Andrew Armstrong

Overview:

1. Predictors of sensitivity and clinical efficacy of therapies in advanced prostate cancer
2. Novel designs of clinical trials and pharmacodynamic/translational studies in prostate, kidney, bladder cancer
3. Pre-operative models for drug development of novel agents in human testing in prostate cancer
4. Novel therapies and drug development for prostate, renal, bladder, and testicular cancer
5. Design of rational combination therapies in men with metastatic hormone-refractory prostate cancer
6. PI3 kinase/mTOR inhibition in prostate cancer: mechanisms of sensitivity and resistance
7. Developing prognostic models for progression and survival in metastatic prostate cancer
8. Examining surrogate markers of mortality in metastatic prostate cancer
9. Clear cell and non-clear cell renal cell carcinoma: natural history, sensitivity to novel agents including mTOR and VEGF inhibition

Positions:

Professor of Medicine

Medicine, Medical Oncology
School of Medicine

Associate Professor in Pharmacology and Cancer Biology

Pharmacology & Cancer Biology
School of Medicine

Professor in Surgery

Surgery, Urology
School of Medicine

Member of the Duke Cancer Institute

Duke Cancer Institute
School of Medicine

Education:

B.S.E. 1996

Duke University

M.D. 2000

University of Virginia School of Medicine

M.Sc. 2008

Johns Hopkins University

Internship/Residency, General Internal Medicine

University of Pennsylvania School of Medicine

Fellowship, Division Of Oncology/Hematology

Johns Hopkins University School of Medicine

Grants:

Propel Protocol ID: D081SC00001

Administered By
Duke Cancer Institute
Role
Principal Investigator
Start Date
End Date

ProSTAR: CPI-1205

Administered By
Duke Cancer Institute
Role
Principal Investigator
Start Date
End Date

VISION PSMA-617-01

Administered By
Duke Cancer Institute
Role
Principal Investigator
Start Date
End Date

A Phase 2 Study of Nivolumab in combination with either Rucaparib, docetaxel, or enzalutamide in men with Castration-resistant metastaic prostate cancer (CheckMate 9KD: CHECKpoint pathway and nivoluMA

Administered By
Duke Cancer Institute
Role
Principal Investigator
Start Date
End Date

MK7123

Administered By
Duke Cancer Institute
Role
Principal Investigator
Start Date
End Date

Publications:

An Integrative Systems Biology and Experimental Approach Identifies Convergence of Epithelial Plasticity, Metabolism, and Autophagy to Promote Chemoresistance.

The evolution of therapeutic resistance is a major cause of death for cancer patients. The development of therapy resistance is shaped by the ecological dynamics within the tumor microenvironment and the selective pressure of the host immune system. These selective forces often lead to evolutionary convergence on pathways or hallmarks that drive progression. Thus, a deeper understanding of the evolutionary convergences that occur could reveal vulnerabilities to treat therapy-resistant cancer. To this end, we combined phylogenetic clustering, systems biology analyses, and molecular experimentation to identify convergences in gene expression data onto common signaling pathways. We applied these methods to derive new insights about the networks at play during transforming growth factor-β (TGF-β)-mediated epithelial⁻mesenchymal transition in lung cancer. Phylogenetic analyses of gene expression data from TGF-β-treated cells revealed convergence of cells toward amine metabolic pathways and autophagy during TGF-β treatment. Knockdown of the autophagy regulatory, ATG16L1, re-sensitized lung cancer cells to cancer therapies following TGF-β-induced resistance, implicating autophagy as a TGF-β-mediated chemoresistance mechanism. In addition, high ATG16L expression was found to be a poor prognostic marker in multiple cancer types. These analyses reveal the usefulness of combining evolutionary and systems biology methods with experimental validation to illuminate new therapeutic vulnerabilities for cancer.
Authors
Xu, S; Ware, KE; Ding, Y; Kim, SY; Sheth, MU; Rao, S; Chan, W; Armstrong, AJ; Eward, WC; Jolly, MK; Somarelli, JA
MLA Citation
URI
https://scholars.duke.edu/individual/pub1368763
PMID
30736412
Source
pubmed
Published In
Journal of Clinical Medicine
Volume
8
Published Date
DOI
10.3390/jcm8020205

Abstract 5702: Characterization of circulating tumor cells during immune checkpoint inhibition in metastatic renal cell carcinoma and malignant melanoma

Authors
Zhang, T; Park, S; Runyambo, D; Poellmann, MJ; Reyes-Martinez, M; Mahbooba, Z; Green, R; Lee, C; George, DJ; Armstrong, AJ; Hong, S; Wang, AZ
MLA Citation
Zhang, Tian, et al. “Abstract 5702: Characterization of circulating tumor cells during immune checkpoint inhibition in metastatic renal cell carcinoma and malignant melanoma.” Clinical Research (Excluding Clinical Trials), American Association for Cancer Research, 2018. Crossref, doi:10.1158/1538-7445.am2018-5702.
URI
https://scholars.duke.edu/individual/pub1393337
Source
crossref
Published In
Clinical Research (Excluding Clinical Trials)
Published Date
DOI
10.1158/1538-7445.am2018-5702

Naming disease states for clinical utility in prostate cancer: a rose by any other name might not smell as sweet.

