical and basic cancer research. As a clinician, I devoted myself to clinical cancer research including chemotherapy and metastasis for 11 years before switching to basic cancer research. As a graduate student at Kyushu University in Japan, I learned molecular biology and carcinogenesis. As a postdoctoral fellow in Dr. Yue Xiong’s lab at UNC-CH, I became interested in mouse genetic approaches to investigating the molecular and cellular basis of tumor suppression. Though time consuming and complicated, utilizing such methodology is a necessary step toward the goal. I generated 5 strains of knock out mice and characterized more than 30 different mouse mutants for various cell cycle inhibitors and tumor suppressors, and demonstrated their functions in the control of stem/progenitor cells and tumorigenesis of multiple tissues. I discovered that p18INK4c is a downstream target of GATA3 and restrains mammary luminal progenitor proliferation and tumorigenesis (Pei XH,CancerCell,2009). As a tenure track assistant and later associate professor at the University of Miami, I published 17 research papers. I discovered that deletion of Brca1 causes luminal-to-basal mammary tumor transformation (BaiF,Oncogene,2013). This paper was published with aspecial “ Commentary ” paper in the same issue of the journal (Ng T,Oncogene, 2013), in which the authors commented my findings as “these findings will hopefully yield new approaches to target BRCA1-deficient tumors”. Further, Idiscovered that BRCA1 suppresses EMT during mammaryand tumor development (BaiF,CancerRes.,2014). I generated a mutant mouse strain lacking p19INK4d and demonstrated that p19INK4d is a tumor suppressor (BaiF,MolCellBiol.,2014). I discovered that p16INK4a suppresses BRCA1-deficient mammary stem cell function and tumorigenesis (ScottA,Oncotarget,2016; CellCycle,2017). I found that GATA3 suppresses B cell lymphomagenesis in p18INK4c deficient background (LiuS,Oncotarget,2016). More recently, I discovered that estrogen promotes estrogen receptor negative BRCA1 deficient tumor metastasis (WangC,BreastCancerRes,2018). In collaboration with Dr. Yanbin Zhang, we demonstrated that FANCA promotes DNA double strand break repair by catalyzing single-strand annealing and strand exchange (Benitez A,MolecularCell,2018). I generated multiple mutant mouse strains that develop ER-positiveand -negative mammary tumors with a serial of tumor cell lines that are transplantable. Through these experiences, I have demonstrated my ability to successfully carry out research project, using a combination of multi-disciplinary approaches (biochemical,cellular,genetic,and histopathological) . In Oct 2018, I moved to China and became a full professor at the Shenzhen University School of Basic Medical Sciences.

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1.?? PeiXH*, Bai F*, Smith MD, Usary J, Fan C, Pai SY, Ho IC, Perou CM, Xiong Y. CDK inhibitor p18INK4c is a down stream target of GATA3 and controls mammary luminal progenitor cell proliferation and tumorigenesis? CancerCell. ?2009;15:389-401. *equal contribution.

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2.? ?BaiF ,Smith MD, Chan HL, Pei XH*.? Germlinemutation of Brca1 alters the fate o fmammary luminal cells and causes luminal-to-basal mammary tumor transformation. Oncogene. 2013;32:2715-2725. Featured Article.*Corresponding Author.

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3.???? BaiF, Chan HL,Scott? A, SmithMD, Fan C, Herschkowitz JI, Perou, CM, Livingstone AS, Robbins DJ, Capobianco AJ, PeiXH*. BRCA1 suppresses epithelial-to-mesenchymal transition and stem cell dedifferentiation during mammary and tumor development. CancerRes.2014;74:6161-6172.*Corresponding Author.

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1.? Investigation ofthe roleoftheINK4 familyofcellcycleinhibitorsincellproliferationand tumorigenesis. I discovered that the function of p18Inkc in suppressing tumor development is fully dependent on Cdk4 and p18Inkc collaborates with Men1? to suppress endocrine tumorigenesis. I also discovered that p19Ink4d 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. We found that p16INK4a suppresses BRCA1-deficient mammary tumorigenesis.

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a.???? Pei XH, BaiF, Tsutsui T,Kiyokawa H, Xiong Y. Genetic evidence for functional dependency of p18Ink4c on Cdk4. MolCellBiol. ?2004; 24:6653-6664.

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b.????BaiF*, PeiXH*, Nishikawa T,Smith MD,Xiong Y. ?p18Ink4c, but not p27Kip1 collaborates with Men1 to suppress neuroendocrine organ tumors.Mol Cell Biol. 2007;27:1495-1504. *equal contribution.

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c.???? BaiF, Chan HL, Smith MD, Kiyokawa H,Pei XH*. ?p19Ink4d is a tumor suppressor and controls pituitary anterior lobe cell proliferation. Mol Cel lBiol. ?2014;34:2121-2134.(Coverarticle). *Corresponding Author.

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d.???? Scott A, Bai F,Chan HL,Liu S, Slingerland JM, Robbins DJ, Capobianco AJ, Pei XH*. p16INK4a

suppresses BRCA1-deficient mammary tumorigenesis. Oncotarget. 2016;7:84496-84507.

*Corresponding Author.

