Curebound 2025 Research Portfolio + Annual Report Available 

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Personalized Immunotherapy; Novel Approaches, Targets, and Therapeutics

Outcomes for pancreatic duct adenocarcinoma (PDAC) patients remain poor by any reasonable metric and thus more effective therapies are needed. We hypothesize that targeting the post translational modification, SUMOylation, will be an effective therapy for PDAC as we have shown SUMO inhibition (SUMOi) activates anti-PDAC immune responses. More recently we have found that SUMOi synergizes with chemotherapeutic agents used to treat PDAC most notably, irinotecan. In this proposal, we will determine the mechanism underlying this synergy and the effectiveness of combining SUMOi with both irinotecan and other immunomodulatory agents in murine and human models of the disease. Given the availability of recent development of clinical grade SUMOi’s and that irinotecan is part of approved first and second-line therapies for PDAC, we believe the results of our studies will provide sufficient rationale to move these strategies directly to the clinic for the treatment of PDAC patients

Pancreatic Cancer

Outcomes for pancreatic duct adenocarcinoma (PDAC) patients remain poor by any reasonable metric and thus more effective therapies are needed. We hypothesize that targeting the post translational modification, SUMOylation, will be an effective therapy for PDAC as we have shown SUMO inhibition (SUMOi) activates anti-PDAC immune responses.

UC San Diego

SUMO Inhibition and Irinotecan: A Novel Synergistic Combination for Pancreatic Cancer Therapy

Novel Approaches, Targets, and Therapeutics

Maximiliano D'Angelo, PhD (Sanford Burnham Prebys)

Susanne Heyen-Genel, PhD (Sanford Burnham Prebys)

Lung cancer is a leading cause of death worldwide, highlighting the need for new therapies. Nuclear pore complexes (NPCs), the channels connecting the nucleus to the cytoplasm, are built from 32 different proteins or nucleoporins. Emerging evidence shows that cells modify NPCs and nucleoporins to regulate specific functions, and cancer cells exploit this plasticity to promote tumorigenesis, making them dependent on these alterations and rendering certain nucleoporins key vulnerabilities. We found that the nucleoporin Nup37 is a critical dependency of lung cancer cells that can be leveraged for targeted therapies. We established and validated a novel high-throughput assay to screen for Nup37 modulators. Our goal is to perform a large-scale screen to identify small molecules that reduce Nup37 levels and validate lead compounds for anti-lung cancer efficacy. We expect to identify the first Nup37 inhibitors and lay the foundation for the development of selective lung cancer therapies.

Lung Cancer

Lung cancer is a leading cause of death worldwide, highlighting the need for new therapies. Nuclear pore complexes (NPCs), the channels connecting the nucleus to the cytoplasm, are built from 32 different proteins or nucleoporins. Emerging evidence shows that cells modify NPCs and nucleoporins to regulate specific functions, and cancer cells exploit this plasticity to promote tumorigenesis, making them dependent on these alterations and rendering certain nucleoporins key vulnerabilities.

Sanford Burnham Prebys

Modulating Nup37 For Novel Cancer Therapies 

Solid tumors with loss-of-function (LOF) mutations in nucleotide-excision repair (NER) genes—particularly ERCC2—are highly sensitive to illudins. Our lead compound, ITX-121, has shown the best therapeutic index in its class (illudins) based on prior in vitro and in vivo studies. We hypothesize that ITX-121 will demonstrate strong efficacy with minimal toxicity in ERCC2-mutant PDO and PDX models, supporting advancement to clinical development. Methods, Aims, and Expected Outcomes Using CROs (Including Certis and Crown in San Diego), we will test ITX-121 in ERCC2-mutant patient-derived organoids (PDOs) in vitro, followed by patient-derived xenografts (PDXs) in vivo. Our goal is to confirm that ITX-121 selectively targets ERCC2-mutant tumors with minimal toxicity, establishing a preclinical foundation for first-in-human trials. We will perform additional, similar work in ERCC6-mutant melanoma.

Solid Tumors; Bladder Cancer; Melanoma and Skin Cancers

Solid tumors with loss-of-function (LOF) mutations in nucleotide-excision repair (NER) genes—particularly ERCC2—are highly sensitive to illudins. Our lead compound, ITX-121, has shown the best therapeutic index in its class (illudins) based on prior in vitro and in vivo studies.

Precision Small-Molecule Targeting Cancers Deficient in Nucleotide-Excision Repair

Glioblastoma recurrence is driven by therapy-induced reprogramming and an immunosuppressive microenvironment. Building upon our published work, we hypothesize that inhibiting activity of bromodomain protein, BRD2, post-radiation therapy, offers dual benefits: disrupting cellular reprogramming toward stem-like states and augmenting anti-tumor immunity through senescence-associated secretory phenotype (SASP) activation. Using a first-in-class brain-penetrant BRD2 inhibitor as adjuvant therapy, we will interrogate its role in SASP reprogramming by epigenetic and functional assays (AIM 1), assess its immunomodulatory effects in immune-competent models by flow cytometry and IHC (Aim 2), and validate therapeutic efficacy when combined with immune checkpoint blockade (ICB) (Aim 3). We expect our results will nominate BRD2 inhibition as a therapeutic strategy to simultaneously block senescence-mediated recurrence and promote immune surveillance by priming the GBM TME to enhance ICB response.

Brain Cancer

Glioblastoma recurrence is driven by therapy-induced reprogramming and an immunosuppressive microenvironment. Building upon our published work, we hypothesize that inhibiting activity of bromodomain protein, BRD2, post-radiation therapy, offers dual benefits: disrupting cellular reprogramming toward stem-like states and augmenting anti-tumor immunity through senescence-associated secretory phenotype (SASP) activation.

