Steven Patierno

Overview:

Patierno's current translational research interests are focused on the genomics molecular biology of cancer disparities, cancer biology, molecular pharmacology and targeted experimental therapeutics to control prostate, breast and lung tumor aggressiveness. He is an internationally recognized expert in cancer control, cancer causation and molecular carcinogenesis, which includes a broad spectrum of laboratory and population level research.   Patierno is also actively engaged in cancer health disparities and healthcare delivery research focused on patient navigation, survivorship, community-based interventions, mHealth, implementation sciences, cancer care economics, and policy.

Positions:

Professor of Medicine

Medicine, Medical Oncology
School of Medicine

Professor of Pharmacology and Cancer Biology

Pharmacology & Cancer Biology
School of Medicine

Professor in Family Medicine and Community Health

Family Medicine and Community Health
School of Medicine

Member of the Duke Cancer Institute

Duke Cancer Institute
School of Medicine

Education:

B.S. 1981

University of Connecticut

Ph.D. 1985

University of Texas Medical School at Houston

Postdoctoral Training, Norris Comprehensive Cancer

University of Southern California

Grants:

3D Biology Signatures defined by Nanostring Max System

Administered By
Medicine, Medical Oncology
Role
Major User
Start Date
End Date

Identification of Genetic Determinates for Disparities in African American Patients with Non-Small Cell Lung Cancer

Administered By
Medicine, Medical Oncology
Awarded By
V Foundation for Cancer Research
Role
Significant Contributor
Start Date
End Date

Targeting RNA splicing in race-related aggressive and lethal prostate cancer

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

PC150506: Small molecule targeting of RNA splice variants driving tumor aggressiveness

Administered By
Chemistry
Role
Collaborator
Start Date
End Date

2/2 NCCU-DUKE Cancer Disparities Translational Research Partnership

Administered By
Duke Cancer Institute
Awarded By
National Institutes of Health
Role
Principal Investigator
Start Date
End Date

Publications:

Findings from the National Navigation Roundtable: A call for competency-based patient navigation training.

Authors
Valverde, PA; Burhansstipanov, L; Patierno, S; Gentry, S; Dwyer, A; Wysocki, KL; Patterson, AK; Krebs, LU; Sellers, J; Johnston, D
MLA Citation
Valverde, Patricia A., et al. “Findings from the National Navigation Roundtable: A call for competency-based patient navigation training..” Cancer, vol. 125, no. 24, Dec. 2019, pp. 4350–59. Pubmed, doi:10.1002/cncr.32470.
URI
https://scholars.duke.edu/individual/pub1409904
PMID
31503340
Source
pubmed
Published In
Cancer
Volume
125
Published Date
Start Page
4350
End Page
4359
DOI
10.1002/cncr.32470

Perspectives on Inflammatory Breast Cancer (IBC) Research, Clinical Management and Community Engagement from the Duke IBC Consortium.

Inflammatory breast cancer (IBC) is an understudied and aggressive form of breast cancer with a poor prognosis, accounting for 2-6% of new breast cancer diagnoses but 10% of all breast cancer-related deaths in the United States. Currently there are no therapeutic regimens developed specifically for IBC, and it is critical to recognize that all aspects of treating IBC - including staging, diagnosis, and therapy - are vastly different than other breast cancers. In December 2014, under the umbrella of an interdisciplinary initiative supported by the Duke School of Medicine, researchers, clinicians, research administrators, and patient advocates formed the Duke Consortium for IBC to address the needs of patients in North Carolina (an ethnically and economically diverse state with 100 counties) and across the Southeastern United States. The primary goal of this group is to translate research into action and improve both awareness and patient care through collaborations with local, national and international IBC programs. The consortium held its inaugural meeting on Feb 28, 2018, which also marked Rare Disease Day and convened national research experts, clinicians, patients, advocates, government representatives, foundation leaders, staff, and trainees. The meeting focused on new developments and challenges in the clinical management of IBC, research challenges and opportunities, and an interactive session to garner input from patients, advocates, and community partners that would inform a strategic plan toward continuing improvements in IBC patient care, research, and education.
Authors
Devi, GR; Hough, H; Barrett, N; Cristofanilli, M; Overmoyer, B; Spector, N; Ueno, NT; Woodward, W; Kirkpatrick, J; Vincent, B; Williams, KP; Finley, C; Duff, B; Worthy, V; McCall, S; Hollister, BA; Palmer, G; Force, J; Westbrook, K; Fayanju, O; Suneja, G; Dent, SF; Hwang, ES; Patierno, SR; Marcom, PK
MLA Citation
Devi, Gayathri R., et al. “Perspectives on Inflammatory Breast Cancer (IBC) Research, Clinical Management and Community Engagement from the Duke IBC Consortium..” J Cancer, vol. 10, no. 15, 2019, pp. 3344–51. Pubmed, doi:10.7150/jca.31176.
URI
https://scholars.duke.edu/individual/pub1395729
PMID
31293637
Source
pubmed
Published In
Journal of Cancer
Volume
10
Published Date
Start Page
3344
End Page
3351
DOI
10.7150/jca.31176

