About

Dr. Alejandro Sanchez is an Assistant Professor in the Division of Urology at the University of Utah School of Medicine and a Huntsman Cancer Institute investigator. He specializes in the surgical care of patients with urologic cancers, utilizing open, laparoscopic, robotic, and endoscopic techniques. His practice at the Huntsman Cancer Institute primarily focuses on the multidisciplinary treatment of prostate, bladder, kidney, testicular, adrenal, urethral, and penile cancers. He received his undergraduate degree from the University of Florida, graduating Summa Cum Laude in Biochemistry. He earned his medical degree from Harvard Medical School and completed his urologic surgery training at Massachusetts General Hospital. Dr. Sanchez further completed a fellowship in urologic oncology at Memorial Sloan Kettering Cancer Center, where he received a Young Investigator Award from the American Society of Urologic Oncology for his research on the mechanisms underlying the association of sarcopenia and poor oncologic outcomes in patients with clear cell renal cell carcinoma. During his fellowship, he also received the Chairman’s Award for Excellence in Basic Science. His research efforts are primarily focused on clinical trial development and translational research, contributing to advancements in the treatment of urologic cancers.

Research topics

• Biology
• Pathology
• Oncology
• Biochemistry
• Biophysics
• Medical physics
• Internal medicine
• Gynecology
• Immunology
• Medicine
• Chemistry
• Cancer research
• Cell biology

Selected publications

• Cardiovascular Disease in a Population-Based Cohort of Prostate Cancer Patients With Long-Term Follow-Up

  Clinical Genitourinary Cancer · 2026-03-28

  article
  PublisherDOI

• Abstract 3627: Metabolomic signatures of physical activity in treatment-naive patients with early-onset vs. late-onset colorectal cancer: Results from the ColoCare Study

  Cancer Research · 2026-04-03

  article

  Abstract Introduction: Emerging studies link physical inactivity to early-onset colorectal cancer (EOCRC), but most rely on subjective measures of physical activity (PA). Metabolite signatures may offer an objective measure of PA that also captures the systemic metabolic response to activity. We assessed a previously validated PA metabolomic signature in patients with recently diagnosed colorectal cancer (CRC) and compared profile scores between patients with EOCRC (<50 yrs) vs. non-EOCRC (>50 yrs). Methods: We examined baseline (pre-surgery) data from 122 stage I-III patients with CRC in the ColoCare Study at Huntsman Cancer Institute (Utah) and Heidelberg University Hospital (Germany). PA for the previous year was measured with the International Physical Activity Questionnaire-Short Form. Untargeted serum metabolites and complex lipids were profiled at the West Coast Metabolomics Center. We calculated a 24-metabolite PA signature developed in >6,000 cancer-free individuals (Papadimitriou et al., CEBP, 2025) consisting of acylcarnitines, glycerophospholipids, monosaccharides, amino acids, and sphingolipids. Following metabolite pre-processing, normalization, and scaling, we performed multivariable linear regression on 20 metabolites available in our dataset, adjusting for age, sex, tumor stage, and body mass index (BMI). Metabolite scores were calculated for each participant by multiplying normalized metabolite concentrations by the previously developed PA metabolite signature coefficients and were then compared between EOCRC vs. non-EOCRC survivors. Results: Compared to patients with non-EOCRC (67±9 years, N=102), those with EOCRC (39±10 years, N=20) were diagnosed with higher stages (55% vs. 43% stage III), had lower prevalence of obese BMI (25% vs. 37%), and were more physically active (16±17 metabolic equivalent (MET) hrs/week vs. 11±17 MET hrs/week), p>0.05. Patients with EOCRC were more likely to meet PA guidelines (>150 min/week of moderate to vigorous PA; 60% vs. 38%) compared to those with non-EOCRC, p>0.05. Among the 20 metabolites investigated in our data, 15 showed a consistent direction of association with the previously developed PA signature. Patients with EOCRC had higher scores of the PA metabolite signature (0.04±0.09) than older patients (-0.01±0.10), t=2.3, p=0.03. This modest association remained significant after adjustment for stage, sex, and BMI (β=0.05, p=0.048). Conclusions: A PA metabolite signature showed comparable associations to questionnaire-derived PA measures in our CRC survivor cohort, consistent with findings in healthy individuals. Patients with EOCRC reported a higher level of PA compared to those with non-EOCRC and had a significantly higher PA metabolite signature score. The metabolite response to PA may clarify how physical inactivity influences EOCRC risk and outcomes. Citation Format: Victoria Maria Bandera, Tengda Lin, Patricia Erickson, Caroline Himbert, Aik Choon Tan, Mary C. Playdon, Alan Maschek, Paul Stewart, Sheetal Hardikar, Elaine M. Glenny, Jennifer Ose, Victoria Damerell, Christy A. Warby, Olena Aksonova, Oliver Fiehn, Kenneth Boucher, Peter Schirmacher, Ildiko Strehli, Megan Mclaws, Alejandro Sanchez, Jolanta Jedrzkiewicz, Lyen C. Huang, Vaia Florou, Jessica N. Cohan, Alexander Brobeil, Hans-Ulrich Kauczor, Christoph Kahlert, Meghana Karchi, Elizabeth H. Wood, Doratha A. Byrd, Erin M. Siegel, Adetunji T. Toriola, David Shibata, Christopher I. Li, Jane C. Figueiredo, Biljana Gigic, Jatin Roper, Stephen Hursting, Cornelia M. Ulrich. Metabolomic signatures of physical activity in treatment-naive patients with early-onset vs. late-onset colorectal cancer: Results from the ColoCare Study [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2026; Part 1 (Regular Abstracts); 2026 Apr 17-22; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2026;86(7 Suppl):Abstract nr 3627.

