Overview

Pingping Hou is an assistant professor at Rutgers University, New Jersey Medical School. Dr. Hou graduated with a bachelor's degree from China Agricultural University in Beijing in 2007. After completing her graduate study mentored by Dr. Hongkui Deng at Peking University in 2014 and postdoctoral training with Dr. Ronald A. DePinho at the University of Texas MD Anderson Cancer Center, she joined the faculty of Rutgers University as an assistant professor in 2021.

Dr. Hou's research focuses on the molecular mechanisms of KRAS-targeted therapy resistance in pancreatic cancer and the development of cell-based therapies. Her work discovered new factors that drive tumorigenesis and the bypass of KRAS dependency, and delineated the intercellular crosstalk in the tumor microenvironment that is sufficient and essential for developing therapy resistance. Dr. Hou has published 15 original articles in leading journals including Science, Nature, Cancer Discovery, and Nature Cancer. Dr. Hou's achievements have been recognized by several awards, including a Faculty of the Year Award at Rutgers NJMS (2024) a Rutgers New Investigator Award (2023), an MD Anderson Cancer Center Wall of Science awardee (2021), and an MD Anderson Outstanding Research Publication Award (2021).

Education

D.Phil, 2014, Perking University

Curriculum Vitae

View CV

Relevant Publications

Gulhati P, Schalck A, Jiang S, Shang X, Wu CJ, Hou P, Ruiz SH, Soto LS, Parra E, Ying H, Han J, Dey P, Li J, Deng P, Sei E, Maeda DY, Zebala JA, Spring DJ, Kim M, Wang H, Maitra A, Moore D, Clise-Dwyer K, Wang YA, Navin NE, DePinho RA. "Targeting T cell checkpoints 41BB and LAG3 and myeloid cell CXCR1/CXCR2 results in antitumor immunity and durable response in pancreatic cancer." Nat Cancer. 2023 Jan;4(1):62-80. doi: 10.1038/s43018-022-00500-z.

Deng D, Patel R, Chiang C.-Y, Hou P. "Role of the Tumor Microenvironment in Regulating Pancreatic Cancer Therapy Resistance." Cells. 2022, 11, 2952. https://doi.org/10.3390/cells11192952.

Hou P*, Wang YA. "Conquering oncogenic KRAS and its bypass mechanisms." Theranostics. 2022, 12(13): 5691-5709. doi:10.7150/thno.71260.

Hou P, Ma X, Yang Z, Zhang Q, Wu CJ, Li J, Tan L, Yao W, Yan L, Zhou X, Kimmelman AC, Lorenzi PL, Zhang J, Jiang S, Spring DJ, Wang YA, DePinho RA. "USP21 deubiquitinase elevates macropinocytosis to enable oncogenic KRAS bypass in pancreatic cancer." Genes Dev. 2021, Sep 16, doi: 10.1101/gad.348787.121.

Zhu M, Peng R, Liang X, Lan Z, Tang M, Hou P, Song JH, Mak CSL, Park J, Zheng SE, Huang A, Ma X, Chen R, Chang Q, Logothetis CJ, Jain AK, Lin SH, Katayama H, Hanash S, Wang G. "P4HA2-induced prolyl hydroxylation suppresses YAP1-mediated prostate cancer cell migration, invasion, and metastasis." Oncogene. 2021 Sep 1. doi: 10.1038/s41388-021-02000-3.

Chakravarti D, Hu B, Mao X, Rashid A, Li J, Liao W, Whitley EM, Dey P, Hou P, LaBella KA, Chang A, Wang G, Spring DJ, Deng P, Zhao D, Liang X, Lan Z, Lin Y, Sarkar S, Terranova C, Deribe YL, Blutt SE, Okhuysen P, Zhang J, Sanchez EV, Nielsen OH, Dupont A, Younes M, Patel KR, Shroyer NF, Rai K, Estes MK, Wang YA, Bertuch AA, DePinho RA. 'Telomere dysfunction activates YAP1 to drive tissue inflammation.' Nature Communications. 2020 Sep 21;11(1):4766. doi: 10.1038/s41467-020-18420-w.

