Christopher B. Dechet
· Professor (Clinical)VerifiedUniversity of Utah · Urology
Active 1999–2026
About
Christopher B. Dechet, MD, FACS, is a professor in the Division of Urology within the Department of Surgery at the Huntsman Cancer Institute at the University of Utah. He serves as the Director for the Section for Urologic Oncology and holds the Anderson Family Endowed Chair in Urologic Oncology. Dr. Dechet specializes in the surgical care of patients with urologic cancers, including prostate, kidney, bladder, adrenal, and testis cancer. His expertise encompasses robotic, laparoscopic, and open surgical approaches, and he has been using the Da Vinci robotic system since 2004, making him the most experienced robotic surgeon in the Intermountain West. He routinely performs robotic prostatectomy, robotic partial nephrectomy, and robotic cystectomy. Dr. Dechet has developed a comprehensive quality of life database aimed at improving surgical outcomes for prostate cancer and has pioneered robotic surgical approaches for treating high-risk prostate cancer. His extensive laparoscopic expertise has been recognized with an achievement award from the Society of Laparoscopic Surgeons. With a background that includes undergraduate studies at Stanford University and medical training at the University of Pennsylvania School of Medicine, where he received an American Heart Association research grant, Dr. Dechet completed his surgery and urology training at the Mayo Clinic. Over the past 20 years, he has received multiple awards, including the Patient Choice Physician Award, Most Compassionate Doctor Award, Vitals Top 10 Doctor Award, and Top Urologist Award. He is also known for his international presentations and visiting professorships in Italy and Austria, where he has performed nerve-sparing prostatectomy, robotic cystectomy, and partial nephrectomy.
Research topics
- Medicine
- Internal medicine
- Oncology
- Urology
- Biology
- Genetics
Selected publications
Cancer Research · 2026-03-13
articleAbstract Clear cell renal cell carcinoma (ccRCC), the most common subtype of kidney cancer, has been strongly associated with dysregulated lipid metabolism in obesity, known to contribute to ccRCC development. The mechanisms connecting obesity to ccRCC initiation and progression remain unclear. Ceramides, bioactive sphingolipids, influence mitochondrial function, metabolism, and cell fate. However, their role in ccRCC initiation and progression is not understood. We hypothesized that ceramides are essential intermediates linking lipid excess to the onset and progression of ccRCC. We leveraged lipidomics and transcriptomics data from the KidneyCare Study, a prospective cohort study that recruited 162 patients undergoing nephrectomy for a renal mass (stage I-IV) at the Huntsman Cancer Institute, University of Utah. After excluding 6 patients with systemic therapy prior to surgery, 68 patients with ccRCC had flash-frozen for downstream omics analyses. Targeted sphingolipid quantification was performed by LC-MS/MS using multiple reaction monitoring (MRM) and RNA sequencing (RNAseq). Among 47 normal and 72 tumor samples, we profiled 119 sphingolipids. We performed differential sphingolipid expression analysis and Lipid Ontology (LION) enrichment analysis comparing tumor vs. normal tissue lipids, and multi-omics analysis using integrative module analysis for multi-omics data (iModMix) integrating sphingolipids and RNAseq data to identify correlated features distinguishing tumor from normal tissue. A total of 79/119 (66%) sphingolipids were differentially expressed between tumor and normal tissue (t-test padjj < 0.05, > 1.5 fold-change). We found the ceramide Cer18:1;O2/24:1 (Cer 24:1) to be overexpressed in tumor vs. normal tissue. Cer 24:1 ceramides are directly associated with poor metabolic health, cardiovascular disease, and mortality. Applying iModMix identified 82 gene modules and 12 sphingolipid modules with ceramide modules being the most abundant. Highly correlated ceramides and transcriptomics module pairs included cell signaling pathways and lipid-related metabolic pathways. Our findings suggest that ceramide metabolism is significantly altered in ccRCC tumor vs. normal kidney. In the future, we will explore the potential link between Cer 24:1 overexpression and ccRCC progression. Citation Format: Augustine Takyi, Kyle Harshany, Gabriela Sandri, Olivia Rodriguez, Adam Taylor, Rebekah Nicolson, Christopher Dechet, Bogdana Schmidt, Brock O’Neil, Mei Koh, Scott Summers, Katsuhiko Funai, Mary Playdon, Cornelia Ulrich, John Alan. Maschek, Bing-Jian Feng, Paul Stewart, Alejandro Sanchez. Defining the role of ceramide metabolism in clear cell renal cell carcinoma progression [abstract]. In: Proceedings of the AACR Special Conference in Cancer Research: Innovations in Kidney Cancer Research: From Molecular Insights to Therapeutic Breakthroughs; 2026 Mar 13-16; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2026;86(5_Suppl_2):Abstract nr A030.
