Shiao-Wen David Hsu

Positions:

Associate Professor of Medicine

Medicine, Medical Oncology
School of Medicine

William Dalton Family Assistant Professor of Medical Oncology, in the School of Medicine

Medicine, Medical Oncology
School of Medicine

Member of the Duke Cancer Institute

Duke Cancer Institute
School of Medicine

Education:

M.D. 2001

University of North Carolina at Chapel Hill

Medical Resident, Medicine

University of Texas at Dallas

Fellow in Hematology-Oncology, Medicine

Duke University

Grants:

Identifying gene-environment interactions that confer metabolic vulnerabilities in cancer

Administered By
Pharmacology & Cancer Biology
Awarded By
National Institutes of Health
Role
Collaborator
Start Date
End Date

Targeting KRAS (G12C) Mutant in Colorectal Cancer

Administered By
Medicine, Medical Oncology
Role
Principal Investigator
Start Date
End Date

Determining the Efficacy of Liposomal Gemcitabine in Patient Derived Xenografts (PDXs)

Administered By
Medicine, Medical Oncology
Role
Principal Investigator
Start Date
End Date

Targeting the TK1 receptor in colorectal and lung PDX using CarT cell and Motorcar cell

Administered By
Medicine, Medical Oncology
Role
Principal Investigator
Start Date
End Date

Targeting Calreticulin in Colorectal Cancer Liver Metastasis

Administered By
Medicine, Medical Oncology
Awarded By
National Institutes of Health
Role
Principal Investigator
Start Date
End Date

Publications:

Mismatch repair gone awry: Management of Lynch syndrome.

The hallmark of Lynch syndrome involves germline mutations of genes important in DNA mismatch repair. Affected family kindreds will have multiple associated malignancies, the most common of which is colorectal adenocarcinoma. Recently, evidence has shown that clinical diagnostic criteria provided by the Amsterdam Criteria and the Bethesda Guidelines must be linked with microsatellite instability testing to correctly diagnose Lynch syndrome. We present a case of metachronous colorectal adenocarcinomas in a patient less than 50 years of age, followed by a discussion of Lynch syndrome, with an emphasis on surveillance and prevention of malignancies.
Authors
Zhang, T; Boswell, EL; McCall, SJ; Hsu, DS
MLA Citation
Zhang, Tian, et al. “Mismatch repair gone awry: Management of Lynch syndrome..” Crit Rev Oncol Hematol, vol. 93, no. 3, Mar. 2015, pp. 170–79. Pubmed, doi:10.1016/j.critrevonc.2014.10.005.
URI
https://scholars.duke.edu/individual/pub1051217
PMID
25459670
Source
pubmed
Published In
Crit Rev Oncol Hematol
Volume
93
Published Date
Start Page
170
End Page
179
DOI
10.1016/j.critrevonc.2014.10.005

Retraction for Garman et al: A genomic approach to colon cancer risk stratification yields biologic insights into therapeutic opportunities.

Authors
Garman, KS; Acharya, CR; Edelman, E; Grade, M; Gaedcke, J; Sud, S; Barry, W; Diehl, AM; Provenzale, D; Ginsburg, GS; Ghadimi, BM; Ried, T; Nevins, JR; Mukherjee, S; Hsu, D; Potti, A
MLA Citation
Garman, Katherine S., et al. “Retraction for Garman et al: A genomic approach to colon cancer risk stratification yields biologic insights into therapeutic opportunities..” Proc Natl Acad Sci U S A, vol. 108, no. 42, Oct. 2011. Pubmed, doi:10.1073/pnas.1115170108.
URI
https://scholars.duke.edu/individual/pub768489
PMID
21969600
Source
pubmed
Published In
Proc Natl Acad Sci U S A
Volume
108
Published Date
Start Page
17569
DOI
10.1073/pnas.1115170108

Gene expression signatures, clinicopathological features, and individualized therapy in breast cancer.

CONTEXT: Gene expression profiling may be useful for prognostic and therapeutic strategies in breast carcinoma. OBJECTIVES: To demonstrate the value in integrating genomic information with clinical and pathological risk factors, to refine prognosis, and to improve therapeutic strategies for early stage breast cancer. DESIGN, SETTING, AND PATIENTS: Retrospective study of patients with early stage breast carcinoma who were candidates for adjuvant chemotherapy; 964 clinically annotated breast tumor samples (573 in the initial discovery set and 391 in the validation cohort) with corresponding microarray data were used. All patients were assigned relapse risk scores based on their respective clinicopathological features. Signatures representing oncogenic pathway activation and tumor biology/microenvironment status were applied to these samples to obtain patterns of deregulation that correspond with relapse risk scores to refine prognosis with the clinicopathological prognostic model alone. Predictors of chemotherapeutic response were also applied to further characterize clinically relevant heterogeneity in early stage breast cancer. MAIN OUTCOME MEASURES: Gene expression signatures and clinicopathological variables in early stage breast cancer to determine a refined estimation of relapse-free survival and sensitivity to chemotherapy. RESULTS: In the initial data set of 573 patients, prognostically significant clusters representing patterns of oncogenic pathway activation and tumor biology/microenvironment states were identified within the low-risk (log-rank P = .004), intermediate-risk (log-rank P = .01), and high-risk (log-rank P = .003) model cohorts, representing clinically important genomic subphenotypes of breast cancer. As an example, in the low-risk cohort, of 6 prognostically significant clusters, patients in cluster 4 had an inferior relapse-free survival vs patients in cluster 1 (log-rank P = .004) and cluster 5 (log-rank P = .03). Median relapse-free survival for patients in cluster 4 was 16 months less than for patients in cluster 1 (95% CI, 7.5-24.5 months) and 19 months less than for patients in cluster 5 (95% CI, 10.5-27.5 months). Multivariate analyses confirmed the independent prognostic value of the genomic clusters (low risk, P = .05; high risk, P = .02). The reproducibility and validity of these patterns of pathway deregulation in predicting relapse risk was established using related but not identical clusters in the independent validation cohort. The prognostic clinicogenomic clusters also have unique sensitivity patterns to commonly used cytotoxic therapies. CONCLUSIONS: These results provide preliminary evidence that incorporation of gene expression signatures into clinical risk stratification can refine prognosis. Prospective studies are needed to determine the value of this approach for individualizing therapeutic strategies.
Authors
Acharya, CR; Hsu, DS; Anders, CK; Anguiano, A; Salter, KH; Walters, KS; Redman, RC; Tuchman, SA; Moylan, CA; Mukherjee, S; Barry, WT; Dressman, HK; Ginsburg, GS; Marcom, KP; Garman, KS; Lyman, GH; Nevins, JR; Potti, A
MLA Citation
Acharya, Chaitanya R., et al. “Gene expression signatures, clinicopathological features, and individualized therapy in breast cancer..” Jama, vol. 299, no. 13, Apr. 2008, pp. 1574–87. Pubmed, doi:10.1001/jama.299.13.1574.
URI
https://scholars.duke.edu/individual/pub715760
PMID
18387932
Source
pubmed
Published In
Jama
Volume
299
Published Date
Start Page
1574
End Page
1587
DOI
10.1001/jama.299.13.1574