  PublisherDOI

• Abstract A030: Defining the role of ceramide metabolism in clear cell renal cell carcinoma progression

  Cancer Research · 2026-03-13

  articleSenior author

  Abstract 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.

  PublisherDOI

• Abstract 4912: Assessing transcriptomic profiles of visceral adipose tissue in colon cancer patients

  Cancer Research · 2025-04-21

  article

  Background: Obesity is a major risk factor for colon cancer (CC) with a number of potential biologic mechanisms. Visceral adipose tissue (VAT) has been identified as a key contributor, partly due to its secretion of adipokines and proinflammatory cytokines. VAT has also been associated with worse cancer-related outcomes. In this study, we evaluated transcriptomic differences in patients with high versus low amounts of VAT among people with CC. Methods: Tumor-adjacent VAT was collected in 60 patients diagnosed with stage I-III CC who underwent primary surgery as part of the ColoCare Study at Huntsman Cancer Institute (HCI), University of Utah, and University of Heidelberg, Germany. Bulk transcriptomic analysis (RNAseq) was performed on VAT at the HCI genomics core. Computed tomography (CT) scans were used to measure visceral fat area (VFA) via body composition analysis performed using the Data Analysis Facilitation Suite (DAFS). The “DESeq2” R package was used to identify differentially expressed genes stratified by VFA (low VFA: <175 cm2, high VFA ≥ 175 cm2), adjusting for age at diagnosis, sex, study site, and tumor stage. Ranked/sorted genes were entered into gene set enrichment analysis (GSEA) software to identify enriched gene sets and pathways. Results: Among the 60 patients included the study, 53% were male, the mean age at diagnosis was 63±13 years, 45% had stage III CC, and the mean VFA was 182±105 cm2. Among patients with high VFA, 173 genes were differentially expressed compared to those with low VFA. GSEA identified 17 significantly upregulated and 20 significantly downregulated gene sets (p-adj. < 0.05). Upregulated gene sets among patients with high VFA included pathways were related to extracellular matrix signaling, pyrimidine metabolism, and cytokine-cytokine receptor interactions, while downregulated gene sets included pathways related to branched-chain amino-acid degradation, propanoate metabolism, and pyruvate metabolism. Discussion: VAT in patients with high levels of visceral adiposity was characterized by the overexpression of pathways that are thought to be associated with CRC development and progression. Our next steps involve further evaluation of these findings in a larger cohort, along with an assessment of VAT gene expression in relation to survival. Citation Format: Patricia A. Erickson, Victoria M. Bandera, Bettina Katalin Budai, Tengda Lin, Caroline Himbert, Sheetal Hardikar, Jeffrey T. Yap, Elaine M. Glenny, Aik Choon Tan, Jennifer Ose, Christy A. Warby, Olena Aksonova, Tobias Nonnenmacher, Chris Stubben, David Nix, Kenneth Boucher, Peter Schirmacher, Ildiko Strehli, Alejandro Sanchez, Jolanta Jedrzkiewicz, Lyen C. Huang, Jessica N. Cohan, Alexander Brobeil, Hans-Ulrich Kauczor, Christoph Kahlert, Victoria Damerell, Erin M. Siegel, Doratha A. Byrd, Adetunji T. Toriola, David Shibata, Christopher I. Li, Jane C. Figueiredo, Jatin Roper, Biljana Gigic, Stephen Hursting, Cornelia M. Ulrich. Assessing transcriptomic profiles of visceral adipose tissue in colon cancer patients [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2025; Part 1 (Regular Abstracts); 2025 Apr 25-30; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2025;85(8_Suppl_1):Abstract nr 4912.