The Journal of Urology · 2025-04-08
articleJournal of Clinical Oncology · 2025-02-10
article38 Background: In a subset of patients with molecular-imaging defined recurrent oligometastatic prostate cancer (PCa), salvage oligometastatectomy with surgery and/or radiation may provide improved androgen deprivation therapy (ADT)-free survival. Methods: This is a phase II trial with oligorecurrent PCa after primary prostatectomy or radiation therapy detected on Axumin (n=11) or Prostate-Specific Membrane Antigen (PSMA) (n=9) positron emission tomography. Oligometastatic disease was defined as ≤ 10 total sites, either of lymph node (LN) only (Group A), bone only (Group B), or LN and bone (Group C). Surgical intervention for patients with LN disease included extended pelvic and/or retroperitoneal LN dissection, depending on the location of the LNs. Groups A and C received adjuvant IMRT without ADT if PSA response was ≥ 1/3 decrease but remained ≥ 0.2 ng/dL. The primary outcome was a reduction in PSA by ≥ 50% at 6 months. Secondary objectives included PSA progression free-survival (PSA-PFS), ADT-free survival, and safety. Results: We accrued a total of 20 patients. The median age was 65 years (IQR 61-70), 95% (19/20) had an ECOG of 0, and 10% (2/20) were Hispanic. All patients had a prior prostatectomy, after which 45% (9/20) received adjuvant/salvage RT, with 33% (3/9) including the pelvis/ prostate bed. 30% (6/20) had exposure to ADT before trial treatment. The median time from definitive prostate cancer treatment to trial treatment was 2.8 years (IQR: 0.9-6.0). Oligorecurrent disease occurred as lymph nodes only (18/20; 90%) or bony (2/20; 10%). Within Group A, one patient completed adjuvant RT. The average number of imaging-identified positive LNs was 1.8 (range 1-6). The primary endpoint of reduction in PSA by ≥ 50% at 6 months was 40% (95%CI 19-64%) (Table 1). The secondary endpoint of PSA-PFS at 12 months was 84.4% (95%CI 66.6-100%). ADT-free survival at 12-months was 71.4% (95% CI 52.7% - 96.6%). There were no Clavien Grade III-IV complications. Conclusions: Salvage treatment of oligometastatic disease after prostatectomy or radiation identified on molecular imaging is feasible and safe. Nearly half the cohort had a good response to salvage treatment, demonstrated by a ≥ 50% reduction in PSA at 6 months. Ongoing analyses include comparing imaging and pathology correlations, and comparing complete/ partial responders and treatment failure. Further research is needed to identify ideal candidates for salvage treatment. Clinical trial information: NCT03796767 . PSA progression-free survival at 6- and 12-months (PFS). Time Estimate 95% Confidence Interval 6 months 100% --- 12 months 84.4% 66.6-100%
Journal for ImmunoTherapy of Cancer · 2025-03-01 · 4 citations
articleOpen accessBACKGROUND: Muscle-invasive urothelial cancer (UC) has a high risk of recurrence after definitive treatment. Nivolumab adjuvant to radical surgery improves disease-free survival in patients with UC with a high risk of recurrence; however, its role adjuvant to chemoradiation therapy (CRT) is unknown. METHODS: The NEXT trial is a single-arm, phase-2 study evaluating the efficacy and tolerability of nivolumab adjuvant to CRT in patients with localized or locoregional UC. The primary endpoint is failure-free survival (FFS) at 2 years. Secondary endpoints include patterns of recurrence, toxicity and quality of life (QoL). Plasma cell-free DNA (cfDNA) was subjected to shallow whole-genome sequencing to correlate with outcomes. RESULTS: 28 patients were enrolled and received 480 mg of nivolumab intravenously every 4 weeks for up to 12 cycles adjuvant to CRT. The FFS at 2 years was 33.2% (95% CI 18.5% to 59.6%). Nine (32%) patients had localized progression, and eight (29%) had distant progression. 25 (89%) had one or more high-risk features (ie, plasmacytoid differentiation, T4, N+, multiple tumors, tumors >5 cm, residual disease before CRT, carcinoma in situ, and hydronephrosis). Patients with ≤2 high-risk features had a median FFS of 45.2 months (95% CI 14.56 to not reached (NR)) compared with 8.2 months (95% CI 7.1 to NR) in those with three or more risk features (p=0.0024). Nivolumab-associated treatment-related adverse events occurred in 18 (64.3%) patients, only 3 had grade 3 TRAEs, with significant changes in QoL. Plasma cfDNA copy number instability (CNI) scores ≤25 before the first dose of adjuvant nivolumab and at cycle 4 were associated with better overall survival compared with CNI scores ≥26 (49.6 months vs 20.5 months, p=0.0024). Genome copy number changes indicated chromatin remodeling and tyrosine kinase pathways, among others, as oncogenic drivers implicated in progression. CONCLUSION: Nivolumab adjuvant to CRT in localized or locally advanced UC is well tolerated. Stratification by risk factors and correlation with plasma cfDNA analyses generate hypotheses for potential patient selection and putative therapeutic targets for future study. TRIAL REGISTRATION NUMBER: NCT03171025.
