Robert W. Hsieh, M.D. Ph.D. is a medical oncologist who specializes in the treatment of prostate cancer, bladder cancer, kidney (renal) cancer and testicular cancer as a member of Stanford's multi-disciplinary Urologic Cancer Program. Dr. Hsieh obtained his M.D. and Ph.D. degrees at the University of Chicago (Pritzker School of Medicine) and subsequently came to Stanford to complete his Internal Medicine residency and Hematology and Oncology fellowship training (with a clinical focus on genitourinary cancers).
Dr. Hsieh has also had extensive experience in basic lab research (cancer stem cells, target identification and validation, pre-clinical drug discovery) having done post-doctoral work in the Clarke Lab in the Institute for Stem Cell Biology and Regenerative Medicine. He is currently involved in early phase clinical trials in immuno-oncology in industry.
- Genitourinary Oncology
- Prostate Cancer
- Kidney (Renal) Cancer
- Bladder Cancer
- Testicular Cancer
- Medical Oncology
Honors & Awards
Project Grant (co-Principal Investigator), SPARK Translational Research Program (2018)
Fellowship Award, Stanford Cancer Institute (2015-2016)
Scholar Award, California Institute of Regenerative Medicine (CIRM) (2015-2016)
Fellows Recognition Award, National Comprehensive Cancer Network (NCCN) (2013)
The Leon O. Jacobson Basic Science Prize, The University of Chicago (2009)
Frank Family Fellowship, The University of Chicago (2006-2009)
Medical Scientist Training Program Award (MSTP), The University of Chicago (2001-2009)
Boards, Advisory Committees, Professional Organizations
Medical Oncology Board Certification, American Board of Internal Medicine (2016 - Present)
Internal Medicine Board Certification, American Board of Internal Medicine (2012 - Present)
Board Certification: American Board of Internal Medicine, Medical Oncology (2016)
Board Certification: American Board of Internal Medicine, Internal Medicine (2012)
Fellowship: Stanford University Hematology and Oncology Fellowship (2016) CA
Residency: Stanford University Internal Medicine Residency (2011) CA
Internship, Stanford University, Internal Medicine (2010)
M.D., The University of Chicago, Medicine (2009)
Ph.D., The University of Chicago, Biochemistry and Molecular Biology (2006)
B.S., Stanford University, Electrical Engineering and Biological Sciences (2001)
Robert W Hsieh. "United StatesCDK19"
Primary analysis of a randomized, double-blind, phase II study of the anti-TIGIT antibody tiragolumab (tira) plus atezolizumab (atezo) versus placebo plus atezo as first-line (1L) treatment in patients with PD-L1-selected NSCLC (CITYSCAPE).
AMER SOC CLINICAL ONCOLOGY. 2020
View details for Web of Science ID 000560368303408
Single-cell transcriptional diversity is a hallmark of developmental potential.
Science (New York, N.Y.)
2020; 367 (6476): 405–11
Single-cell RNA sequencing (scRNA-seq) is a powerful approach for reconstructing cellular differentiation trajectories. However, inferring both the state and direction of differentiation is challenging. Here, we demonstrate a simple, yet robust, determinant of developmental potential-the number of expressed genes per cell-and leverage this measure of transcriptional diversity to develop a computational framework (CytoTRACE) for predicting differentiation states from scRNA-seq data. When applied to diverse tissue types and organisms, CytoTRACE outperformed previous methods and nearly 19,000 annotated gene sets for resolving 52 experimentally determined developmental trajectories. Additionally, it facilitated the identification of quiescent stem cells and revealed genes that contribute to breast tumorigenesis. This study thus establishes a key RNA-based feature of developmental potential and a platform for delineation of cellular hierarchies.
View details for DOI 10.1126/science.aax0249
View details for PubMedID 31974247
Role of epithelial to mesenchymal transition associated genes in mammary gland regeneration and breast tumorigenesis.
2017; 8 (1): 1669
Previous studies have proposed that epithelial to mesenchymal transition (EMT) in breast cancer cells regulates metastasis, stem cell properties and chemo-resistance; most studies were based on in vitro culture of cell lines and mouse transgenic cancer models. However, the identity and function of cells expressing EMT-associated genes in normal murine mammary gland homeostasis and human breast cancer still remains under debate. Using in vivo lineage tracing and triple negative breast cancer (TNBC) patient derived xenografts we demonstrate that the repopulating capacity in normal mammary epithelial cells and tumorigenic capacity in TNBC is independent of expression of EMT-associated genes. In breast cancer, while a subset of cells with epithelial and mesenchymal phenotypes have stem cell activity, in many cells that have lost epithelial characteristics with increased expression of mesenchymal genes, have decreased tumor-initiating capacity and plasticity. These findings have implications for the development of effective therapeutic agents targeting tumor-initiating cells.
View details for PubMedID 29162812
View details for PubMedCentralID PMC5698470
Cryptococcal osteomyelitis and meningitis in a patient with non-hodgkin's lymphoma treated with PEP-C.