  PublisherDOI

• Abstract PR007: Tumor-adjacent visceral adipose tissue displays an altered transcriptomic landscape in early-onset colorectal cancer patients: Results from the ColoCare Study

  Clinical Cancer Research · 2025-12-10

  article

  Abstract Introduction: Obesity is commonly characterized by high levels of internal (visceral) adiposity. Visceral adipose tissue (VAT) is highly metabolically active and secretes proteins and metabolites in paracrine and endocrine signaling pathways. The phenotype of tumor-adjacent VAT may be an unexplored factor for risk and progression of early-onset colorectal cancer (EOCRC). Thus, we aimed to identify transcriptomic differences in tumor-adjacent visceral adipose tissue (VAT) in patients with EOCRC (<50 years at diagnosis) vs. those diagnosed with later-onset colorectal cancer (LOCRC; >50 years at diagnosis). Methods: VAT samples were collected from 332 patients with stage 0-III colorectal cancer enrolled in the ColoCare Study and recruited at Huntsman Cancer Institute (Utah), Heidelberg University Hospital (Germany), University of Tennessee Health Science Center (Tennessee), and Moffitt Cancer Center (Florida). Patients in our study were treatment naïve. VAT tissue was collected 1-3 cm from the colorectal tumor during surgery. VAT transcriptomes were measured with bulk RNA sequencing. Participants were classified as EOCRC vs. LOCRC. Normalized differentially expressed genes were identified (DESeq2), with analyses adjusted for sex, body mass index (BMI), study site, and tumor stage. Gene set enrichment analysis (GSEA) identified enriched pathways within the 2025 Hallmark gene sets. Significance was assessed using false discovery rate (FDR) p-adj<0.05. We replicated our analyses, adjusting for tumor site (colon vs. rectal), to account for potential differences by anatomical subgroup. Results: Patients with EOCRC (n=45, average age: 41±9 years) had higher disease stages compared to LOCRC patients (n=287, average age: 66±10 years) (EOCRC: 64% Stage III vs LOCRC: 39% Stage III) and similar BMI (EOCRC: 28.8±7.0 kg/m2 vs. LOCRC: 28.5±5.9 kg/m2). GSEA revealed 5 significantly enriched gene sets (FDR p-adj<0.05) in VAT when comparing EOCRC to LOCRC patients. VAT of EOCRC patients exhibited upregulation of immune pathways (Interferon Alpha Response, Interferon Gamma Response, TNFA Signaling via NF- κB), and fibrosis Hallmark pathways (Epithelial Mesenchymal Transition) (Normalized Enrichment Score (NES) >1.5, p-adj<0.05). Additionally, the VAT of patients with EOCRC showed upregulation of the glycolysis gene set relative to LOCRC (NES>1.5, p-adj<0.05). These pathways remained significantly enriched regardless of tumor site adjustment. Conclusions: VAT of patients with EOCRC displays a differential gene expression landscape relative to LOCRC patients, suggesting enhanced immune, fibrotic, and metabolic activity. These findings suggest that tumor-adjacent VAT physiology may be a relevant factor of the tumor-microenvironment in EOCRC progression. Citation Format: Victoria M. Bandera, Patricia Erickson, Caroline Himbert, Elaine M. Glenny, Tengda Lin, Sheetal Hardikar, Aik Choon Tan, Jennifer Ose, Victoria Damerell, Christy Warby, Olena Aksonova, Chris Stubben, David Nix, Kenneth Boucher, Peter Schirmacher, Ildiko Strehli, Megan Mclaws, Alejandro Sanchez, Jolanta Jedrzkiewicz, Lyen C. Huang, Vaia Florou, Jessica N. Cohan, Alexander Brobeil, Hans-Ulrich Kauczor, Christoph Kahlert, Meghana Karchi, Elizabeth H. Wood, Doratha A. Byrd, Erin M. Siegel, Adetunji T. Toriola, David Shibata, Christopher I. Li, Jane C. Figueiredo, Biljana Gigic, Jatin Roper, Stephen Hursting, Cornelia M. Ulrich. Tumor-adjacent visceral adipose tissue displays an altered transcriptomic landscape in early-onset colorectal cancer patients: Results from the ColoCare Study [abstract]. In: Proceedings of the AACR Special Conference in Cancer Research: The Rise in Early-Onset Cancers—Knowledge Gaps and Research Opportunities; 2025 Dec 10-13; Montreal, QC, Canada. Philadelphia (PA): AACR; Clin Cancer Res 2025;31(23_Suppl):Abstract nr PR007.