ESMO Open · 2025-09-01
articleOpen accessJournal of Clinical Oncology · 2025-05-28
articlee17057 Background: Currently non-specific protein factors (Alkaline Phosphatase-ALK, LDH, albumin) are used for identifying prognostic risk groups in mCRPC. We explored NGS-based proteome sequencing for scalable and high-throughput plasma proteomic profiling for developing an integrated approach of mCRPC tumor-biology associated proteins with existing biomarkers based on patient-centric nomograms that estimate 6-, 12- and 24-months overall survival (OS) probabilities. Methods: Proteomic profiling of plasma for 3,072 proteins using Olink Explore NGS platform was performed in 32 local stage prostate cancer, 123 metastatic hormone-sensitive (mHSPC) and 157 mCRPC state samples (Total N = 312) in a clinically annotated real-world cohort study. Proteins were measured in Normalized Protein eXpression (NPX) units. NPX values of all proteins across all three cancer states were compared to identify Differentially Expressed Proteins (DEPs) exclusively to mCRPC using t-test with multiple corrections. Clinical outcome in the mCRPC was overall survival (OS) and Hazard Ratios (HRs) for mCRPC-DEPs with significant (P<0.05) association with survival at a univariate level were build into an aggregated composite score generated by multiplying each individual DEP’s univariate-level survival HR coefficient with the corresponding NPX value. The “Composite Proteome Prognostic Score (CPPS)” range for the mCRPC cohort (N = 121 pts) was dichotomized above and below the cohort median as “High” and “Low” and evaluated using Cox Proportional Hazard Regression along with current prognostic protein biomarkers (PSA, LDH, Alkaline Phosphatase and Albumin) at the univariate level and included in multi-variable analysis (MVA) for univariate-level significant (P<0.05) variables. Prognostic nomogram integrating MVA significant clinical factors with the CPPS was developed and nomogram performance with and without CPPS for estimating 6-,12- and 24-months survival was determined using Area Under Curve (AUC). Results: Median OS of the mCRPC cohort (N = 157) was 28 months (range: 0.3-45). 866/3072 DEPs were exclusive to mCRPC and 252/866 associated with OS (HR > 1; P < 0.05). 102/252 DEPs were significant after multiple correction (FDR < 0.05). The top 20 DEPs were used to generate CPPS. The CPPS HR value of 3.48 (95% CI: 1.77-6.83) was higher compared to known clinical factors including PSA, LDH , Alkaline Phosphatase, Albumin. AUCs for estimating mCRPC OS probabilities integrating CPPS with clinical factors versus clinical factors alone increased to 0.90 from 0.83 (6-months); 0.86 from 0.72 (12-months) and 0.76 from 0.69 (24-months). Conclusions: A patient-centric nomogram to estimate survival in mCRPC which includes novel protein classifiers can enhance current prognostication models.
International Journal of Radiation Oncology*Biology*Physics · 2025-02-07 · 2 citations
articleClinical Proteomics · 2025-04-18 · 1 citations
articleOpen accessBACKGROUND: Plasma-based high-plex proteomic profiling were performed in prostate cancer (PC) patients using the Olink® Explore Proximity Extension Assay to identify plasma proteins associated in different PC states and to explore potential prognostic biomarkers. The progressive PC states include local, organ-confined PC (local PC), metastatic hormone-sensitive PC (mHSPC) and metastatic castrate-resistant PC (mCRPC). METHODS: Plasma samples were uniformly processed from 84 PC patients (10 patients with local PC; 29 patients with mHSPC; 45 patients with mCRPC). A proteome-wide association study was performed to identify proteins differentially overexpressed in progressive cancer states. Specifically, a sequential screening approach was employed where proteins overexpressed from one disease state were assessed for overexpression in the progressive disease state. Linear regression, analysis of variance, and t-tests were used for this approach. Differentially expressed proteins (DEPs) in mCRPC were then used to construct a prognostic model for overall survival (OS) in mCRPC patients using the Cox Proportional Hazard Model. The predictive performance of this model was assessed using time-dependent area under the receiver operating characteristic curves (tAUC) in an independent sample of mCRPC patients. The tAUC of the prognostic model was then compared to that of a model excluding DEPs to evaluate the added value of circulatory proteins in predicting survival. RESULTS: Of 736 tumor-associated proteins, 26 were differentially expressed across local PC, mHSPC, and mCRPC states. Among these, 20 were overexpressed in metastatic states compared to local, and in mCRPC compared to mHSPC states. Of these 20 proteins, Ribonucleoside-diphosphate reductase subunit M2 (RRM2) was identified as a prognostic biomarker for OS in mCRPC, with a hazard ratio of 2.30 (95% confidence interval (CI) 1.17-4.51) per normalized expression unit increase. The tAUC of the model including previously identified clinical prognostic factors was 0.62 (95% CI 0.29-0.91), whereas the model that includes RRM2 with clinical prognostic factors was 0.87 (95% CI 0.51-0.98). CONCLUSIONS: Plasma proteome profiling can identify novel circulatory DEPs associated with mCRPC state survivals. Overexpression of RRM2 is linked to poor mCRPC survival and its inclusion alongside conventional prognostic factors enhances the predictive performance of the prognostic model.