Alternative splicing promotes tumour aggressiveness and drug resistance in African American prostate cancer.

Clinical challenges exist in reducing prostate cancer (PCa) disparities. The RNA splicing landscape of PCa across racial populations has not been fully explored as a potential molecular mechanism contributing to race-related tumour aggressiveness. Here, we identify novel genome-wide, race-specific RNA splicing events as critical drivers of PCa aggressiveness and therapeutic resistance in African American (AA) men. AA-enriched splice variants of PIK3CD, FGFR3, TSC2 and RASGRP2 contribute to greater oncogenic potential compared with corresponding European American (EA)-expressing variants. Ectopic overexpression of the newly cloned AA-enriched variant, PIK3CD-S, in EA PCa cell lines enhances AKT/mTOR signalling and increases proliferative and invasive capacity in vitro and confers resistance to selective PI3Kδ inhibitor, CAL-101 (idelalisib), in mouse xenograft models. High PIK3CD-S expression in PCa specimens associates with poor survival. These results highlight the potential of RNA splice variants to serve as novel biomarkers and molecular targets for developmental therapeutics in aggressive PCa.
Authors
Wang, B-D; Ceniccola, K; Hwang, S; Andrawis, R; Horvath, A; Freedman, JA; Olender, J; Knapp, S; Ching, T; Garmire, L; Patel, V; Garcia-Blanco, MA; Patierno, SR; Lee, NH
MLA Citation
Wang, Bi-Dar, et al. “Alternative splicing promotes tumour aggressiveness and drug resistance in African American prostate cancer..” Nat Commun, vol. 8, June 2017. Pubmed, doi:10.1038/ncomms15921.
URI
https://scholars.duke.edu/individual/pub1264786
PMID
28665395
Source
pubmed
Published In
Nature Communications
Volume
8
Published Date
Start Page
15921
DOI
10.1038/ncomms15921

Impact of patient navigation on timely cancer care: the Patient Navigation Research Program.

