Jiaoti Huang

Overview:

I am a physician-scientist with clinical expertise in the pathologic diagnosis of genitourinary tumors including tumors of the prostate, bladder, kidney and testis. Another area of interest is gynecologic tumors. In my research laboratory we study prostate cancer, focusing on molecular mechanisms of carcinogenesis and tumor progression, as well as biomarkers, imaging and novel therapeutic strategies. In addition to patient care and research, I am also passionate about education. I have trained numerous residents, fellows, graduate students and postdocs.

Positions:

Endowed Department Chair of Pathology

Pathology
School of Medicine

Professor of Pathology

Pathology
School of Medicine

Chair

Pathology
School of Medicine

Professor of Pharmacology and Cancer Biology

Pharmacology & Cancer Biology
School of Medicine

Member of the Duke Cancer Institute

Duke Cancer Institute
School of Medicine

Education:

M.D. 1983

Anhui Medical University (China)

Ph.D. 1991

New York University

Grants:

Histologic and Immunohistochemical Biomarkers for Heavily Treated Metastatic Prostate Cancer

Administered By
Pathology
Awarded By
National Institutes of Health
Role
Principal Investigator
Start Date
End Date

Role and targeting of PRMT5 in prostate cancer

Administered By
Pathology
Awarded By
Purdue University
Role
Principal Investigator
Start Date
End Date

A novel strategy to identify prostate cancer biomarkers for patient management

Administered By
Pathology
Awarded By
National Institutes of Health
Role
Principal Investigator
Start Date
End Date

Stand Up 2 Cancer West Coast Dream Team Grant

Administered By
Pathology
Role
Principal Investigator
Start Date
End Date

Confirmation of histologic SCNC (NEPC)

Administered By
Pathology
Role
Principal Investigator
Start Date
End Date

Publications:

Prostate Cancer Cell Phenotypes Remain Stable Following PDE5 Inhibition in the Clinically Relevant Range.

Widespread cGMP-specific phosphodiesterase 5 (PDE5) inhibitor use in male reproductive health and particularly in prostate cancer patients following surgery has generated interest in how these drugs affect the ability of residual tumor cells to proliferate, migrate, and form recurrent colonies. Prostate cancer cell lines were treated with PDE5 inhibitors at clinically relevant concentrations. Proliferation, colony formation, and migration phenotypes remained stable even when cells were co-treated with a stimulator of cGMP synthesis that facilitated cGMP accumulation upon PDE5 inhibition. Surprisingly, supraclinical concentrations of PDE5 inhibitor counteracted proliferation, colony formation, and migration of prostate cancer cell models. These findings provide tumor cell-autonomous evidence in support of the field's predominant view that PDE5 inhibitors are safe adjuvant agents to promote functional recovery of normal tissue after prostatectomy, but do not rule out potential cancer-promoting effects of PDE5 inhibitors in the more complex environment of the prostate.
Authors
Hankey, W; Sunkel, B; Yuan, F; He, H; Thomas-Ahner, JM; Chen, Z; Clinton, SK; Huang, J; Wang, Q
MLA Citation
Hankey, William, et al. “Prostate Cancer Cell Phenotypes Remain Stable Following PDE5 Inhibition in the Clinically Relevant Range.Transl Oncol, vol. 13, no. 9, May 2020, p. 100797. Pubmed, doi:10.1016/j.tranon.2020.100797.
URI
https://scholars.duke.edu/individual/pub1442201
PMID
32454444
Source
pubmed
Published In
Translational Oncology
Volume
13
Published Date
Start Page
100797
DOI
10.1016/j.tranon.2020.100797

Transcriptional profiling identifies an androgen receptor activity-low, stemness program associated with enzalutamide resistance.

The androgen receptor (AR) antagonist enzalutamide is one of the principal treatments for men with castration-resistant prostate cancer (CRPC). However, not all patients respond, and resistance mechanisms are largely unknown. We hypothesized that genomic and transcriptional features from metastatic CRPC biopsies prior to treatment would be predictive of de novo treatment resistance. To this end, we conducted a phase II trial of enzalutamide treatment (160 mg/d) in 36 men with metastatic CRPC. Thirty-four patients were evaluable for the primary end point of a prostate-specific antigen (PSA)50 response (PSA decline ≥50% at 12 wk vs. baseline). Nine patients were classified as nonresponders (PSA decline <50%), and 25 patients were classified as responders (PSA decline ≥50%). Failure to achieve a PSA50 was associated with shorter progression-free survival, time on treatment, and overall survival, demonstrating PSA50's utility. Targeted DNA-sequencing was performed on 26 of 36 biopsies, and RNA-sequencing was performed on 25 of 36 biopsies that contained sufficient material. Using computational methods, we measured AR transcriptional function and performed gene set enrichment analysis (GSEA) to identify pathways whose activity state correlated with de novo resistance. TP53 gene alterations were more common in nonresponders, although this did not reach statistical significance (P = 0.055). AR gene alterations and AR expression were similar between groups. Importantly, however, transcriptional measurements demonstrated that specific gene sets-including those linked to low AR transcriptional activity and a stemness program-were activated in nonresponders. Our results suggest that patients whose tumors harbor this program should be considered for clinical trials testing rational agents to overcome de novo enzalutamide resistance.
Authors
Alumkal, JJ; Sun, D; Lu, E; Beer, TM; Thomas, GV; Latour, E; Aggarwal, R; Cetnar, J; Ryan, CJ; Tabatabaei, S; Bailey, S; Turina, CB; Quigley, DA; Guan, X; Foye, A; Youngren, JF; Urrutia, J; Huang, J; Weinstein, AS; Friedl, V; Rettig, M; Reiter, RE; Spratt, DE; Gleave, M; Evans, CP; Stuart, JM; Chen, Y; Feng, FY; Small, EJ; Witte, ON; Xia, Z
MLA Citation
Alumkal, Joshi J., et al. “Transcriptional profiling identifies an androgen receptor activity-low, stemness program associated with enzalutamide resistance.Proceedings of the National Academy of Sciences of the United States of America, May 2020. Epmc, doi:10.1073/pnas.1922207117.
URI
https://scholars.duke.edu/individual/pub1441320
PMID
32424106
Source
epmc
Published In
Proceedings of the National Academy of Sciences of the United States of America
Published Date
DOI
10.1073/pnas.1922207117