Authors
Armstrong, AJ; Antonarakis, ES; Taplin, M-E; Kelly, WK; Beltran, H; Fizazi, K; Dahut, WL; Shore, N; Slovin, S; George, D; Carducci, MA; Corn, P; Danila, D; Dreicer, R; Heath, E; Rathkopf, D; Liu, G; Nanus, D; Stein, M; Smith, MR; Sternberg, C; Wilding, G; Nelson, PS; Halabi, S; Kantoff, P; Clarke, NW; Evans, CP; Heidenreich, A; Mottet, N; Gleave, M; Morris, MJ; Scher, HI
MLA Citation
Armstrong, A. J., et al. “Naming disease states for clinical utility in prostate cancer: a rose by any other name might not smell as sweet..” Ann Oncol, vol. 29, no. 1, Jan. 2018, pp. 23–25. Pubmed, doi:10.1093/annonc/mdx648.
URI
https://scholars.duke.edu/individual/pub1284326
PMID
29088323
Source
pubmed
Published In
Ann Oncol
Volume
29
Published Date
Start Page
23
End Page
25
DOI
10.1093/annonc/mdx648

Drug development in prostate cancer: time to embrace RECIST?

Authors
Sonpavde, G; Armstrong, AJ
MLA Citation
Sonpavde, Guru, and Andrew J. Armstrong. “Drug development in prostate cancer: time to embrace RECIST?.” Lancet Oncol, vol. 18, no. 4, Apr. 2017, pp. 419–21. Pubmed, doi:10.1016/S1470-2045(17)30149-3.
URI
https://scholars.duke.edu/individual/pub1241332
PMID
28283283
Source
pubmed
Published In
Lancet Oncol
Volume
18
Published Date
Start Page
419
End Page
421
DOI
10.1016/S1470-2045(17)30149-3

Association Between RECIST Changes and Survival in Patients with Metastatic Castration-resistant Prostate Cancer Receiving Docetaxel.

UNLABELLED: We explored the association between Response Evaluation Criteria in Solid Tumors (RECIST) 1.0 and 1.1 changes and overall survival (OS) in patients with metastatic castration-resistant prostate cancer (mCRPC) from the control arms of the VENICE and MAINSAIL phase 3 trials, respectively, receiving docetaxel, prednisone, and placebo. We used Cox proportional hazards regression to evaluate the OS prognostic ability of RECIST changes after adjusting for prognostic factors. In the VENICE trial, the OS hazard ratio (HR) was 0.64 (95% confidence interval [CI] 0.42-0.99; p=0.045) for patients with a partial response (PR) compared to those without PR, and 1.78 (95% CI 1.07-2.95; p=0.026) for those with progressive disease (PD) compared to those without PD. After adjusting for prostate-specific antigen (PSA) changes, PD remained significant (HR 1.85, 95% CI 1.10-3.12; p=0.020). Data from the MAINSAIL trial corroborated the association of PR (HR 0.51, 95% CI 0.22-1.18; p=0.12) and PD (HR 3.51, 95% CI 1.92-6.43; p<0.001) with OS. After adjusting for PSA changes, PD was associated with poor OS (HR 2.36, 95% CI 1.11-5.04; p=0.026). Given the association between RECIST changes and OS, more frequent detection of measurable disease with current imaging techniques, and the poor reliability of bone scan and PSA changes, assessment of RECIST changes on treatment with novel agents in patients with measurable tumors may provide an objective signal of efficacy. PATIENT SUMMARY: In this study, we found an association between changes in objectively measurable tumors according to Response Evaluation Criteria in Solid Tumors (RECIST) and survival in patients with metastatic prostate cancer receiving docetaxel chemotherapy. Since bone scan and prostate-specific antigen changes are unreliable and measurable tumors are more frequently detected now because of better radiographic technology, a focus on RECIST changes should be considered during drug development to provide an objective signal of efficacy.
Authors
Sonpavde, G; Pond, GR; Templeton, AJ; Fandi, A; Tombal, B; Rosenthal, M; Armstrong, AJ; Petrylak, DP
MLA Citation
Sonpavde, Guru, et al. “Association Between RECIST Changes and Survival in Patients with Metastatic Castration-resistant Prostate Cancer Receiving Docetaxel..” Eur Urol, vol. 69, no. 6, June 2016, pp. 980–83. Pubmed, doi:10.1016/j.eururo.2015.10.008.
URI
https://scholars.duke.edu/individual/pub1091611
PMID
26497922
Source
pubmed
Published In
Eur Urol
Volume
69
Published Date
Start Page
980
End Page
983
DOI
10.1016/j.eururo.2015.10.008