BACKGROUND: Patient navigation is a promising intervention to address cancer disparities but requires a multisite controlled trial to assess its effectiveness. METHODS: The Patient Navigation Research Program compared patient navigation with usual care on time to diagnosis or treatment for participants with breast, cervical, colorectal, or prostate screening abnormalities and/or cancers between 2007 and 2010. Patient navigators developed individualized strategies to address barriers to care, with the focus on preventing delays in care. To assess timeliness of diagnostic resolution, we conducted a meta-analysis of center- and cancer-specific adjusted hazard ratios (aHRs) comparing patient navigation vs usual care. To assess initiation of cancer therapy, we calculated a single aHR, pooling data across all centers and cancer types. We conducted a metaregression to evaluate variability across centers. All statistical tests were two-sided. RESULTS: The 10521 participants with abnormal screening tests and 2105 with a cancer or precancer diagnosis were predominantly from racial/ethnic minority groups (73%) and publically insured (40%) or uninsured (31%). There was no benefit during the first 90 days of care, but a benefit of navigation was seen from 91 to 365 days for both diagnostic resolution (aHR = 1.51; 95% confidence interval [CI] = 1.23 to 1.84; P < .001)) and treatment initiation (aHR = 1.43; 95% CI = 1.10 to 1.86; P < .007). Metaregression revealed that navigation had its greatest benefits within centers with the greatest delays in follow-up under usual care. CONCLUSIONS: Patient navigation demonstrated a moderate benefit in improving timely cancer care. These results support adoption of patient navigation in settings that serve populations at risk of being lost to follow-up.
Authors
Freund, KM; Battaglia, TA; Calhoun, E; Darnell, JS; Dudley, DJ; Fiscella, K; Hare, ML; LaVerda, N; Lee, J-H; Levine, P; Murray, DM; Patierno, SR; Raich, PC; Roetzheim, RG; Simon, M; Snyder, FR; Warren-Mears, V; Whitley, EM; Winters, P; Young, GS; Paskett, ED; Writing Group of the Patient Navigation Research Program,
MLA Citation
Freund, Karen M., et al. “Impact of patient navigation on timely cancer care: the Patient Navigation Research Program..” J Natl Cancer Inst, vol. 106, no. 6, June 2014. Pubmed, doi:10.1093/jnci/dju115.
URI
https://scholars.duke.edu/individual/pub1035603
PMID
24938303
Source
pubmed
Published In
J Natl Cancer Inst
Volume
106
Published Date
Start Page
dju115
DOI
10.1093/jnci/dju115

Acquisition of mitochondrial dysregulation and resistance to mitochondrial-mediated apoptosis after genotoxic insult in normal human fibroblasts: a possible model for early stage carcinogenesis.

Acquisition of death-resistance is critical in the evolution of neoplasia. Our aim was to model the early stages of carcinogenesis by examining intracellular alterations in cells that have acquired apoptosis-resistance after exposure to a complex genotoxin. We previously generated sub-populations of BJ-hTERT human diploid fibroblasts, which have acquired death-resistance following exposure to hexavalent chromium [Cr(VI)], a broad-spectrum genotoxicant. Long-term exposure to certain forms of Cr(VI) is associated with respiratory carcinogenesis. Here, we report on the death-sensitivity of subclonal populations derived from clonogenic survivors of BJ-hTERT cells treated with 5 μM Cr(VI) (DR1, DR2), or selected by dilution-based cloning without treatment (CC1). Following Cr(VI) treatment, CC1 cells downregulated expression of the anti-apoptotic protein Bcl-2 and exhibited extensive expression of cleaved caspase 3. In contrast, the DR cells exhibited no cleaved caspase 3 expression and maintained expression of Bcl-2 following recovery from 24 h Cr(VI) exposure. The DR cells also exhibited attenuated mitochondrial-membrane depolarization and mitochondrial retention of cytochrome c and SMAC/DIABLO following Cr(VI) exposure. The DR cells exhibited less basal mtDNA damage, as compared to CC1 cells, which correlates with intrinsic (non-induced) death-resistance. Notably, there was no difference in p53 protein expression before or after treatment among all cell lines. Taken together, our data suggest the presence of more resilient mitochondria in death-resistant cells, and that death-resistance can be acquired in normal human cells early after genotoxin exposure. We postulate that resistance to mitochondrial-mediated cell death and mitochondrial dysregulation may be an initial phenotypic alteration observed in early stage carcinogenesis.
Authors
Nickens, KP; Han, Y; Shandilya, H; Larrimore, A; Gerard, GF; Kaldjian, E; Patierno, SR; Ceryak, S
MLA Citation
Nickens, Kristen P., et al. “Acquisition of mitochondrial dysregulation and resistance to mitochondrial-mediated apoptosis after genotoxic insult in normal human fibroblasts: a possible model for early stage carcinogenesis..” Biochim Biophys Acta, vol. 1823, no. 2, Feb. 2012, pp. 264–72. Pubmed, doi:10.1016/j.bbamcr.2011.10.005.
URI
https://scholars.duke.edu/individual/pub985012
PMID
22057391
Source
pubmed
Published In
Biochimica Et Biophysica Acta
Volume
1823
Published Date
Start Page
264
End Page
272
DOI
10.1016/j.bbamcr.2011.10.005