Targeting BRD2 to Block Therapy-Induced Reprogramming and Immune Evasion in Glioblastoma

Humberto Prada, PhD (San Diego State Research Foundation)

Noe Crespo, PhD (San Diego State Research Foundation)

We hypothesize that community-based supervised exercise and nutritional counseling, integrating culturally adapted and patient-directed strategies, will improve physical fitness, metabolic health, and clinical outcomes in Hispanic/Latino (H/L) men with prostate cancer (PCa) undergoing androgen deprivation therapy (ADT). The first aim will evaluate lipidomic changes in H/L men with PCa following initiation of ADT. The second aim will implement a prospective trial that integrates the YMCA Livestrong program with nutrition guidance for H/L men undergoing ADT. Gaining insight into lipidomic alterations in response to ADT may enhance our understanding of the mechanisms driving disparate cardiometabolic outcomes among H/L men. This multimodal lifestyle intervention study focuses on bridging cancer care disparities for H/L men with PCa. The results of this study can be integrated into strategies applied in clinic to enhance physical and metabolic health for H/L men with PCa in our community.

We hypothesize that community-based supervised exercise and nutritional counseling, integrating culturally adapted and patient-directed strategies, will improve physical fitness, metabolic health, and clinical outcomes in Hispanic/Latino (H/L) men with prostate cancer (PCa) undergoing androgen deprivation therapy (ADT).

Structured Exercise and Nutritional Guidance in Hispanic/Latino Men with Prostate Cancer: A Pilot Study of SALUD-PC

Novel Approaches, Targets, and Therapeutics; Childhood Cancers

Susanne Heynen-Genel, PhD (Sanford Burnham Prebys)

Pancreatic cancer (PC) is lethal, treatment-resistant and marked by a KRAS-driven, immune-cold stroma. MICAL2 is overexpressed in >75% of PCs and drives MRTF/SRF transcription. Overexpression predicts poor survival, and boosts KRAS, RTK and EMT signaling. MICAL2 knock-down (KD) reduces cancer-associated fibroblasts and extracellular matrix, and recruits cycling, granzyme-rich CD8 T cells. CD8 depletion restores tumor growth, and adoptive transfer of MICAL2-KD-derived T cells shrinks tumors, demonstrating immune-mediated control. Large PC tumors regress in an inducible MICAL2-KD system demonstrating the power of this therapeutic approach. Thus, MICAL2 links oncogenic KRAS to desmoplasia and immune exclusion, and dual KRAS/MICAL2 targeting may yield durable, immune-potentiated responses. The MICAL2-MRTF-SRF transcriptional axis has never been targeted clinically, and the available tool compounds show sub-therapeutic potency. Here, we will identify and test novel MICAL2 inhibitors.

Pancreatic cancer (PC) is lethal, treatment-resistant and marked by a KRAS-driven, immune-cold stroma. MICAL2 is overexpressed in >75% of PCs and drives MRTF/SRF transcription. Overexpression predicts poor survival, and boosts KRAS, RTK and EMT signaling. MICAL2 knock-down (KD) reduces cancer-associated fibroblasts and extracellular matrix, and recruits cycling, granzyme-rich CD8 T cells. CD8 depletion restores tumor growth, and adoptive transfer of MICAL2-KD-derived T cells shrinks tumors, demonstrating immune-mediated control.

Targeting MICAL2 For Pancreatic Cancer Therapy

Dannielle Engle, PhD (The Salk Institute)

KRAS inhibitors (KRASis) are on track to be FDA approved for use in pancreatic ductal adenocarcinoma (PDA). However, not all patients will realize their full potential due to resistance mechanisms, including stromal activation of compensatory pathways. This proposal will test the hypothesis that VDR agonist can promote KRASi responses through inhibition of macrophage-mediated therapeutic resistance and immunosuppression. In Aim1, we will test the ability of VDR agonist to prevent and reverse KRASi resistance in human PDA organoid transplants and dissect the functional contribution of macrophage VDR activity. In Aim2, we will determine the potential for VDR agonist to promote KRASi synergy with immunotherapy and improve long-term survival in syngeneic orthotopic PDA transplants. As VDR agonists are FDA approved and recent clinical trials have shown they are safe for use in PDA patients, this work is poised to rapidly translate to the clinic and improve patient outcomes.

KRAS inhibitors (KRASis) are on track to be FDA approved for use in pancreatic ductal adenocarcinoma (PDA). However, not all patients will realize their full potential due to resistance mechanisms, including stromal activation of compensatory pathways.

Salk Institute

Overcoming Stromal Barriers to KRAS Inhibition in Pancreatic Cancer with VDR Agonist Therapy

Despite excellent outcomes for many children with B-cell acute lymphoblastic leukemia (B-ALL), infants with B-ALL remain difficult to cure. During physiologic development, fetal HSCs activate the heat shock response through heat shock factor 1 (Hsf1) to maintain protein homeostasis (proteostasis) and HSC function. However, we found that in some contexts, pre-leukemic can co-opt this adaptive mechanism to resist stress and fuel clonal expansion and leukemia. This raises the question of whether normal developmental activation of Hsf1 is hijacked to promote the development of infant B-ALL. In this proposal, we will test the hypothesis that Hsf1 promotes initiation and progression of infant B-ALL by promoting proteostasis. Additionally, we will evaluate the impact of Hsf1 on gene expression programs in B-ALL. These studies will reveal whether Hsf1-driven fetal hematopoietic programs preferentially influence the onset of infant B-ALL, with the potential to reveal a new therapeutic target.

Leukemias & Lymphomas 

Despite excellent outcomes for many children with B-cell acute lymphoblastic leukemia (B-ALL), infants with B-ALL remain difficult to cure. During physiologic development, fetal HSCs activate the heat shock response through heat shock factor 1 (Hsf1) to maintain protein homeostasis (proteostasis) and HSC function. However, we found that in some contexts, pre-leukemic can co-opt this adaptive mechanism to resist stress and fuel clonal expansion and leukemia.

