About

Veera Baladandayuthapani is the Jeremy M.G. Taylor Collegiate Professor and Chair in the Department of Biostatistics at the University of Michigan. He also serves as the Associate Director of Quantitative Data Sciences and the Director of the Cancer Data Science Shared Resource at the UM Rogel Cancer Center. He obtained his PhD in Statistics from Texas A&M University in 2005, an M.A. in Statistics from the University of Rochester in 2000, and a BSc in Mathematics from the Indian Institute of Technology, Kharagpur in 1998. His research explores the potential of Bayesian probabilistic models and machine learning methods to assist in medical and health sciences, focusing on large and complex datasets such as high-throughput genomics, epigenomics, transcriptomics, proteomics, and high-resolution neuro- and cancer-imaging. A special focus of his work is on developing integrative and spatial models that combine different sources of data for biomarker discovery and clinical prediction to aid in precision and translational medicine. His contributions include over 160 published papers in top statistical, biostatistical, bioinformatics, biomedical, and oncology journals, as well as co-authoring a book on Bayesian analysis of gene expression data. He has received numerous awards, including the Myrto Lefkopoulou Distinguished Lectureship from Harvard School of Public Health, the H. O. Hartley award from Texas A&M University, and the MD Anderson Faculty Scholar Award. He is a fellow of the American Association for the Advancement of Science and the American Statistical Association, and an elected member of the International Statistical Institute. He serves on editorial boards for major journals such as the Journal of the American Statistical Association, Annals of Applied Statistics, and Biometrics.

Research topics

• Biology
• Genetics
• Medicine
• Cancer research
• Immunology
• Internal medicine
• Molecular biology
• Oncology

Selected publications

• A Linear Analysis Mixed Model Phenotyper (LAMP) for Bipolar Disorder: Evaluating the Impact of Medication, Substance Use Disorders, and Comorbidities on Mood Trajectories

  medRxiv · 2025-09-08

  preprintOpen access

  Background: Bipolar disorder is a complex psychiatric condition characterized by recurrent mood episodes and fluctuating symptom severity. Our study investigates post-diagnosis complexities using 17-year longitudinal data from the Prechter Bipolar Research Program. Methods: We analyzed mood trajectories of 525 bipolar I disorder (BP1) and 150 bipolar II disorder (BP2) patients, using the Linear Analysis Mixed Model Phenotyper (LAMP) to identify subgroups. This approach revealed shared and distinct patterns across individual trajectories, classifying these subgroups into meaningful longitudinal phenotypes. Regression modeling was then applied to identify associations between these phenotypes and relevant factors. Results: We found that medication use and alcohol use disorder significantly impacted long-term mood trajectories. Polypharmacy was associated with resistant/worsening trajectories in both BP1 (PHQ-9: OR: 1.09, CI: 1.02-1.17) and BP2 (GAD-7: OR: 1.21, CI: 1.05-1.43), with each additional medication increasing the risk of a worse trajectory by 9% and 21%, respectively. In BP1, antidepressant use improved trajectories (PHQ-9: OR: 0.40, CI: 0.19-0.83), but when combined with antipsychotics, increasing use frequency from 0% to 20% raised the risk of resistant/worsening trajectories (OR: 2.09, CI: 1.33- 3.28). In BP2, antipsychotic use was associated with improved trajectories (PHQ-9: OR: 0.04, CI: 0.00-0.56). Alcohol use disorder in BP1 increased resistant/worsening risk by 83% (PHQ-9: OR: 1.83, CI: 1.15-2.93). Conclusions: Our results indicate that polypharmacy and alcohol use disorder contribute to resistant or worsening mood trajectories. In BP1, while antidepressants are beneficial, their combination with antipsychotics substantially increases risk, highlighting the need for individualized, diagnosis-specific treatment approaches. Highlights: LAMP analysis pipeline aided in improving treatment approaches in bipolar disorder.17 years of PrBP data provided comprehensive analysis of long-term mood trajectories.Polypharmacy and alcohol use disorder worsened mood trajectory.The combination of antidepressants and antipsychotics worsened mood trajectory.