BMJ case reports
The authors present the first case report of a patient with lymphoma who developed disseminated cryptococcal osteomyelitis and meningitis while being treated with the PEP-C (prednisone, etoposide, procarbazine and cyclophosphamide) chemotherapy regimen. During investigation of fever and new bony lesions, fungal culture from a rib biopsy revealed that the patient had cryptococcal osteomyelitis. Further evaluation demonstrated concurrent cryptococcal meningitis. The patient's disseminated cryptococcal infections completely resolved after a full course of antifungal treatment. Cryptococcal osteomyelitis is itself an extremely rare diagnosis, and the unique presentation with concurrent cryptococcal meningitis in our patient with lymphoma was likely due to his PEP-C treatment. It is well recognised that prolonged intensive chemotherapeutic regimens place patients at risk for atypical infections; yet physicians should recognise that even chronic low-dose therapies can put patients at risk for fungal infections. Physicians should consider fungal infections as part of the infectious investigation of a lymphopaenic patient on PEP-C.
View details for DOI 10.1136/bcr.08.2011.4578
View details for PubMedID 22962380
Molecular characterization of a B-ring unsaturated estrogen: Implications for conjugated equine estrogen components of Premarin
2008; 73 (1): 59-68
Conjugated equine estrogens (CEEs) are routinely used for hormone replacement therapy (HRT), making it important to understand the activities of individual estrogenic components. Although 17beta-estradiol (17beta-E2), the most potent estrogen in CEE, has been extensively characterized, the actions of nine additional less potent estrogens are not well understood. Structural differences between CEEs and 17beta-E2 result in altered interactions with the two estrogen receptors (ERalpha and ERbeta) and different biological activities. To better understand these interactions, we have determined the crystal structure of the CEE analog, 17beta-methyl-17alpha-dihydroequilenin (NCI 122), in complex with the ERalpha ligand-binding domain and a peptide from the glucocorticoid receptor-interacting protein 1 (GRIP1) coactivator. NCI 122 has chemical properties, including an unsaturated B-ring and 17alpha-hydroxyl group, which are shared with some of the estrogens found in CEEs. Structural analysis of the NCI 122-ERalpha LBD-GRIP1 complex, combined with biochemical and cell-based comparisons of CEE components, suggests that factors such as decreased ligand flexibility, decreased ligand hydrophobicity and loss of a hydrogen bond between the 17-hydroxyl group and His524, contribute significantly to the reduced potency of CEEs on ERalpha.
View details for DOI 10.1016/j.ste.roids.2007.08.014
View details for Web of Science ID 000252602600007
View details for PubMedID 17949766
Identification of ligands with bicyclic scaffolds provides insights into mechanisms of estrogen receptor subtype selectivity
JOURNAL OF BIOLOGICAL CHEMISTRY
2006; 281 (26): 17909-17919
Estrogen receptors alpha (ERalpha) and beta (ERbeta) have distinct functions and differential expression in certain tissues. These differences have stimulated the search for subtype-selective ligands. Therapeutically, such ligands offer the potential to target specific tissues or pathways regulated by one receptor subtype without affecting the other. As reagents, they can be utilized to probe the physiological functions of the ER subtypes to provide information complementary to that obtained from knock-out animals. A fluorescence resonance energy transfer-based assay was used to screen a 10,000-compound chemical library for ER agonists. From the screen, we identified a family of ERbeta-selective agonists whose members contain bulky oxabicyclic scaffolds in place of the planar scaffolds common to most ER ligands. These agonists are 10-50-fold selective for ERbeta in competitive binding assays and up to 60-fold selective in transactivation assays. The weak uterotrophic activity of these ligands in immature rats and their ability to stimulate expression of an ERbeta regulated gene in human U2OS osteosarcoma cells provides more physiological evidence of their ERbeta-selective nature. To provide insight into the molecular mechanisms of their activity and selectivity, we determined the crystal structures of the ERalpha ligand-binding domain (LBD) and a peptide from the glucocorticoid receptor-interacting protein 1 (GRIP1) coactivator complexed with the ligands OBCP-3M, OBCP-2M, and OBCP-1M. These structures illustrate how the bicyclic scaffolds of these ligands are accommodated in the flexible ligand-binding pocket of ER. A comparison of these structures with existing ER structures suggests that the ERbeta selectivity of OBCP ligands can be attributed to a combination of their interactions with Met-336 in ERbeta and Met-421 in ERalpha. These bicyclic ligands show promise as lead compounds that can target ERbeta. In addition, our understanding of the molecular determinants of their subtype selectivity provides a useful starting point for developing other ER modulators belonging to this relatively new structural class.
View details for DOI 10.1074/jbc.M513684200
View details for Web of Science ID 000238490300041
View details for PubMedID 16648639
- Label-free detection of protein-protein interactions on biochips ANGEWANDTE CHEMIE-INTERNATIONAL EDITION 2005; 44 (34): 5480-5483
Interdigital cantilever as a biological sensor
1st IEEE Conference on Nanotechnology (IEEE-NANO 2001)
IEEE. 2001: 562–566
View details for Web of Science ID 000173446400104
High-speed atomic force microscopy in liquid
REVIEW OF SCIENTIFIC INSTRUMENTS
2000; 71 (5): 2097-2099
View details for Web of Science ID 000086794300027
High-speed tapping mode imaging with active Q control for atomic force microscopy
APPLIED PHYSICS LETTERS
2000; 76 (11): 1473-1475
View details for Web of Science ID 000085735800041