The Role of Proteostasis Pathways in Pediatric Leukemia

Lukas Chavez, PhD (Sanford Burnham Prebys)

Megan Paul, MD (Rady Children’s Hospital)

Extrachromosomal DNA (ecDNA) drives oncogene amplification and therapy resistance in aggressive cancers, such as Group 3 medulloblastoma (G3 MB), a lethal pediatric brain tumor. We hypothesize that small molecules capable of selectively reducing or eliminating ecDNA in G3 MB cells will disrupt oncogene-driven tumor growth and uncover novel therapeutic vulnerabilities. Our aims are: (1) to optimize and validate a high-throughput, image-based assay for ecDNA quantification, and (2) to screen a custom library of ~1,000 bioactive compounds to find ecDNA-targeting hits. Using high-content confocal imaging and machine learning-based analysis, we will quantify ecDNA in metaphase cells and assess compound effects across multiple concentrations and timepoints. Expected outcomes include identification of potent, ecDNA-suppressive compounds and insights into ecDNA biology, with potential for translation into therapies for aggressive tumors driven by ecDNA oncogene amplifications.

Extrachromosomal DNA (ecDNA) drives oncogene amplification and therapy resistance in aggressive cancers, such as Group 3 medulloblastoma (G3 MB), a lethal pediatric brain tumor. We hypothesize that small molecules capable of selectively reducing or eliminating ecDNA in G3 MB cells will disrupt oncogene-driven tumor growth and uncover novel therapeutic vulnerabilities.

Targeting ecDNA in High-Risk Medulloblastoma: A High-Throughput Assay to Discover Novel Therapeutic Probes

Novel Approaches, Targets, and Therapeutics; Personalized Immunotherapy; Childhood Cancers

Charles Spruck, PhD (Sanford Burnham Prebys)

Eduard Sergienko (Sanford Burnham Prebys)

Viral mimicry is an emerging therapeutic approach that reactivates retroelements in cancer cells to elicit an immune response. We found that FBXO44 is required for retroelement silencing in cancer cells and its inhibition stimulated antiviral pathways, IFN signaling, and PD-L1 expression. FBXO44 targeting exhibited stand-alone antitumor activity and sensitized refractory tumors to checkpoint inhibitor. To identify FBXO44 inhibitors, we conducted a HTP screen and identified SBI-1620718, which blocks FBXO44 functions in vitro and induces viral mimicry in cancer cells. Here, we will optimize SBI-1620718 by analog-by-catalog and de novo synthesis and evaluate its drug-like properties by ADME testing (Aim 1). Viral mimicry/immunomodulatory activities will be confirmed in breast cancer and pediatric glioma cells (Aim 2). These data will form the basis of a future R01 application to develop and validate a potent FBXO44 drug for the treatment of diverse cancer types in a 3–5-year timeframe.

Breast Cancer; Pediatric Solid Tumors

Viral mimicry is an emerging therapeutic approach that reactivates retroelements in cancer cells to elicit an immune response. We found that FBXO44 is required for retroelement silencing in cancer cells and its inhibition stimulated antiviral pathways, IFN signaling, and PD-L1 expression. FBXO44 targeting exhibited stand-alone antitumor activity and sensitized refractory tumors to checkpoint inhibitor.

Therapeutic Targeting of Immunomodulator FBXO44 in Cancer

Novel Approaches, Targets, and Therapeutics; Personalized Immunotherapy; Cancer Equity

Pancreatic ductal adenocarcinoma (PDA) is a lethal malignancy with a 13% five-year survival rate, driven in part by an immunosuppressive microenvironment resistant to immunotherapy. Oncostatin M (OSM) and its receptor OSMR, members of the IL-6 cytokine family, are associated with poor prognosis in cancer, but their role in PDA is poorly defined. We show that OSM-OSMR signaling promotes immunosuppression and fibrosis in PDA. Spatial transcriptomics of human tumors revealed that high OSMR expression correlates with macrophage infiltration, CAF activation, and CD8? T cell exclusion. Functional assays using OSMR WT, KO, and rescue PDA lines demonstrated that tumor proliferation, invasion, and macrophage polarization are dependent on OSMR. Neutralizing antibodies against OSM and OSMR suppressed STAT3 activation, tumor growth, and stromal remodeling in in vitro and ex vivo models. These findings nominate the OSM-OSMR axis as a mechanistic driver and promising therapeutic target in PDA.

Pancreatic ductal adenocarcinoma (PDA) is a lethal malignancy with a 13% five-year survival rate, driven in part by an immunosuppressive microenvironment resistant to immunotherapy. Oncostatin M (OSM) and its receptor OSMR, members of the IL-6 cytokine family, are associated with poor prognosis in cancer, but their role in PDA is poorly defined.

Perturbing the OSM-OSMR Signaling Axis in Pancreatic Ductal Adenocarcinoma (PDA)

Scott Kopetz, MD, PhD (University of Texas MD Anderson)

There is an urgent need for new approaches to treat colorectal cancer (CRC) and limit its resistance to targeted therapies. This proposal will test the hypothesis that CRC growth and therapeutic resistance can be blocked via inhibition of the lysine fatty acid deacylase HDAC11, which we have identified as a novel regulator of CRC oncogenic signaling pathways. In Aim1, we will validate the efficacy of a set of HDAC11 inhibitors (HDAC11is) evolved for clinical application, evaluating their therapeutic impact on CRC patient derived organoids, xenografts, and primary tumor slices. In Aim2, we will determine the ability for the lead HDAC11i to overcome CRC resistance to clinically relevant targeted therapies. By determining how HDAC11i is impacted by patient mutational background and evaluating its potential for intercepting therapeutic resistance, this work will be critical for advancing this new class of pharmacological inhibitor to the clinic and improving outcomes for CRC patients.

Gastrointestinal Cancers

There is an urgent need for new approaches to treat colorectal cancer (CRC) and limit its resistance to targeted therapies. This proposal will test the hypothesis that CRC growth and therapeutic resistance can be blocked via inhibition of the lysine fatty acid deacylase HDAC11, which we have identified as a novel regulator of CRC oncogenic signaling pathways.