  PublisherOA PDFDOI

• Abstract 935: HPV16 E6 splicing induces partial epithelial-mesenchymal transition in oropharyngeal squamous cell carcinoma

  Cancer Research · 2025-04-21

  article

  Abstract The incidence of HPV16-positive oropharyngeal squamous cell carcinoma (HPV+ OPSCC) is rising at an alarming rate and has overtaken cervical cancer to become the most prevalent HPV+ cancer in the United States. Although most patients with HPV+ OPSCC respond favorably to standard chemoradiation, a substantial proportion of patients have highly aggressive tumors that recur. Biomarkers are needed to reliably stratify patients into risk subgroups. Using multiple complementary models that recapitulate HPV+ OPSCC, our group demonstrated that enhanced splicing of HPV16 E6 oncogene increased migration and invasion. In vivo, HPV+OPSCC with higher spliced E6 (E6*) generated more isolated clusters of tumor cells that spread further away from the main tumor relative to the original full-length isoform (E6FL). This is consistent with an adverse phenotype seen in human HPV+ OPSCC. However, the mechanisms of how spliced E6 enhanced invasion remain unclear.Epithelial-mesenchymal transition (EMT) drives invasion in OPSCC, and is commonly characterized by a loss of epithelial genes and gain in mesenchymal genes. However, recent studies also identified a partial EMT (p-EMT) phenotype, where cancer cells co-express both epithelial and mesenchymal genes. In this study, we explored whether spliced E6 enhances invasion via EMT in OPSCC. Immunofluorescence staining of E-cadherin (epithelial phenotype) and vimentin (mesenchymal phenotype) was performed on formalin-fixed paraffin-embedded tissue of 46 human HPV+ OPSCC. Analysis of the tumor regions on whole-slide images showed that patients with increased E6* relative to E6FL had reduced membrane localization of E-cadherin. In contrast, total expression of E-cadherin and vimentin were unchanged. This finding corroborates with our in vivo chick chorioallantoic membrane model and in vitro studies in OPSCC cell lines, where E-cadherin was more localized at cell-cell junctions in cancer cells with increased E6 splicing. Therefore, we propose that splicing of HPV16 E6 oncogene promotes p-EMT by inhibiting translocation of epithelial E-cadherin from the cell membrane to cytoplasm to reduce cell-cell adhesion. Overall, our findings may shed valuable insights into the mechanisms driving aggressive HPV+ OPSCC and substantiate E6* as a prognostic biomarker to distinguish HPV+ OPSCC risk subgroups for personalized treatment. Citation Format: Yvonne Xinyi Lim, Min Liu, Allison Furgal, Jake McGue, Shiting Li, Bailey Garb, Timothy Frankel, Veera Baladandayuthapani, Laura Rozek, Maureen Sartor, Nisha D'Silva. HPV16 E6 splicing induces partial epithelial-mesenchymal transition in oropharyngeal squamous cell carcinoma [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 935.

  PublisherDOI

• Spatial analysis reveals a novel inflammatory tumor transition state which promotes a macrophage-driven induction of sarcomatoid renal cell carcinoma

  bioRxiv (Cold Spring Harbor Laboratory) · 2025-06-14 · 1 citations

  preprintOpen access

  SUMMARY Sarcomatoid renal cell carcinoma (sRCC) is an aggressive transdifferentiation of epithelioid clear cell RCC (ccRCC) tumors that shows heightened response to immunotherapy. The underlying biology leading to sarcomatoid transformation and mechanisms contributing to immunotherapy response are not well understood. Novel single cell spatial techniques were used in ccRCC and sRCC tumors from 40 patients to understand the spatial sRCC transformation and corresponding immune changes. A transcriptional transition state in epithelioid ccRCC cells along a continuum to mesenchymal sRCC was identified which expresses high levels of pro-inflammatory cytokines and an immune infiltrate. In vitro studies demonstrated that M2-like macrophages, recruited to the tumor by the transition state, induce full transition to the sarcomatoid state. A combination of increased PD-L1 expression and T-cells recruited by the transition state was observed, consistent with the increased immunotherapy response. This study enriches our understanding of the mechanisms leading to development and immune responsiveness of sRCC paving the way for novel approaches to diminish RCC progression.