  PublisherDOI

• Supplementary Tables S6-S8 from Associations between Pretreatment Body Composition Features and Clinical Outcomes among Patients with Metastatic Clear Cell Renal Cell Carcinoma Treated with Immune Checkpoint Blockade

  2025-11-25

  articleOpen access

  <p>Table S6. Associations between SMI and length of prior treatment exposure before starting ICB among the 144 patients that received ICB in the second+ line setting Table S7. The prevalence of SMI by the number of prior treatments received before starting ICB among the 144 patients that received ICB in the second+ line setting Table S8. Characteristics of the TCGA cohort used for gene expression analysis by SMI</p>

  PublisherDOI

• Prostate Cancer Imaging Stewardship: a multimodal, physician-centered intervention for guideline-concordant imaging

  JNCI Journal of the National Cancer Institute · 2025-08-06

  article

  BACKGROUND: Inappropriate imaging to stage low-risk prostate cancer is considered low-value care. Determining the effectiveness of a theory-based intervention-Prostate Cancer Imaging Stewardship (PCIS)-to promote guideline-concordant imaging. METHODS: A stepped-wedge, cluster-randomized trial, PCIS, was conducted between March 2018 and March 2021 at 10 Veterans Health Administration medical centers (VAMCs) initially selected for prostate cancer volume, geographic diversity, and willingness to participate. Intervention initiations at sites were randomized in 3-month intervals. We enrolled 61 urology providers who treat prostate cancer at participating sites. Outcomes were assessed among 2302 patients with incident prostate cancer aged 18-85 years. PCIS combines 3 evidence-based provider-focused behavior change strategies: (1) Clinical Reminder Order Check triggered when a provider attempted to order imaging for a patient with prostate-specific antigen < 20 ng/mL, (2) VAMC-level academic detailing at initiation and every 3 months thereafter, and (3) Audit and Feedback for providers to improve their imaging performance. The main outcome was guideline-discordant nuclear medicine bone scan (NMBS) imaging for low-risk prostate cancer patients. RESULTS: NMBS imaging would be consistent with National Comprehensive Cancer Network guidelines in 878 patients (38%) and inconsistent in 1424 patients (62%). Among patients not requiring NMBS, 141/690 (20.4%) received guideline-discordant imaging (ie, NMBS ordered) during Control compared with 109/734 (14.9%) during Intervention (odds ratio [OR] = 0.54, P = .04). Among patients requiring a NMBS, 29 of 425 (6.8%) did not receive one (ie, guideline-discordant imaging) during Control compared with 25 of 453 (5.5%) during the Intervention (OR = 1.36, P = .36). CONCLUSION: PCIS significantly reduced low-value, guideline-discordant NMBS imaging among low-risk prostate cancer patients without negatively affecting necessary imaging for high-risk patients. CLINICAL TRIALS REGISTRATION: NCT03445559.