Intercepting Colorectal Cancer Growth and Therapeutic Resistance Through Inhibition 

Eduard Sergienko, PhD (Sanford Burnham Prebys)

We recently identified BRD8 as a selective vulnerability in glioblastoma (GBM) retaining wildtype p53, which represents ~71% of all GBM cases. This discovery not only explains how most GBMs maintain aggressive growth despite intact p53 but also offers a promising new therapeutic target for GBM. Despite its druggable bromodomain (BD) and high oncogenic potential, no effective BRD8 inhibitor is available. Notably, we find that BRD8 is not stable unless its BD is bound by MRGBP. We hypothesize that disrupting the BRD8/MRGBP interaction will degrade BRD8 and inhibit GBM. We aim to leverage our optimized high-throughput BRD8 BD/MRGBP binding assay to screen curated compound library, identify small-molecule inhibitors of this interaction, and validate candidate compounds in human iPSC- and patient-derived GBM models. This project will lay the groundwork for BRD8-targeted therapy and establish its therapeutic relevance in GBM and beyond.

Brain and CNS Cancers; Solid Tumors

We recently identified BRD8 as a selective vulnerability in glioblastoma (GBM) retaining wildtype p53, which represents ~71% of all GBM cases. This discovery not only explains how most GBMs maintain aggressive growth despite intact p53 but also offers a promising new therapeutic target for GBM. Despite its druggable bromodomain (BD) and high oncogenic potential, no effective BRD8 inhibitor is available.

Targeting a Novel Epigenetic Vulnerability in Glioblastoma

This project addresses a key barrier in neoantigen-based cancer immunotherapy: the poor immunogenicity of many tumor neoantigens. We hypothesize that co-formulating mRNA neoantigen vaccines with innate immune adjuvants can enhance antitumor immunity by promoting stronger, more durable T cell responses. Our aims are to (1) evaluate the immunogenicity of mRNA vaccines co-formulated with two distinct adjuvants—1V270 (a modified TLR7 agonist) and Sanford Burnham Prebys-0686844 (bufalin, a known molecule with novel STAT1-dependent immune activity), and (2) assess therapeutic efficacy in a colorectal cancer model. Methods include mRNA-LNP formulation, in vivo immune profiling, and tumor challenge studies. Expected outcomes include stronger neoantigen-specific CD8+ and CD4+ T cell responses, enhanced tumor control, and robust memory formation. These results will define a strategy to overcome immunogenicity barriers and significantly improve mRNA vaccine efficacy in cancer.

Solid Tumors

This project addresses a key barrier in neoantigen-based cancer immunotherapy: the poor immunogenicity of many tumor neoantigens. We hypothesize that co-formulating mRNA neoantigen vaccines with innate immune adjuvants can enhance antitumor immunity by promoting stronger, more durable T cell responses.

Scripps Research

Targeted Immunopotentiation of Neoantigen Vaccines Using Innate Immune Agonists

Corinne McDaniels-Davidson, PhD (San Diego State)

This study hypothesizes that pre-diagnostic care, including primary care provider (PCP) utilization and cancer screening, is an overlooked but critical mediator of cancer health disparities. It aims to (1) characterize pre-diagnostic care utilization across racial and ethnic groups, (2) test how pre-diagnostic care is associated with stage at diagnosis and cancer-specific mortality, and (3) conduct mediation analyses to quantify the relationship between pre-diagnostic care and disparities in cancer outcomes. Using SEER-Medicare data, the team will assess associations between pre-diagnostic care, diagnostic stage, and cancer outcomes through multivariable models, and will apply mediation analysis to better understand how pre-diagnostic care contributes to cancer health disparities. The expected outcome is a clearer understanding of how PCP utilization influences cancer outcomes and disparities, helping to inform strategies to improve outcomes for underserved communities

Prostate Cancer; Breast Cancer; Colorectal Cancer

This study hypothesizes that pre-diagnostic care, including primary care provider (PCP) utilization and cancer screening, is an overlooked but critical mediator of cancer health disparities. It aims to (1) characterize pre-diagnostic care utilization across racial and ethnic groups, (2) test how pre-diagnostic care is associated with stage at diagnosis and cancer-specific mortality, and (3) conduct mediation analyses to quantify the relationship between pre-diagnostic care and disparities in cancer outcomes.

Addressing Cancer Disparities Through Pre-Diagnostic Care: A SEER-Medicare Analysis of Prostate, Breast, and Colorectal Cancer

Linda Lara-Jacobo, PhD (San Diego State Research Foundation)

Nicolas Lopez-Galvez, PhD (San Diego State Research Foundation)

Gastrointestinal (GI) cancers are a major contributor to overall United States cancer burden. Most cases arise from modifiable exposures, but prevention depends on access to resources and information. In Imperial Valley, a predominantly Latino, agricultural region in southeast California, a farmworker advocacy organization raised concerns to our research team about GI cancer risk linked to environmental and occupational exposures. In response, we propose a study in Imperial Valley evaluating the correlation of environmental exposures and stool-based biomarkers with GI cancer risk among 40 farmworkers and 40 non-farmworkers. Participants will wear a silicone wristband to monitor exposures (Aim 1a), and provide a stool sample for biomarker analysis (Aim 1b). We will also interview community stakeholders to explore GI cancer risk awareness (Aim 2). This community-based project will generate foundational data to inform culturally tailored GI cancer prevention and detection strategies.

Colorectal Cancer; Pancreatic Cancer 

Gastrointestinal (GI) cancers are a major contributor to overall United States cancer burden. Most cases arise from modifiable exposures, but prevention depends on access to resources and information. In Imperial Valley, a predominantly Latino, agricultural region in southeast California, a farmworker advocacy organization raised concerns to our research team about GI cancer risk linked to environmental and occupational exposures.

