Honors & Awards


  • The National Scholarship, Ministry of Education of the People's Republic of China (2010-2012)
  • “Excellent graduates of Hunan” Award, Department of Education of Hunan province, China (2012)
  • Top Prize in the All China Medical Student Clinical skill competition, Department of Higher Education of Ministry of education (2012)
  • “The best contestant” award in the All China Medical Student Clinical skill competition, Department of Higher Education of Ministry of education (2012)
  • Joint PhD Student Scholarship, China Scholarship Council (2014-2016)

Professional Education


  • Joint PhD student, University of Miami, Surgery (2016)
  • Bachelor of Medicine, Central South University (2013)
  • Doctor of Philosophy, Peking University (2017)

All Publications


  • Trop2 is a driver of metastatic prostate cancer with neuroendocrine phenotype via PARP1. Proceedings of the National Academy of Sciences of the United States of America Hsu, E. C., Rice, M. A., Bermudez, A., Marques, F. J., Aslan, M., Liu, S., Ghoochani, A., Zhang, C. A., Chen, Y. S., Zlitni, A., Kumar, S., Nolley, R., Habte, F., Shen, M., Koul, K., Peehl, D. M., Zoubeidi, A., Gambhir, S. S., Kunder, C. A., Pitteri, S. J., Brooks, J. D., Stoyanova, T. 2020

    Abstract

    Resistance to androgen deprivation therapy, or castration-resistant prostate cancer (CRPC), is often accompanied by metastasis and is currently the ultimate cause of prostate cancer-associated deaths in men. Recently, secondary hormonal therapies have led to an increase of neuroendocrine prostate cancer (NEPC), a highly aggressive variant of CRPC. Here, we identify that high levels of cell surface receptor Trop2 are predictive of recurrence of localized prostate cancer. Moreover, Trop2 is significantly elevated in CRPC and NEPC, drives prostate cancer growth, and induces neuroendocrine phenotype. Overexpression of Trop2 induces tumor growth and metastasis while loss of Trop2 suppresses these abilities in vivo. Trop2-driven NEPC displays a significant up-regulation of PARP1, and PARP inhibitors significantly delay tumor growth and metastatic colonization and reverse neuroendocrine features in Trop2-driven NEPC. Our findings establish Trop2 as a driver and therapeutic target for metastatic prostate cancer with neuroendocrine phenotype and suggest that high Trop2 levels could identify cancers that are sensitive to Trop2-targeting therapies and PARP1 inhibition.

    View details for DOI 10.1073/pnas.1905384117

    View details for PubMedID 31932422

  • A specific immune tolerance toward offspring cells is to exist after the mother lymphocyte infusion IMMUNOBIOLOGY Xing, H., Liu, S., Chen, X., Fang, F., Wu, X., Zhu, P. 2017; 222 (4): 658–63

    Abstract

    To examine immune tolerance between maternal lymphocytes and offspring tissue after a donor lymphocyte infusion.Mouse models were established by mating female BALB/c mice with male C57BL mice. Splenic lymphocytes from donors of different genetic backgrounds were labeled with carboxyfluorescein succinimidyl ester (CFSE), and 1×107 of the labeled cells were intravenously injected into a recipient. At 6h, 24h, 72h and 120h after the infusion, mononuclear cells in recipient spleen, liver, thymus, lymph nodes, and peripheral blood were collected. CFSE+, CFSE-, CD3+, CD8+, CD4+, CD19+, NK1.1+, CD25+, and CD127+ lymphocytes in those samples were analyzed by flow cytometry. The distribution of donor T cells, B cells, NK cells, helper T cells, cytotoxic T cells, and recipient regulatory T cells in the tissues were then analyzed.Maternal lymphocytes were more likely to survive in offspring. At 120h after infusion, the percentages of maternal cells in the offspring were 0.52±0.11% in lymph nodes, 0.97±0.04% in peripheral blood, and 0.97±0.11% in the spleen. Few donor cells, if any, were detected in these tissues at 120h after aunt to child, father to child, and unrelated allogeneic infusions were performed. The subtype proportion of donor lymphocytes changed significantly in the recipient tissues. Recipient Treg cells increased in the mother to child group, but not in the aunt to child, father to child, and unrelated allogeneic groups, suggesting a decreased cellular immune response to allogeneic cells in the mother to child group. At 120h after the infusion, no donor cells were detected in the recipient livers and thymuses of all groups, implying that donor cells were barely able to colonize in the liver and thymus.Specific immune tolerance to maternal lymphocytes exists in offspring. An infusion of maternal donor lymphocytes may produce a relatively persistent effect of adoptive immunotherapy with reduced side-effects.