  PublisherDOI

• Combined sedentarism and high-fat diet induce early signs of kidney injury in C57BL/6J mice

  American Journal of Physiology-Renal Physiology · 2025-05-06 · 3 citations

  articleOpen access

  Physical inactivity is a risk factor for chronic kidney disease. Our laboratory recently developed a new mouse model of physical inactivity (small mouse cage housing) that more closely recapitulates the metabolic disturbances that occur with sedentary behavior. In this paper, we performed an in-depth phenotyping of kidney function and metabolic parameters in response to small mouse cage housing.

  PublisherDOI

• PD13-02 PHASE II TRIAL OF IMAGE-GUIDED OLIGOMETASTATECTOMY AND RADIATION THERAPY IN RECURRENT PROSTATE CANCER (SOAR)

  The Journal of Urology · 2025-04-08

  article1st authorCorresponding
  PublisherDOI

• Germline whole-exome sequencing reveals <i>FOXP3</i>-related gene variants conferring urinary cancer susceptibility and associated with immune escape

  Journal for ImmunoTherapy of Cancer · 2025-09-01

  articleOpen access

  Background The heritability of urinary tract cancer (UTC) remains unexplained by known pathogenic germline variants, and the influence of germline variants on treatment response to immune checkpoint inhibition (ICI) has yet to be fully elucidated. Methods In this case–control study, we performed a germline whole-exome sequencing of 810 UTC patients from the Oncology Research Information Exchange Network. A rare-variant burden test was conducted on the 810 patients and 2354 healthy controls from the Centre d'Etudes du Polymorphisme Humain families, the University of Utah Heritage 1000 Projects, and the 1000 Genomes Project, stratified into discovery and confirmation sets. We used a gene set-based rare-variant association test (GSRVAT) with near-match confirmation, testing for the association of pathways with UTC susceptibility and accounting for multiple testing. We then studied the impact of the identified pathways on tumor biology and clinical course among the 810 cases by analyzing their tumor exomes, transcriptomes, and clinical features. Results GSRVAT revealed forkhead box p3 ( FOXP3 ) as a susceptibility pathway in 16% of patients with UTC, with an epistasis with DNA mismatch repair. Carriers of germline truncating variants in FOXP3 -related susceptibility genes exhibited decreased tumor FOXP3 expression levels, which were associated with a cold tumor microenvironment and significantly reduced overall and progression-free survival following ICI. Conclusions Germline variants in a set of FOXP3 -related genes confer inherent susceptibility to UTC and contribute to resistance against ICI. The immune-evading trait resulting from these variants and the downregulation of FOXP3 expression introduce a novel avenue for personalized medicine through germline and tumor sequencing.

  PublisherOA PDFDOI

Frequent coauthors

• A. Ari Hakimi

  Memorial Sloan Kettering Cancer Center

  59 shared

• Roy Mano

  Tel Aviv University

  59 shared

• Andrew W. Silagy

  52 shared

• Paul Russo

  Memorial Sloan Kettering Cancer Center

  52 shared

• Renzo G. DiNatale

  50 shared

• Kyle A. Blum

  The University of Texas MD Anderson Cancer Center

  48 shared

• Fengshen Kuo

  47 shared

• Robert J. Motzer

  46 shared

Labs

• University of Utah School of Medicine Urology DivisionPI

Education

• B.S., Biochemistry

  University of Florida

• M.D.

  Harvard Medical School

• Other, Urologic Oncology

  Memorial Sloan Kettering Cancer Center

Awards & honors

• Young Investigator Award from the American Society of Urolog…
• Chairman’s Award for Excellence in Basic Science