  PublisherOA PDFDOI

• Durvalumab and guadecitabine in advanced clear cell renal cell carcinoma: results from the phase Ib/II study BTCRC-GU16-043

  Nature Communications · 2024-02-01 · 8 citations

  articleOpen access

  Abstract Epigenetic modulation is well established in hematologic malignancies but to a lesser degree in solid tumors. Here we report the results of a phase Ib/II study of guadecitabine and durvalumab in advanced clear cell renal cell carcinoma (ccRCC; NCT03308396). Patients received guadecitabine (starting at 60 mg/m 2 subcutaneously on days 1-5 with de-escalation to 45 mg/m2 in case of dose limiting toxicity) with durvalumab (1500 mg intravenously on day 8). The study enrolled 57 patients, 6 in phase Ib with safety being the primary objective and 51in phase II, comprising 2 cohorts: 36 patients in Cohort 1 were treatment naive to checkpoint inhibitors (CPI) with 0-1 prior therapies and 15 patients in Cohort 2 were treated with up to two prior systemic therapies including one CPI. The combination of guadecitabine 45 mg/m2 with durvalumab 1500 mg was deemed safe. The primary objective of overall response rate (ORR) in cohort 1 was 22%. Sixteen patients (44%) experienced stable disease (SD). Secondary objectives included overall survival (OS), duration of response, progression-free survival (PFS), clinical benefit rate, and safety as well as ORR for Cohort 2. Median PFS for cohort 1 and cohort 2 were 14.26 and 3.91 months respectively. Median OS was not reached. In cohort 2, one patient achieved a partial response and 60% achieved SD. Asymptomatic neutropenia was the most common adverse event. Even though the trial did not meet the primary objective in cohort 1, the tolerability and PFS signal in CPI naive patients are worth further investigation.

  PublisherOA PDFDOI

• Developing a Bayesian workshop for full-time staff statisticians

  Journal of Clinical and Translational Science · 2024-01-01 · 1 citations

  articleOpen access

  Introduction: There are two main schools of thought about statistical inference: frequentist and Bayesian. The frequentist approach relies solely on available data for predictions, while the Bayesian approach incorporates both data and prior knowledge about the event of interest. Bayesian methods were developed hundreds of years ago; however, they were rarely used due to computational challenges and conflicts between the two schools of thought. Recent advances in computational capabilities and a shift toward leveraging prior knowledge for inferences have led to increased use of Bayesian methods. Methods: Many biostatisticians with expertise in frequentist approaches lack the skills to apply Bayesian techniques. To address this gap, four faculty experts in Bayesian modeling at the University of Michigan developed a practical, customized workshop series. The training, tailored to accommodate the schedules of full-time staff, focused on immersive, project-based learning rather than traditional lecture-based methods. Surveys were conducted to assess the impact of the program. Results: All 20 participants completed the program and when surveyed reported an increased understanding of Bayesian theory and greater confidence in using these techniques. Capstone projects demonstrated participants' ability to apply Bayesian methodology. The workshop not only enhanced the participants' skills but also positioned them to readily apply Bayesian techniques in their work. Conclusions: Accommodating the schedules of full-time biostatistical staff enabled full participation. The immersive project-based learning approach resulted in building skills and increasing confidence among staff statisticians who were unfamiliar with Bayesian methods and their practical applications.

  PublisherOA PDFDOI

• Abstract 1230: MTX-531, a first-in-class pan-PI3K inhibitor spares hyperinsulinemia yielding durable tumor regressions and resilience to adaptive resistance