Promotora-Led Cancer Prevention in the Fields: A Pilot Study Linking Environmental Pollutants and GI Cancer Risk in Imperial Valley

Pancreatic ductal adenocarcinoma (PDAC) is among the deadliest cancers, with >80% diagnosed at advanced stages and <15% 5-year survival for locally advanced disease. Early detection markedly improves outcomes, yet current risk models miss most high-risk individuals. We hypothesize that integrating clinical, imaging, lifestyle, and genomic data through multi-modal artificial intelligence (AI) will enable accurate early PDAC risk prediction. We will develop: (1) an EHR/imaging model trained on >1M scans with matched clinical data from the UC Cancer Consortium, (2) a lifestyle/genomic model using Mutographs questionnaires and whole-genome sequencing, and (3) a unified predictive framework via ensemble learning. Validation in the independent prospective PRECEDE cohort (150 PDAC cases, 300 controls) will assess accuracy. The expected outcome is a clinically scalable tool for early PDAC detection, enabling targeted surveillance and earlier intervention to improve survival.

Pancreatic ductal adenocarcinoma (PDAC) is among the deadliest cancers, with >80% diagnosed at advanced stages and <15% 5-year survival for locally advanced disease. Early detection markedly improves outcomes, yet current risk models miss most high-risk individuals. 

Multi-Modal AI Framework for Early Detection of Pancreatic Cancer

Rebecca Rakow-Penner, MD, PhD (UC San Diego)

This study hypothesizes that combining multiparametric MRI, including advanced diffusion imaging with restriction spectrum imaging (RSI), and extracellular vesicle (EV)-based liquid biopsy will improve early ovarian cancer detection by enhancing sensitivity and specificity in high-risk women. The aims are to evaluate quantitative imaging and liquid biopsy biomarkers for early detection and to develop and prospectively assess a risk model that integrates MRI findings, liquid biopsy results, genetic risk, and age. In this study, high-risk women (such as those with BRCA1/2 mutations) and newly diagnosed ovarian cancer patients will undergo multiparametric pelvic MRI with high-resolution anatomical, perfusion, and multi-shell diffusion sequences for RSI modeling, while blood samples will be collected for EV-based liquid biopsy. Data will be combined with clinical information using multivariate modeling to construct the risk model. The expected outcome is a preliminary model with high sensitivity and specificity for ovarian cancer detection, validated against pathology.

Ovarian Cancer

This study hypothesizes that combining multiparametric MRI, including advanced diffusion imaging with restriction spectrum imaging (RSI), and extracellular vesicle (EV)-based liquid biopsy will improve early ovarian cancer detection by enhancing sensitivity and specificity in high-risk women.

Ovarian Cancer Comprehensive Screening and Risk Assessment with Extracellular Vesicle Circulating Blood Tumor Marker And MRI

Kelly Kersten, PhD (Sanford Burnham Prebys)

Christina Towers, PhD (The Salk Institute)

While immunotherapy has shown impressive response rates in some cancer patients, many develop resistance. A causal role has been implicated for tumor-associated macrophages, which are notoriously immunosuppressive. But how they acquire this immunosuppressive state is largely unknown. We previously showed that the uptake of tumor-derived material by macrophages induces a metabolic and phenotypic reprogramming that could dictate their function. Amongst the cargo ingested were tumor-derived mitochondria. Here, we hypothesize that cancer cells expel their mitochondria through mitochondrial-derived vesicles and, upon transfer into macrophages, cause reprogramming into an immunosuppressive state that supports tumor growth and drives immunotherapy resistance. This innovative and collaborative proposal will elucidate the mechanisms of mitochondrial transfer in macrophage reprogramming in immunotherapy resistant tumors, to ultimately, improve anti-cancer therapies.

Melanoma and Skin Cancers; Pancreatic Cancer

While immunotherapy has shown impressive response rates in some cancer patients, many develop resistance. A causal role has been implicated for tumor-associated macrophages, which are notoriously immunosuppressive. But how they acquire this immunosuppressive state is largely unknown.

Elucidating How Tumor Mitochondrial Transfer Affects Macrophage Function in Cancer

Pancreas cancer is among the most lethal forms of human cancers. This is based on several factors including the inability to detect it at an early stage and the fact that a typical pancreas tumor is largely comprised of activated stromal cells and their extracellular matrix. In fact, approximately 80 percent of a pancreatic tumor involves stromal cells and the collagen containing extracellular protein matrix that these cells produce. Importantly, this extracellular matrix is used by the tumor cells to invade and metastasize. Also, this matrix is so dense that it limits blood flow to the tumor thereby minimizing the amount of anti-cancer drugs that can reach the tumor. As such, there are no effective therapeutics for patients with pancreatic cancer.

Our grant will focus on our newly developed bispecific antibody that not only targets pancreatic cancer cells directly but also targets the stromal cells within the tumor. In fact, this antibody disrupts the development of the stromal derived extracellular matrix which greatly contributes to disease progression. In collaboration with Dr. Andy Lowy we will explore the anti-tumor activity of this antibody directly on live tumor specimens surgically removed from patients. This represents a form of a clinical trial in a dish. We will also evaluate the anti-tumor activity of this antibody in models of pancreas cancer and assess if this antibody can enhance drug delivery to tumors based on its anti-stromal activity. If successful, this project will provide important information needed to move this antibody into clinical trials in patients with pancreatic cancer.

Pancreas cancer is among the most lethal forms of human cancers. This is based on several factors including the inability to detect it at an early stage and the fact that a typical pancreas tumor is largely comprised of activated stromal cells and their extracellular matrix. In fact, approximately 80 percent of a pancreatic tumor involves stromal cells and the collagen containing extracellular protein matrix that these cells produce.

A Human Bispecific Antibody to Target Pancreatic Cancer Stroma

Oncogenic mutations in K-Ras occur in >95% of PDAC, but resistance rapidly arises to K-Ras inhibitors, driven by elevated levels of OXPHOS. Current OXPHOS inhibitors have dose-limiting toxicities, so developing orthogonal modulators of OXPHOS is an urgent unmet need. We discovered that the transcription factor ZBTB11 mediates the metabolic reprogramming that drives resistance, and developed degraders that countered this resistance with minimal toxicity to healthy cells. The next step in translation is to optimize the ADME/PK properties of our lead degrader. Using a chemical biology platform and hPDAC models, we seek to advance our ZBTB11 degraders to murine models, and use them to demonstrate efficacy in K-Rasi resistant tumors. Our aims are: (1) Develop advanced ZBTB11-targeting degraders suitable as drug prototypes; (2) Validate ZBTB11 degradation as a strategy to overcome KRasi resistance in vivo.