    View details for DOI 10.1016/j.imbio.2016.12.003

    View details for Web of Science ID 000396960500008

    View details for PubMedID 28065449

  • p16 loss rescues functional decline of Brca1-deficient mammary stem cells CELL CYCLE Scott, A., Bai, F., Chan, H., Liu, S., Slingerland, J. M., Robbins, D. J., Capobianco, A. J., Pei, X. 2017; 16 (8): 759–64

    Abstract

    Recent evidence indicates that the accumulation of endogenous DNA damage can induce senescence and limit the function of adult stem cells. It remains elusive whether deficiency in DNA damage repair is associated with the functional alteration of mammary stem cells. In this article, we reported that senescence was induced in mammary epithelial cells during aging along with increased expression of p16Ink4a (p16), an inhibitor of CDK4 and CKD6. Loss of p16 abrogated the age-induced senescence in mammary epithelial cells and significantly increased mammary stem cell function. We showed that loss of Brca1, a tumor suppressor that functions in DNA damage repair, in the mammary epithelium induced senescence with induction of p16 and a decline of stem cell function, which was rescued by p16 loss. These data not only answer the question as to whether deficiency in DNA damage repair is associated with the functional decline of mammary stem cells, but also identify the role of p16 in suppressing Brca1-deficient mammary stem cell function.

    View details for DOI 10.1080/15384101.2017.1295185

    View details for Web of Science ID 000399738300011

    View details for PubMedID 28278054

    View details for PubMedCentralID PMC5405722

  • p16(INK4a) suppresses BRCA1-deficient mammary tumorigenesis ONCOTARGET Scott, A., Bai, F., Chan, H., Liu, S., Ma, J., Slingerland, J. M., Robbins, D. J., Capobianco, A. J., Pei, X. 2016; 7 (51): 84496–507

    Abstract

    Senescence prevents the proliferation of genomically damaged, but otherwise replication competent cells at risk of neoplastic transformation. p16INK4A (p16), an inhibitor of CDK4 and CDK6, plays a critical role in controlling cellular senescence in multiple organs. Functional inactivation of p16 by gene mutation and promoter methylation is frequently detected in human breast cancers. However, deleting p16 in mice or targeting DNA methylation within the murine p16 promoter does not result in mammary tumorigenesis. How loss of p16 contributes to mammary tumorigenesis in vivo is not fully understood.In this article, we reported that disruption of Brca1 in the mammary epithelium resulted in premature senescence that was rescued by p16 loss. We found that p16 loss transformed Brca1-deficient mammary epithelial cells and induced mammary tumors, though p16 loss alone was not sufficient to induce mammary tumorigenesis. We demonstrated that loss of both p16 and Brca1 led to metastatic, basal-like, mammary tumors with the induction of EMT and an enrichment of tumor initiating cells. We discovered that promoter methylation silenced p16 expression in most of the tumors developed in mice heterozygous for p16 and lacking Brca1. These data not only identified the function of p16 in suppressing BRCA1-deficient mammary tumorigenesis, but also revealed a collaborative effect of genetic mutation of p16 and epigenetic silencing of its transcription in promoting tumorigenesis. To the best of our knowledge, this is the first genetic evidence directly showing that p16 which is frequently deleted and inactivated in human breast cancers, collaborates with Brca1 controlling mammary tumorigenesis.

