AACR-KidneyCAN Kidney Cancer Innovation and Discovery Grant
The AACR-KidneyCAN Kidney Cancer Innovation and Discovery Grant is a new grant mechanism that seeks to stimulate creative approaches to translate basic research into new treatment options for kidney cancer.
2026 Grantees
Scientific Statement of Research
Hereditary leiomyomatosis and renal cell carcinoma (HLRCC) is a rare but highly aggressive kidney cancer caused by germline inactivation of fumarate hydratase (FH), the enzyme responsible for converting fumarate to malate. HLRCC tumors display enlarged nucleoli and markedly elevated ribosome biogenesis, a process essential for tumor growth but historically difficult to target therapeutically due to its essential role in normal cells. This project seeks to identify cancer-specific regulators of ribosome biogenesis that may represent selective therapeutic vulnerabilities in FH-mutant tumors. Preliminary studies have identified a novel nucleolar complex that is highly upregulated in HLRCC tumors and patient-derived FH-mutant cells, with expression levels strongly associated with tumor aggressiveness. Building on these findings, Dr. Sorrell will evaluate this pathway as a therapeutic target and seek to develop small-molecule inhibitors for the treatment of HLRCC.
Biography
Dr. Sorrell earned her undergraduate degree in Biology and master’s degree from the University of São Paulo, and a doctoral degree in Molecular Cell Biology from the Weizmann Institute of Science.She completed postdoctoral training at the Fred Hutchinson Cancer Research Center. She is currently an Associate Professor in the Department of Cell Biology at the Simmons Comprehensive Cancer Center at University of Texas Southwestern Medical Center. Her laboratory investigates how cancer cells reprogram nutrient utilization and biomass production to sustain growth, with a focus on identifying cancer-specific vulnerabilities that can be exploited as biomarkers or therapeutic targets.
Statement of Support
“Receiving the 2026 AACR-KidneyCAN Kidney Cancer Innovation and Discovery Grant is a great honor, and I am deeply grateful for this support. This award will allow us to initiate studies and establish the foundation for a new therapeutic strategy targeting ribosome biogenesis in aggressive kidney cancers. It will enable the generation of essential preliminary data, accelerate translational studies, and position the project to secure additional federal and foundation funding focused on targeting this rare and highly aggressive disease.”
Scientific Statement of Research
Translocation renal cell carcinoma (tRCC) is a rare and aggressive kidney cancer driven by TFE3/TFEB gene fusions, with poor responses to standard therapies. Dr. Kotecha seeks to address a major barrier to the development of theranostic strategies in RCC, namely the lack of a validated cell-surface target for tRCC. Emerging evidence suggests that cadherin-17 (CDH17) may be selectively expressed in tRCC, and the investigators have developed a CDH17-targeted immunoPET imaging agent that demonstrated high tumor uptake in preclinical models of other cancer types. Dr. Kotecha will assess CDH17 expression in tRCC tumor specimens and evaluate CDH17-directed imaging and radioligand therapy in fusion-distinct patient-derived xenograft models, including the use of serial PET imaging to assess target expression, predict treatment response, and identify mechanisms of resistance. These studies aim to establish the preclinical foundation for translating CDH17-directed theranostic strategies for patients with tRCC.
Biography
Dr. Kotecha earned his undergraduate degree in biology from Rensselaer Polytechnic Institute and his medical degree from Albany Medical College. During medical school, he spent a year as a Medical Research Scholar at the National Institutes of Health. He completed an Internal Medicine residency at Beth Israel Deaconess Medical Center, Harvard Medical School, followed by a Hematology and Medical Oncology fellowship at Memorial Sloan Kettering Cancer Center. He is currently an Assistant Attending Physician on the Genitourinary Oncology and Cellular Therapy Services at Memorial Sloan Kettering Cancer Center and Assistant Professor of Medicine at Weill Cornell Medical College.
Statement of Support
“This award will enable Dr. Kotecha to establish CDH17 as a theranostic target in translocation RCC, generating the imaging and therapeutic data needed for clinical translation. It will also strengthen his transition from early-career investigator to independent physician-scientist advancing therapeutic discovery for rare RCC subtypes.”
Scientific Statement of Research
Identifying tumor-specific metabolic adaptations that drive progression and therapeutic resistance remains a major unmet need in clear cell renal cell carcinoma (ccRCC). Dr. Spinelli previously identified rhodoquinone (RQ), a previously unrecognized mammalian electron carrier that transfers electrons to fumarate rather than oxygen, and found that RQ accumulates in ccRCC tumors compared with healthy kidney tissue. These findings suggest that ccRCC may use an alternative energy pathway to survive in low-oxygen environments. In this project, Dr. Spinelli and her laboratory will examine how kidney tumors produce and use RQ and test whether disrupting RQ biosynthesis or RQ-dependent electron transfer can slow tumor growth. Their work could uncover a previously unrecognized metabolic vulnerability in kidney cancer and inform new strategies for diagnosis and treatment.
Biography
Dr. Spinelli received her doctoral degree in Chemical Biology from Harvard University and pursued postdoctoral training at the Whitehead Institute for Biomedical Research. She is currently an Associate Professor of Molecular Medicine at UMass Chan Medical School and a Howard Hughes Medical Institute Freeman Hrabowski Scholar.