Oncogenic mutations in K-Ras occur in >95% of PDAC, but resistance rapidly arises to K-Ras inhibitors, driven by elevated levels of OXPHOS. Current OXPHOS inhibitors have dose-limiting toxicities, so developing orthogonal modulators of OXPHOS is an urgent unmet need. We discovered that the transcription factor ZBTB11 mediates the metabolic reprogramming that drives resistance, and developed degraders that countered this resistance with minimal toxicity to healthy cells.

Overcoming K-Ras Inhibitor Resistance in PDAC

Childhood Cancers; Personalized Immunotherapy

Mitchell Kronenberg, PhD (La Jolla Institute for Immunology)

Anusha Ganesan, MD, PhD (Rady Children’s Hospital)

Hilde Cheroutre, PhD (La Jolla Institute for Immunology)

Kyu Hye Chun, PhD (UC San Diego and La Jolla Institute for Immunology)

Nicolas Thiault, PhD (La Jolla Institute for Immunology)

Regulatory CD4 T cells (Treg) infiltrate tumors, respond to antigens in the tumor microenvironment, and suppress anti-tumor responses. Using mouse models, we have identified a mechanism for generation of CD4 cytotoxic T cells (CTL). Most important, we developed a method that reliably converts suppressive Treg, and other helper CD4 T cell (Th) subsets, to stable populations of CD4 CTL, with effective cell killing capacity. Humans also are known to have CD4 CTL, but the means to generate them have not been characterized. Based on our mechanistic findings, we will develop a method for generating human CD4 CTL from CD4 Treg and from CD4 Th, with a combination of antigen activation, two cytokines and retinoic acid. We will test human CD4 CTL for function and phenotypic stability, using T cells from peripheral blood and also tumor infiltrating CD4 T cells from pediatric brain tumors (PBT). This will provide a new tool for adoptive T cell and other immune therapies.

Brain & CNS Cancer

Regulatory CD4 T cells (Treg) infiltrate tumors, respond to antigens in the tumor microenvironment, and suppress anti-tumor responses. Using mouse models, we have identified a mechanism for generation of CD4 cytotoxic T cells (CTL). Most important, we developed a method that reliably converts suppressive Treg, and other helper CD4 T cell (Th) subsets, to stable populations of CD4 CTL, with effective cell killing capacity

La Jolla Institute for Immunology

Enlisting Cytotoxic CD4+ T Cells to Fight Childhood Cancers

Steven Olson, PhD (Sanford Burnham Prebys)

Dan Theodorescu, MD, PhD (University of Arizona)

Targeting cisplatin resistance will improve survival in muscle-invasive bladder cancer (MIBC) while reducing platinum dosage, minimizing toxicity. We discovered that the protein, NPEPPS, drives cisplatin resistance in bladder cancer cells because it binds and inhibits anion channels (VRACs), which ordinarily transport cisplatin into cells. In proof-of-concept studies, we have shown inhibitors of NPEPPS, which prevent binding to VRACs, can overcome cisplatin resistance in MIBC. As these inhibitors are relatively non-specific, our goal is to discover novel selective inhibitors with drug-like properties suitable to target engagement in tumor tissue. Using cancer cell lines, patient-derived organoids, and in vivo models, we will demonstrate how NPEPPS inhibition restores platinum sensitivity in resistant tumors. This work will validate NPEPPS as a therapeutic target and deliver optimized lead compounds, transforming the therapeutic outcomes of platinum-based treatments in bladder cancer.

Bladder Cancer; Solid Tumors

Targeting cisplatin resistance will improve survival in muscle-invasive bladder cancer (MIBC) while reducing platinum dosage, minimizing toxicity. We discovered that the protein, NPEPPS, drives cisplatin resistance in bladder cancer cells because it binds and inhibits anion channels (VRACs), which ordinarily transport cisplatin into cells. In proof-of-concept studies, we have shown inhibitors of NPEPPS, which prevent binding to VRACs, can overcome cisplatin resistance in MIBC.

Discovery Of NPEPPS Inhibitors for the Treatment of Muscle-invasive Bladder Cancer

While Hispanic youth will comprise 33% of the U.S. population by 2030 and have higher incidence of cancers, their participation in cancer research
is critically low, and they have poorer survival rates than non-Hispanic Whites. The goal of this Curebound Equity award is to increase adolescent Hispanic participation in cancer clinical trials. We will implement a navigation intervention in which trained adolescent peers deliver culturally concordant education to Hispanic adolescents during recruitment for cancer clinical trials. This is significant because by increasing minority participation in clinical trials, we can translate discoveries and treatment benefits equally, and, ultimately, improve equity of survival among underserved Hispanics. This study has a particular impact in San Diego and California, where Hispanics are the fastest growing racial-ethnic group and are projected to comprise 50% of the population.


“As a Hispanic physician-scientist, I have witnessed firsthand the disparities in access to cancer care, particularly among our minority Hispanic populations. My goal is to provide the same opportunities to all children and adolescents with cancer, regardless of their background. Hispanics are significantly underrepresented in cancer clinical trials; we need effective interventions to overcome this very low clinical trial participation. This Curebound Equity grant is instrumental to help reduce health disparities in Hispanic adolescents with cancer and lays the foundation for future interventions to change the course of cancer research and care for underserved communities in San Diego.” – Paula Aristizabal, MD, MAS

Cancer Equities

While Hispanic youth will comprise 33% of the U.S. population by 2030 and have higher incidence of cancers, their participation in cancer research
is critically low, and they have poorer survival rates than non-Hispanic Whites.