Hou P, Kapoor A, Zhang Q, Li J, Wu CJ, Li J, Lan Z, Tang M, Ma X, Ackroyd JJ, Kalluri R, Zhang J, Jiang S, Spring DJ, Wang YA, DePinho RA. 'Tumor microenvironment remodeling enables bypass of oncogenic KRAS dependency in pancreatic cancer.' Cancer Discov. 2020 Apr 27:CD-19-0597. doi: 10.1158/2159-8290.CD-19-0597.

Hou P, Ma X, Zhang Q, Wu CJ, Liao W, Li J, Wang H, Zhao J, Zhou X, Guan C, Ackroyd J, Jiang S, Zhang J, Spring DJ, Wang YA, DePinho RA. 'USP21 deubiquitinase promotes pancreas cancer cell stemness via Wnt pathway activation.' Genes Dev. 2019 Sep 5. doi: 10.1101/gad.326314.119.

Yao W, Rose JL, Wang W, Seth S, Jiang H, Taguchi A, Liu J, Yan L, Kapoor A, Hou P, Chen Z, Wang Q, Nezi L, Xu Z, Yao J, Hu B, Pettazzoni PF, Ho IL, Feng N, Ramamoorthy V, Jiang S, Deng P, Ma GJ, Den P, Tan Z, Zhang SX, Wang H, Wang YA, Deem AK, Fleming JB, Carugo A, Heffernan TP, Maitra A, Viale A, Ying H, Hanash S, DePinho RA, Draetta GF. 'Syndecan 1 is a critical mediator of macropinocytosis in pancreatic cancer.' Nature. 2019 Apr;568(7752):410-414.

Wang G, Lu X, Dey P, Deng P, Wu CC, Jiang S, Fang Z, Zhao K, Konaparthi R, Hua S, Zhang J, Li-Ning-Tapia EM, Kapoor A, Wu CJ, Patel NB, Guo Z, Ramamoorthy V, Tieu TN, Heffernan T, Zhao D, Shang X, Khadka S, Hou P, Hu B, Jin EJ, Yao W, Pan X, Ding Z, Shi Y, Li L, Chang Q, Troncoso P, Logothetis CJ, McArthur MJ, Chin L, Wang YA, DePinho RA. 'Targeting YAP-Dependent MDSC Infiltration Impairs Tumor Progression.' Cancer Discov. 2016 Jan;6(1):80-95.

Areas Of Interest

KRAS

Pancreatic ductal adenocarcinoma

cancer immunity

cell plasticity

chimeric antigen receptors

macrophages

therapy resistance

tumor microenvironment

Course List

MBGC5020Q

Cancer Biology: Intrinsic

Understand and exploit the intercellular crosstalk to combat pancreatic cancer

Decode KRAS targeted therapy resistance

The RTK-RAS-MAPK pathway is the most frequently altered signaling pathway at the rate of 46% across all cancer types. KRAS alternation is the top common event across all samples at 9%, and particularly predominant in pancreatic cancer (72%), colon cancer (69%) and lung cancer (33%). Oncogenic KRAS not only initiates tumorigenesis, but is also required for tumor maintenance, implying KRAS as an ideal therapeutic target for cancer treatment. Due to great advances of targeting RAS achieved in the past decade, KRAS can be druggable now by various methods. However, drug resistance occurs as expected, emphasizing that to overcome KRAS targeted therapy (KRASi) resistance is the key for favorable disease control.

Current projects focus on understanding tumor cell autonomous and non-autonomous KRASi resistance mechanisms, including exploring resistance-associated immune cells in the tumor microenvironment and dissecting how cell fate transition regulates KRASi resistance via epigenetic modulation.


Develop novel cell therapies

Cells of the tumor microenvironment (TME) are plastic and mostly immune suppressive. Pancreatic cancer belongs to cold tumor with sparse cytotoxic immune cell infiltration. Thus, patients benefit little from current progress in immunotherapy. To change the scenario, our lab will exploit the hallmarks of pancreatic TME and take the advantage of our strength in cellular reprogramming to engineer myeloid cells. Our research goal is to rewire the TME from pro- to anti-tumor phenotype for achieving a durable disease control.

Current projects include developing chimeric antigen receptor (CAR) macrophage cell therapy and creating novel safety switches.