    View details for DOI 10.18632/oncotarget.13015

    View details for Web of Science ID 000391353200057

    View details for PubMedID 27811360

    View details for PubMedCentralID PMC5356676

  • Gata3 restrains B cell proliferation and cooperates with p18(INK4c) to repress B cell lymphomagenesis ONCOTARGET Liu, S., Chan, H., Bai, F., Ma, J., Scott, A., Robbins, D. J., Capobianco, A. J., Zhu, P., Pei, X. 2016; 7 (39): 64007–20

    Abstract

    GATA3, a lineage specifier, controls lymphoid cell differentiation and its function in T cell commitment and development has been extensively studied. GATA3 promotes T cell specification by repressing B cell potential in pro T cells and decreased GATA3 expression is essential for early B cell commitment. Inherited genetic variation in GATA3 has been associated with lymphoma susceptibility. However, it remains elusive how the loss of function of GATA3 promotes B cell development and induces B cell lymphomas. In this study, we found that haploid loss of Gata3 by heterozygous germline deletion increased B cell populations in the bone marrow (BM) and spleen, and decreased CD4 T cell populations in the thymus, confirming that Gata3 promotes T and suppresses B cell development. We discovered that haploid loss of Gata3 reduced thymocyte proliferation with induction of p18Ink4c (p18), an inhibitor of CDK4 and CDK6, but enhanced B cell proliferation in the BM and spleen independent of p18. Loss of p18 partially restored Gata3 deficient thymocyte proliferation, but further stimulated Gata3 deficient B cell proliferation in the BM and spleen. Furthermore, we discovered that haploid loss of Gata3 in p18 deficient mice led to the development of B cell lymphomas that were capable of rapidly regenerating tumors when transplanted into immunocompromised mice. These results indicate that Gata3 deficiency promotes B cell differentiation and proliferation, and cooperates with p18 loss to induce B cell lymphomas. This study, for the first time, reveals that Gata3 is a tumor suppressor specifically in B cell lymphomagenesis.

    View details for DOI 10.18632/oncotarget.11746

    View details for Web of Science ID 000387167800094

    View details for PubMedID 27588406

    View details for PubMedCentralID PMC5325421

  • Immunophenotypic analysis of abnormal plasma cell clones in bone marrow of primary systemic light chain amyloidosis patients CHINESE MEDICAL JOURNAL Hu Yang, Wang Mangju, Chen Yan, Chen Xue, Fang Fang, Liu Shiqin, Zhang Ying, Wu Xueqiang, Zhu Ping 2014; 127 (15): 2765–70

    Abstract

    Primary systemic light chain amyloidosis (AL) is a rare plasma cell disease, our purpose was to analyze the immunophenotypic characteristics of the plasma cells in bone marrow in AL patients, and explore whether the detection of abnormal plasma cell clones in bone marrow by flow cytometry (FCM) could be used as an important indicator of AL diagnosis.Fresh bone marrow samples were collected from 51 AL, 21 multiple myeloma (MM), and 5 Waldenström's macroglobulinemia (WM) patients. The immunophenotype of bone marrow cells were analyzed and compared by FCM using a panel of antibodies including CD45, CD38, CD138, CD117, CD56, and CD19.In AL, light chain restriction could be identified in 31 cases (60.9%), in which the λ light chain restriction was found in 24 cases (77.4%). In MM, κ light chain restriction was found in 13 cases (61.9%), and λ light chain restriction in eight cases. CD45 on abnormal plasma cells was negative to weakly positive in both AL and MM, but was positive to strongly positive in WM. In the bone marrow plasma cells of the 51 AL, 78.4% were CD56+, 68.6% were CD117+, and 88.2% were CD19-. While in the 21 MM cases, 66.7% were CD56+, 38.1% were CD117+, and 90.4% were CD19-. The plasmacytoid lymphocytes in the five WM patients were CD19+ and CD56-, CD117-.Detection of abnormal plasma cell clones in bone marrow by FCM is valuable for the diagnosis of AL.

    View details for DOI 10.3760/cma.j.issn.0366-6999.20141053

    View details for Web of Science ID 000340691000008

    View details for PubMedID 25146610