Rady Children’s Hospital

COMPRENDO-A: Peer-Navigation to Improve Accrual of Adolescents with cancer into Clinical Trials

Novel Approaches and New Therapeutic Platforms

Half a million patients in the United States suffer from cancers that are driven by mutant forms of the protein NRAS. Unfortunately, there are a lack of effective drugs that target NRAS, resulting in poor clinical outcomes for these patients. We are overcoming prior hurdles to developing NRAS-targeted therapies by developing drugs that inhibit NRAS palmitoylation, a fatty acid modification essential for its cancer- driving function. This project will fund critical pre-clinical research and development activities in our NRAS program and support our goal of reaching First-in-Human trials by 2028.

“At Palm Therapeutics, we are committed to developing new therapies for some of the most difficult to treat cancers. We are thrilled and honored to receive the Catalyst Grant, which will help us reach key scientific milestones in our NRAS inhibitor program and support our ultimate mission of providing better treatment options for NRAS-mutant cancer patients.” – Andrew Rudd, PhD

Precision Oncology

Half a million patients in the United States suffer from cancers that are driven by mutant forms of the protein NRAS. 

Palm Therapeutics: Preclinical Development of NRAS Palmitoylation Inhibitors for NRAS Mutant Cancers

Novel Therapeutics & Platforms, Immunotherapies & Personalized Vaccines

Immunotherapy is rapidly gaining its place as a mainstream treatment of solid cancers, Nonetheless, less than 30% of patients with lung cancer benefit from this approach. This is the result of large gaps in our knowledge of how immunotherapies work and how to choose the right treatment or treatment combination for a particular patient. Cancer immunotherapy aims to stimulate the patient's immune system to attack and kill tumor cells. Our laboratory identified an important immune cell type and a novel surface target to enhance their anti-tumor function. Here, we team with experts in drug development to identify agents to boost tumor immune responses. Studies in this discovery grant have the potential to identify a new class of immunotherapy drugs for patients with lung cancer.

Immunotherapy

Immunotherapy is rapidly gaining its place as a mainstream treatment of solid cancers, Nonetheless, less than 30% of patients with lung cancer benefit from this approach.

A novel approach to boost anti-tumor immune responses 

Cancer Equities, Novel Therapeutics & Platforms, Immunotherapies & Personalized Vaccines

In 2030, pancreatic cancer (PC) will be the #1 cause of cancer-related death. This is due to a very low survival rate and limited treatment options that have poor responses. Our current chemotherapy does not work due to a thick barricade that surrounds PC that makes it hard for therapies to get into the tumor. Our team has discovered and validated new small molecules called peptides that can target drugs directly to these tumor barriers and then pass through them to access the cancer and immune cells within PC. A benefit to the peptide-targeting technique is that we avoid damaging healthy tissue. We will use these peptides to boost the immune system's ability to fight cancer cells and then reduce cells that block this response. We anticipate moving these into early clinical trials at UCSD.

In 2030, pancreatic cancer (PC) will be the #1 cause of cancer-related death. This is due to a very low survival rate and limited treatment options that have poor responses. Our current chemotherapy does not work due to a thick barricade that surrounds PC that makes it hard for therapies to get into the tumor.

Moores Cancer Center, UCSD

Harnessing Tumor-Penetrating Peptides to Modulate the Pancreatic Tumor Immune Microenvironment

Children with bone marrow failure syndromes are pre-disposed to developing leukemia. The only way to prevent leukemia in these children is a bone marrow transplant to remove the diseased cells that ultimately turn into leukemia. However, current methods for bone marrow transplant have high rates of complications and death due to toxicity of the chemotherapy used to prepare a patient for receiving transplanted cells and inappropriate immune system activation after transplant. We will address these complications by developing less toxic chemotherapy alternatives and developing ways to shield the immune system from inappropriate activation. These advances will overcome obstacles that limit performing bone marrow transplant to prevent leukemia in children with bone marrow failure syndromes.

Leukemia

Children with bone marrow failure syndromes are pre-disposed to developing leukemia. The only way to prevent leukemia in these children is a bone marrow transplant to remove the diseased cells that ultimately turn into leukemia.

Prevention of leukemia in cancer predisposition syndromes

Triple Negative Breast Cancer (TNBC) is an aggressive and highly recurrent type of cancer that is resistant to most therapies.


Our goal is to develop a new approach that uses our previous immunity against viruses to fight tumors. We will deliver viral proteins to tumor cells to make our immune system think it is fighting an infection, and instead turn against the tumor. We chose cytomegalovirus as a model because it infects >50% of the population, and generates a strong immune memory. We have tested our strategy in pancreatic tumors, and have delayed tumor growth and increased survival by 68%.

We believe this approach will also work for TNBC. This strategy is broadly applicable to many people and different types of cancer, making it a major medical advance.

Breast Cancer

Triple Negative Breast Cancer (TNBC) is an aggressive and highly recurrent type of cancer that is resistant to most therapies. Our goal is to develop a new approach that uses our previous immunity against viruses to fight tumors.

Harnessing cytomegalovirus T-cells to combat triple-negative breast cancer

Checkpoint inhibitor immunotherapy has revolutionized cancer treatment. Despite durable responses in some patients, the majority either fail to respond or develop resistance to current immunotherapy. Therefore, a significant unmet clinical need remains to treat patients with progressive disease after immunotherapy. We made the paradoxical observation that an immune suppressive drug in combination with checkpoint blockade is effective in Hodgkin lymphoma patients who fail/relapse after immunotherapy treatment. Our studies revealed that modulation of specific immune cells by JAK inhibition correlates with response and these cells are required for response. In this proposal, we will address the hypothesis that the novel combination therapy could also help patients with solid tumors.

Checkpoint inhibitor immunotherapy has revolutionized cancer treatment. Despite durable responses in some patients, the majority either fail to respond or develop resistance to current immunotherapy. Therefore, a significant unmet clinical need remains to treat patients with progressive disease after immunotherapy.