Multiparametric Ultrasound for the Targeting of Prostate Cancer using ARFI, SWEI, B-mode, and QUS

© 2019 IEEE. Prostate cancer diagnosis using standard transrectal ultrasound (TRUS) and systematic biopsy is challenging. To improve the performance of TRUS imaging, we combined it with acoustic radiation force impulse (ARFI) imaging and shear wave elasticity imaging (SWEI) to enhance lesion contrast into a multiparametric ultrasound (mpUS) synthesized image using a linear support vector machine (SVM). The SVM was trained on one subset of patients (N=15) and applied to a second subset (N=15) imaged with a different transducer. mpUS imaging identified 79% of clinically significant PCa in the second cohort with a PPV of 95%.
Authors
Morris, DC; Chan, DY; Chen, H; Palmeri, ML; Polascik, TJ; Foo, WC; Huang, J; Mamou, J; Nightingale, KR
MLA Citation
Morris, D. C., et al. “Multiparametric Ultrasound for the Targeting of Prostate Cancer using ARFI, SWEI, B-mode, and QUS.” Ieee International Ultrasonics Symposium, Ius, vol. 2019-October, 2019, pp. 880–83. Scopus, doi:10.1109/ULTSYM.2019.8926035.
URI
https://scholars.duke.edu/individual/pub1427968
Source
scopus
Published In
Ieee International Ultrasonics Symposium, Ius
Volume
2019-October
Published Date
Start Page
880
End Page
883
DOI
10.1109/ULTSYM.2019.8926035

Clinical and genomic characterization of Low PSA Secretors: a unique subset of metastatic castration resistant prostate cancer.

BACKGROUND: Metastatic disease burden out of proportion to serum PSA has been used as a marker of aggressive phenotype prostate cancer but is not well defined as a distinct subgroup. We sought to prospectively characterize the molecular features and clinical outcomes of Low PSA Secretors. METHODS: Eligible metastatic castration resistant prostate cancer (mCRPC) patients without prior small cell histology underwent metastatic tumor biopsy with molecular characterization. Low PSA secretion was defined as serum PSA < 2, 5, or 10 ng/mL plus >5 metastases with radiographic progression at study entry. Clinical and molecular features were compared between low PSA vs. normal secretors in a post-hoc fashion. RESULTS: 183 patients were enrolled, including 15 (8%) identified as Low PSA Secretors using optimal PSA cut point of 5 ng/mL. Biopsies from Low PSA Secretors demonstrated higher t-SCNC and RB1 loss and lower AR transcriptional signature scores compared with normal secretors. Genomic loss of RB1 and/or TP53 was more common in Low PSA Secretors (80% vs. 41%). Overall survival (OS) was shorter in Low PSA Secretors (median OS = 26.7 vs. 46.0 months, hazard ratio = 2.465 (95% CI: 0.982-6.183). Progression-free survival (PFS) on post-biopsy treatment with AR-targeted therapy was shorter than with chemotherapy (median PFS 6.2 vs. 4.1 months). CONCLUSIONS: Low PSA secretion in relation to metastatic tumor burden may be a readily available clinical selection tool for de-differentiated mCRPC with molecular features consistent with t-SCNC. Prospective validation is warranted.
Authors
Aggarwal, R; Romero, GR; Friedl, V; Weinstein, A; Foye, A; Huang, J; Feng, F; Stuart, JM; Small, EJ
MLA Citation
Aggarwal, Rahul, et al. “Clinical and genomic characterization of Low PSA Secretors: a unique subset of metastatic castration resistant prostate cancer.Prostate Cancer Prostatic Dis, Apr. 2020. Pubmed, doi:10.1038/s41391-020-0228-0.
URI
https://scholars.duke.edu/individual/pub1438332
PMID
32286548
Source
pubmed
Published In
Prostate Cancer Prostatic Dis
Published Date
DOI
10.1038/s41391-020-0228-0

Corrigendum to 'Roles of alternative RNA splicing of the Bif-1 gene by SRRM4 during the development of treatment-induced neuroendocrine prostate cancer'. [EBioMedicine 31 (2018) 267-275>.

Authors
Gan, Y; Li, Y; Long, Z; Lee, AR; Xie, N; Lovnicki, JM; Tang, Y; Chen, X; Huang, J; Dong, X
URI
https://scholars.duke.edu/individual/pub1436881
PMID
32268279
Source
pubmed
Published In
Ebiomedicine
Volume
54
Published Date
Start Page
102741
DOI
10.1016/j.ebiom.2020.102741