Journal of Clinical Oncology · 2025-02-10
article225 Background: Currently non-specific clinical factors including non-tumor biology proteins (Alkaline Phosphatase-ALK, LDH, albumin) are used for identifying high, intermediate or low prognostic survival risk in mCRPC. We integrated these biomarkers with plasma proteins overexpressed exclusively in mCRPC to develop patient-centric nomograms for estimating 1,2 and 3-year (yr) overall survival (OS) probabilities. Methods: Proteomic profiling of plasma for 3072 proteins using Olink Explore NGS platform was performed in 32 local stage prostate cancer, 123 metastatic hormone-sensitive (mHSPC) and 157 mCRPC state samples (Total N=312) in a clinically annotated real-world cohort study that enrolled patients (pts) between 2020 and 2024. Protein assays were measured in normalized protein expression (NPX) units through a normalization process. We compared NPX values of all protein assays across all three cancer states to identify Differentially Expressed Proteins (DEPs) exclusively overexpressed in mCRPC using t-test with multiple corrections. Clinical outcome in the mCRPC was OS. A composite score was generated aggregating DEPs overexpressed in mCRPC with OS, by multiplying each individual DEP’s univariate-level survival Hazard Ratio (HR) coefficient with their corresponding NPX value. The composite score range for the mCRPC cohort (N=121 pts) was dichotomized above and below the cohort median as “High” and “Low” and evaluated for survival using Cox Proportional Hazard Regression along with current prognostic protein biomarkers (ALK, LDH, albumin) at the univariate followed by multi-variable analysis (MVA) for variables observed with univariate significance (P<0.05). Prognostic nomograms integrating MVA significant clinical factors with the DEP composite score was developed and performance of the nomogram with and without the composite score for estimating 1,2 and 3-years survival probabilities was determined using ROC curves and Area Under Curve (AUC). All analyses were conducted in RStudio. Results: Median OS of the mCRPC cohort (N=121) was 28 months (range: 0.3-45). There were 353/3072 DEPs exclusive to mCRPC and 19/353 DEPs were associated with OS (univariate P<0.05) (SCRN1, GP2, NFU1, DPY30, SNRPB2, KRT19, FKBP5, PGD, IL6, L3HYPDH, MYDGF, DH1, IQGAP2, TOMM20, YAP1, CLGN, IMMT, PKD2, PALM2). MVA Hazard Ratios (HR) with 95% CIs for nomogram input included: DEP score HR-3.48 (1.77-6.83; P<0.0003); LDH: HR-1.01 (1-1; P=0.13); ALK: HR-1 (1-1; P=0.000035); Albumin: HR-0.61 (0.24-1.51; P=0.28). AUCs for estimating mCRPC OS probabilities integrating the DEP score with current factors versus clinical factors alone increased to 0.87 from 0.85 (1-yr); to 0.78 from 0.73(2-yr) and to 0.79 from 0.70 (3-yr). Conclusions: A patient-centric approach using nomograms to estimate survival in mCRPC which includes novel protein classifiers can enhance current prognostication models.
Clinical Genitourinary Cancer · 2024-02-17 · 4 citations
article
Frequent coauthors
- 63 shared
Jonathan D. Tward
- 62 shared
William T. Lowrance
Bon Secours Hospital
- 55 shared
Benjamin L. Maughan
Huntsman Cancer Institute
- 48 shared
Sumati Gupta
Huntsman Cancer Institute
- 48 shared
Brock O’Neil
Community Living
- 46 shared
Neeraj Agarwal
University of Utah
- 39 shared
Alejandro Sánchez
The University of Texas at El Paso
- 36 shared
Robert A. Stephenson
University of Utah
Education
B.S.
Stanford University
M.D.
University of Pennsylvania, School of Medicine
Other, Surgery and Urology
Mayo Clinic
Awards & honors
- Achievement award from the Society of Laparoscopic Surgeons
- American Heart Associate research grant
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