Statement of Support
“The 2026 Kidney Cancer Innovation and Discovery Grant will significantly advance my career by providing critical support to pursue high-risk, high-impact research in kidney cancer metabolism. This funding will accelerate development of my independent research program, generate preliminary data for future federal funding, and foster new collaborations. The award will strengthen my trajectory as an emerging leader in translational cancer metabolism research.”
2025 Grantees
Scientific Statement of Research
Most patients who die of kidney cancer do so due to metastatic disease. Dr. DeBerardinis and his team previously observed that metastases activate oxidative mitochondrial metabolism. In this project, he will evaluate the impact of a well-tolerated mitochondrial inhibitor, ONC201, on kidney cancer growth and metastasis in vivo. Additionally, he plans to use deuterium MRI, a new non-invasive imaging tool, to monitor mitochondrial activity and assess the effects of ONC201 on these pathways. This study may give rise to clinical trials in kidney cancer in the near term.
Biography
Dr. DeBerardinis received his medical and doctoral degrees from the University of Pennsylvania and pursued clinical training at Children’s Hospital of Philadelphia in pediatrics and medical genetics. He is now professor and director of the Eugene McDermott Center for Human Growth and Development at UT Southwestern Medical Center. His lab studies altered metabolic pathways in cancer and inborn errors of metabolism. They use metabolomics and isotope tracing to characterize disease-associated metabolic states directly in patients, and mouse models to explore how metabolic perturbations contribute to tissue dysfunction.
Acknowledgment of Support
“I am grateful for this AACR KidneyCAN Innovation and Discovery Grant. It comes at a pivotal time in our efforts to understand kidney cancer progression and translate this knowledge into practice. We believe this grant project will provide foundational data for imaging and therapeutic clinical trials in kidney cancer.”
Scientific Statement of Research
High-risk and relapsed Wilms tumors remain a major clinical challenge with poor outcomes. Dr. Petrosyan’s team has identified COL2A1, an extracellular matrix (ECM) protein absent in normal kidney but upregulated in aggressive tumors, as a potential driver of cancer stem cell (CSC) plasticity and chemoresistance. Their findings indicate that COL2A1 negatively regulates the tumor suppressor KLF4, facilitates epithelial-mesenchymal transition (EMT), and drives therapeutic resistance. Targeted inhibition of COL2A1 restores KLF4 expression, reverses EMT, and re-sensitizes CSCs to chemotherapy. Using CSC organoid cultures, patient-derived decellularized ECM scaffolds, and in vivo xenograft models, Dr. Petrosyan aims to elucidate the molecular mechanisms behind COL2A1-mediated KLF4 suppression and evaluate pharmacological KLF4 activation as a therapeutic approach in high-risk Wilms tumor.
Biography
Dr. Petrosyan earned her undergraduate degree from the University of California, Riverside, and her doctorate from the University of Southern California (USC). She completed her postdoctoral fellowship at Children’s Hospital Los Angeles (CHLA) and joined the faculty in 2022 as an assistant professor at USC/CHLA. Her research investigates extracellular matrix-driven mechanisms of cancer progression and chemoresistance, emphasizing the therapeutic targeting of cancer stem cells using advanced 3D in vitro models.
Acknowledgment of Support
“The ECM actively regulates tumor progression, therapy resistance, and cellular crosstalk within the tumor microenvironment. This AACR-KidneyCAN Innovation and Discovery Grant will support research into ECM-driven mechanisms in kidney cancer and foster interdisciplinary efforts to develop tumor microenvironment–targeted therapies with translational potential.”
Scientific Statement of Research
Translocation renal cell carcinoma (tRCC) is an aggressive kidney cancer that affects both adults and children and is driven by gene fusions of the TFE3 transcription factor. While TFE3 fusions create critical oncogenic dependencies in tRCC, direct targeting of TFE3 is challenging because it is a transcription factor with many disordered regions. Dr. Viswanathan and his team developed a phenotypic screening strategy to identify small molecules that disrupt TFE3-chromatin interactions essential for oncogenesis. Screening 25,000 compounds identified 62 hits, with compounds acting via two complementary mechanisms: retention/trapping of TFE3 on chromatin or displacement of TFE3 from chromatin. Dr. Viswanthan will focus on further functional validation of these hits and mechanistic characterization via a suite of cell-based and biochemical deconvolution assays. This effort aims to establish a robust pipeline for screening for TFE3 inhibitors, paving the way for future large-scale screens with the development of a first-in-class targeted therapy for tRCC.
Biography
Dr. Viswanathan is an MD/PhD graduate of Harvard Medical School. He completed his residency in internal medicine at the Massachusetts General Hospital and his fellowship in hematology/oncology at Dana-Farber/Harvard Cancer Center. He is a genitourinary medical oncologist at Dana-Farber Cancer Institute and an associate professor of Medicine at Harvard Medical School. His laboratory uses genomic and functional genetic technologies to discover the molecular underpinnings and vulnerabilities of cancer, with focus on cancers of the kidney and prostate, and a special emphasis on rare kidney cancer subtypes including translocation renal cell carcinoma.
Acknowledgment of Support
“This award will help establish foundational data to support efforts in discovering inhibitors of TFE3 fusions for translocation renal cell carcinoma, a kidney cancer of great unmet need that currently lacks specifically approved therapies.”