  Cancer Research · 2024-03-22 · 1 citations

  article

  Abstract Adaptive resistance mechanisms compromise the long-term effectiveness of kinase-targeted agents dictating the need for strategic combination approaches. MTX-531 was computationally designed to selectively target both PI3K and wild type EGFR. MTX-531 exhibits low nanomolar potency against the PI3K isoform family and EGFR with a high degree of specificity predicted by co-crystal structural analyses. Full kinome screening confirmed that MTX-531 is exquisitely selective for its intended targets. We evaluated the pharmacological profile of MTX-531, whereupon single agent treatment with this lead molecule elicited a high incidence of durable tumor regressions in a broad panel of PIK3CA mutant CDX and PDX squamous head and neck (HNSCC) models. The combination of MTX-531 with RAS pathway inhibitors, including agents directed against KRAS G12C, led to durable regressions of KRAS mutant colorectal and pancreatic xenografts, resulting in striking increases in median survival. MTX-531 is exceptionally well tolerated in mice and uniquely does not lead to hyperglycemia and hyperinsulinemia commonly seen with predecessor pan PI3K inhibitors. MTX-531 acts as an agonist of PPARγ, a structural feature of the molecule that is thought to mitigate hyperglycemia induced by PI3K inhibition. This unique attribute of MTX-531 confers a favorable therapeutic index not typically seen with PI3K inhibitors. To the best of our knowledge, MTX-531 is the first reported pan-PI3K inhibitor that does not lead to hyperglycemia. The pharmaceutical profile of MTX-531 includes favorable cross-species oral bioavailability, microsomal stability, and a facile 3 step chemical synthesis. MTX-531, which has the unique capability of concurrently and selectively inhibiting PI3K and EGFR, illustrates the power of rational computational drug design to target multiple adaptive resistance mechanisms in a single molecule. The versatility of MTX-531 in both the single agent and combination settings offers a breadth of development strategies that continue to evolve as new combination candidates become available. MTX-531 is currently undergoing advanced preclinical development for anticipated first in human clinical trials in late 2024. Citation Format: Christopher E. Whitehead, Elizabeth K. Ziemke, Christy L. Frankowski-McGregor, Rachel A. Mumby, June Chung, Jinju Li, Nathaniel Osher, Oluwadara Coker, Michelle Norris, Scott Kopetz, Veera Baladandayuthapani, Melinda Hollingshead, Sharad Verma, Judith S. Sebolt-Leopold. MTX-531, a first-in-class pan-PI3K inhibitor spares hyperinsulinemia yielding durable tumor regressions and resilience to adaptive resistance [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2024; Part 1 (Regular Abstracts); 2024 Apr 5-10; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2024;84(6_Suppl):Abstract nr 1230.

  PublisherDOI

• Supplementary Figure S2 from <i>Fusobacterium Nucleatum</i> Subspecies <i>Animalis</i> Influences Proinflammatory Cytokine Expression and Monocyte Activation in Human Colorectal Tumors

  2023-04-03

  preprintOpen access

  <p>Identification of Fusobacterium spp. and subspecies in human colorectal tumors using Fusobacterium genus 16S V2 - V4 amplicon cloning and sequencing, as well as amplicon-targeted direct sequencing</p>

  PublisherDOI

• Supplementary Figure S1 from <i>Fusobacterium Nucleatum</i> Subspecies <i>Animalis</i> Influences Proinflammatory Cytokine Expression and Monocyte Activation in Human Colorectal Tumors

  2023-04-03

  preprintOpen access

  <p>Identification of <i>Fusobacterium</i> spp. in normal colorectal mucosal and tumor specimens.</p>

  PublisherDOI

• Supplementary Figure S5 from <i>Fusobacterium Nucleatum</i> Subspecies <i>Animalis</i> Influences Proinflammatory Cytokine Expression and Monocyte Activation in Human Colorectal Tumors

  2023-04-03

  preprintOpen access

  <p>Morphological changes in THP-1 monocytes induced by co-culture with <i>F. nucleatum</i> ssp. <i>animalis</i> under normoxic conditions.</p>

  PublisherDOI

• Supplementary Figure S6 from <i>Fusobacterium Nucleatum</i> Subspecies <i>Animalis</i> Influences Proinflammatory Cytokine Expression and Monocyte Activation in Human Colorectal Tumors

  2023-04-03

  preprintOpen access

  <p>Migration of HCP1 CRC cells in a Boyden chamber system.</p>

  PublisherDOI

Recent grants

• Integrative methods for high-dimensional genomics data

  NIH · $1.4M · 2011–2017

• Graph-based Bayesian analysis of Genomics and Proteomics Data

  NIH · $2.0M · 2015–2022

Frequent coauthors

• Gregory N. Fuller

  25 shared

• Markus M. Luedi

  University Hospital of Bern

  24 shared

• Pascal O. Zinn

  University of Pittsburgh Medical Center

  23 shared

• Frederick F. Lang

  The University of Texas MD Anderson Cancer Center

  22 shared

• Nabil Elshafeey

  22 shared

• Raymond Sawaya

  American University of Beirut Medical Center

  22 shared

• Rivka R. Colen

  University of Pittsburgh

  22 shared

• Islam Hassan

  Servier (France)

  22 shared

Awards & honors

• Myrto Lefkopoulou Distinguished Lectureship from Harvard Sch…
• H. O. Hartley award from the Department of Statistics at Tex…
• Theodore G. Ostrom Award from Washington State University
• MD Anderson Faculty Scholar Award
• Young Investigator Award from the International Indian Stati…