Adjuvant chemotherapy for t1 node-positive colon cancers provides significant survival benefit.

BACKGROUND: Contemporary treatment of node-positive (N+) colon cancer consists of adjuvant chemotherapy; however, randomized data supporting this practice were derived from lesions T2 or greater. Minimal data exist regarding the use and need for adjuvant chemotherapy in T1N+ disease. OBJECTIVE: The aim of this study was to determine treatment trends and the effects of adjuvant chemotherapy on T1N+ colon cancers by using the National Cancer Database. DESIGN: This was a retrospective study. Baseline demographics, tumor, and cancer treatment characteristics were compared. Groups were matched on the propensity to receive chemotherapy. Adjusted long-term survival stratified by chemotherapy use was compared by using the Kaplan-Meier method with the log-rank test. Predictors of not receiving chemotherapy were identified by using a multivariable logistic regression model. SETTINGS: Data were collected from the National Cancer Database, which collects cancer data from over 1500 cancer centers. PATIENTS: We identified patients from 1998 to 2006 with T1N+ disease, excluding those with metastatic disease or previous cancer. Patients were stratified based on whether or not they received chemotherapy. MAIN OUTCOME MEASURES: The primary outcome measure of this study was long-term survival. RESULTS: Three thousand one hundred thirty-seven patients had T1N+ disease; 70.6% (n = 2216) received chemotherapy, and utilization significantly increased from 1998 to 2011 (p < 0.001). Unadjusted analysis revealed that patients treated with chemotherapy were statistically younger and healthier, and had shorter postoperative lengths of stay (all p < 0.001). Unadjusted 5-year survival was higher in patients receiving chemotherapy (87.9% vs 63.0% in patients with no chemotherapy; p < 0.001) and this persisted after propensity matching with (83.4% and 63.0% in patients with or without chemotherapy; p < 0.001). Only age (OR, 0.29; p < 0.001) predicted not receiving chemotherapy. LIMITATIONS: Limitations include potential selection bias as well as the inability to compare disease-free survival/recurrence. CONCLUSIONS: Adjuvant chemotherapy appears to significantly improve long-term survival in patients receiving chemotherapy in T1N+ disease. Thus, the use of chemotherapy in T1N+ disease is justified and provides a highly significant survival benefit.
Authors
Ganapathi, AM; Speicher, PJ; Englum, BR; Castleberry, AW; Migaly, J; Hsu, DS; Mantyh, CR
MLA Citation
Ganapathi, Asvin M., et al. “Adjuvant chemotherapy for t1 node-positive colon cancers provides significant survival benefit..” Dis Colon Rectum, vol. 57, no. 12, Dec. 2014, pp. 1341–48. Pubmed, doi:10.1097/DCR.0000000000000245.
URI
https://scholars.duke.edu/individual/pub1049452
PMID
25379998
Source
pubmed
Published In
Dis Colon Rectum
Volume
57
Published Date
Start Page
1341
End Page
1348
DOI
10.1097/DCR.0000000000000245

Erratum: Characterizing the developmental pathways TTF-1, NKX2-8, and PAX9 in lung cancer (Proceedings of the National Academy of Sciences of the United States of America (2009) 106, 13 (5312-5317) DOI: 10.1073/pnas.0900827106)

Authors
Hsu, DS; Acharya, CR; Balakumaran, BS; Riedel, RF; Kim, MK; Stevenson, M; Tuchman, S; Mukherjee, S; Barry, W; Dressman, HK; Nevins, JR; Powers, S; Mu, D; Potti, A
MLA Citation
Hsu, D. S., et al. “Erratum: Characterizing the developmental pathways TTF-1, NKX2-8, and PAX9 in lung cancer (Proceedings of the National Academy of Sciences of the United States of America (2009) 106, 13 (5312-5317) DOI: 10.1073/pnas.0900827106).” Proceedings of the National Academy of Sciences of the United States of America, vol. 108, no. 35, Aug. 2011. Scopus, doi:10.1073/pnas.1111196108.
URI
https://scholars.duke.edu/individual/pub769520
Source
scopus
Published In
Proceedings of the National Academy of Sciences of the United States of America
Volume
108
Published Date
Start Page
14705
DOI
10.1073/pnas.1111196108