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??2.? Investigation of the physiological function of INK4genes.?? I discovered that p18Ink4c collaborates with Men1 to constrain lungstem cell expansion and suppress non-small-cell lung cancers, and with Gata3 to repress B cell lymphomagenesis. I found that loss of Cdk4 completely rescues early on set hearing loss in mice lacking p19Ink4d. I also discovered that p16INK4a suppresses BRCA1-deficient mammary stem cell function.

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a.???? Pei XH*,? BaiF*,Smith MD,Xiong Y. ?p18Ink4c collaborates with Men1 to constrain lung stem cell expansion and suppress non-small-cell lung cancers.CancerRes.2007; 67:3162-3170. *equal contribution.

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b.???? 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. CellDeath&Disease.? 2016;10; 7:e2131. doi:10.1038/cddis. 2016.38. *equalcontribution.

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c.???? Liu S,Chan HL,Bai F,Ma J, Scott A,Capobianco AJ, Zhu P,Pei XH*. ?Gata3 restrains B cell proliferation and cooperates with p18INK4c? to repress B cell lymphomagenesis. Oncotarget. 2016; 7:64007-64020.PMID:27588406.*CorrespondingAuthor.

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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. CellCycle. 2017;6:759-764. PMID: 28278054. *CorrespondingAuthor.

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3.? Investigation of the physiological function o fCUL9 (formerlyPARC) and FANCA genes.? I discovered that Cul9 is a tumor suppressor and promotes p53-dependent apoptosis . I also discovered that CUL9 mediates the functions of the 3M complexand ubiquitylates Survivin to maintain genome integrity. ?In addition, I found that CUL9 mediates the degradation of cytosolic cytochrome c to promote survival in neurons and cancer cells.? Through collaboration with Dr. Yanbin Zhang, we demonstrated that FANCA promotes DNA double strand break repair by catalyzing single-strand annealing and strand exchange.

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a.???? Pei XH, Bai F, Li Z, Smith MD,Whitewolf G, Jin R, and Xiong Y. Cytoplasmic CUL9/PARC ubiquitin ligase is a tumor suppressor and promotes p53-dependent apoptosis.? CancerRes. 2011;71:2969- 2977.

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b.???? LiZ, Pei XH, Yan J, Yan F, Cappell KM, Whitehurst AW, Xiong Y. ?CUL9 Mediates the Functions of the 3M Complex and Ubiquitylates Survivin to Maintain Genome Integrity.MolCell. 2014;54:805-19

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c.???? Gama V, Swahari V, SchaferJ, Kole AJ, Evans A, Huang Y,Cliffe A, Golitz B, Sciaky N, Pei XH, Xiong Y, Deshmukh M. ?The E3 ligase PARC mediates the degradation of cytosolic cytochrome c to promote survival in neurons and cancer cells.Sci Signal.2014;7(334):ra67.doi:10.1126.

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d.???? 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.MolCell. 2018;71(4):621-628.

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Complete List of Published Work in NCBI My Bibliography (a total of 43 peer reviewed publications):

http://www.ncbi.nlm.nih.gov/sites/myncbi/18gFybgHwUAkO/bibliography/47457326/public/?sort=date&direction

=ascending.

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

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PI:????? Pei XH

Amount:?????????? $554,491(￥3,800,000)

Period:???????????? 4/15/2010–12/31/2012

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2.? Title: Function of Brca1 in maintaining mammary luminalcellfateandsuppressingepithelialto mesenchymaltransitionand tumorigenesis.

PI:?????? Pei XH

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

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

PI:??? Pei XH

Agency:?????????? Flight Attendant Medical Research Institute (FAMRI)

Amount:?????????? $50,000(￥343,000)

Period:???????????? 07/01/2014– 6/30/15

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4.? Title:Therole o fBrca1 in suppressing dedifferentiation in breast tumorigenesis.

PI:??? Pei XH

Agency:?????????? American cancer society institutional research grant

Type:?????????????? Pilot project grant

Amount:?????????? $45,000(￥309,000)

Period:???????????? 10/1/2013–9/30/15

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5.? Title:The Role of BRCA1 in Suppressing Epithelial-Mesenchymal Transition in Mammary Gland and Tumor Development

PI:???? Pei XH

Agency:???? DOD Idea Expansion Award

Type:???????? Idea Expansion Award (W81XWH1310282)

Amount:???? $537,779(￥3,690,000)

Period:?????? 9/1/2013–8/31/2016

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6.??? Title:Controlling adult stem cells and tumorigenesis by cell cycle inhibitors

PI:???? Pei XH

Agency:???? Sylvester Comprehensive Cancer Institute, University of Miami

Amount:???? $25,000(￥170,000)

Period:?????? 6/1/2014–5/31/2015

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7.??? Mentor, Studyab road scholarship to Ms.Shiqin Liu (Peking University, China)

Agency:??? China Scholarship Council

Amount:???? $40,800($20,400/year) (￥280,000)

Period:???? 9/1/2014–8/31/2016

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8.??? Title:Targeting breast cancer stem cells

PI:???? Pei XH

Agency:???? Sylvester Comprehensive Cancer Institute, University of Miami

Amount:???? $121,585(￥840,000)

Period:?????? 6/1/2015–5/31/2016

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