Overcoming immunotherapy resistance in solid tumors with JAK inhibitor with anti-PD1 combination therapy

Pancreatic ductal adenocarcinoma has a very low 5-year survival rate of 13%. Current chemotherapy treatments often fail due to drug resistance and side effects. CDK4/6 inhibitors are a promising approach but lack reliable markers to predict patient response. This project aims to improve treatment by identifying biomarkers that predict how the cancer responds to chemotherapy and CDK4/6 inhibition. Using advanced machine learning models called visible neural networks, we will refine these models to better predict drug responses. Collaboration between experts will test these models on patient samples. The goal is to develop more effective treatments and pave the way for clinical trials in San Diego.

Pancreatic ductal adenocarcinoma has a very low 5-year survival rate of 13%. Current chemotherapy treatments often fail due to drug resistance and side effects. CDK4/6 inhibitors are a promising approach but lack reliable markers to predict patient response.

Using AI Models for Predicting Human Pancreatic Cancer Response to Cell Cycle Targeted Therapy

Prevention & Diagnostic Tools, Novel Therapeutics & Platforms, Pediatric Cancers

This proposal, from a transdisciplinary team of scientists, seeks to develop a new treatment for hereditary colorectal cancer (CRC) syndromes such as familial adenomatous polyposis (FAP) and Lynch syndromes, both representing conditions that greatly increase the risk of cancer. Currently there is no treatment that is effective in mitigating CRC risk in the predisposed children. We have developed innovative and precise computational tools and engineered bacteria whose use together can estimate, reduce and track the risk of cancer. This 12-month study tests the safety and effectiveness of this treatment in mice and human preclinical models. Success will advance us towards regulatory approval and could revolutionize treatment for CRC predispositions, offering new hope to those at high risk.

This proposal, from a transdisciplinary team of scientists, seeks to develop a new treatment for hereditary colorectal cancer (CRC) syndromes such as familial adenomatous polyposis (FAP) and Lynch syndromes, both representing conditions that greatly increase the risk of cancer.

Bugs as drugs to fight hereditary cancer syndromes in children 

In the US, the high costs of cancer care force many patients to go without basic needs like food, housing and utilities, which often leads to treatment delays and care interruptions that affect their quality of life and can lead
to worse survival. Recognizing the importance of this issue, the U.S. Department of Health and Human Services implemented new policies, which began in 2024, to enable health systems to begin to address patients’ social needs. The overall project goal is to guide implementation of these policies at UC San Diego Moores Cancer Center, taking a mixed- methods approach that uses electronic health record data and qualitative data from the lived experiences of patients and caregivers, community- based organizations, and healthcare staff. Findings from our project will help ensure equitable access to whole person care for all patients, we hope that our project will reduce cancer health disparities in patient populations with historically poor outcomes.

“This funding mechanism is a testament to Curebound’s uniqueness and importance as a major funder of cancer research, because it illustrates their willingness to support projects that may lead to groundbreaking advancements (i.e., discovery), as well as projects that focus on what’s affecting patients right now (i.e., health equity). Our team will engage with stakeholders to inform new policy options that can address inequities in cancer care and to better understand the needs and experiences of the people we serve to advance health equity in our community.” – Matthew Banegas, PhD

In the US, the high costs of cancer care force many patients to go without basic needs like food, housing and utilities, which often leads to treatment delays and care interruptions that affect their quality of life and can lead
to worse survival.

San Diego State University

Improving Health Equity and Cancer Care Quality through Tailored Navigation

Novel Therapeutics & Platforms, Immunotherapies & Personalized Vaccines, Pediatric Cancers

What if we could engineer our own cells to become potent cancer fighters? We have developed a new technology of targeted virus-like particles (VLPs) that enable specific immune cells to directly express chimeric antigen receptors (CARs). Unlike current methods that require production of engineered immune cells outside the body, this approach enables direct injection of the targeted VLPs into the patient to produce CAR-expressing immune cells with anti-tumor activity. These studies will use both ovarian cancer and neuroblastoma (pediatric cancer) models to demonstrate this approach can be readily adopted to treat most any tumor type. Success with these studies will enable us to quickly translate this system to clinical trials for treatment of patients with refractory malignancies.

Ovarian Cancer and Neuroblastoma

What if we could engineer our own cells to become potent cancer fighters? We have developed a new technology of targeted virus-like particles (VLPs) that enable specific immune cells to directly express chimeric antigen receptors (CARs). 

Targeted virus-like particles to engineer immune cells in vivo for treatment of ovarian cancer and neuroblastoma. 

Prevention & Diagnostic Tools, Novel Therapeutics & Platforms

Platinating agents, particularly cisplatin, are the most widely used group of cytotoxic drugs worldwide, treating many adult- and pediatric-onset cancers. Nearly 40% of common childhood malignant tumors rely on cisplatin chemotherapy for cure exposing ~2,000 children in the United States to cisplatin each year. These agents cause severe off-target toxicities, such as hearing loss. Cisplatin crosses the blood-labyrinth barrier leading to damage to the sensory cells of the cochlea. This results in severe, progressive, and permanent hearing loss in ~75% of cisplatin-treated children and ~80% of young adults with testicular cancer. Our group has identified a small molecule that, in preliminary studies, demonstrates near complete protection against the ototoxic effects of cisplatin. 

Hearing Loss Prevention

Platinating agents, particularly cisplatin, are the most widely used group of cytotoxic drugs worldwide, treating many adult- and pediatric-onset cancers. Nearly 40% of common childhood malignant tumors rely on cisplatin chemotherapy for cure exposing ~2,000 children in the United States to cisplatin each year.

California Institute of Technology

Advancing Pharmacological Interventions for Mitigating Ototoxicity

The standard of care treatment for locally advanced cervical cancer remains combined radiotherapy with cisplatin. Although patients have improved outcomes with chemo-radiotherapy, tumor recurrence remains a problem. Moreover, combining chemotherapy with radiotherapy increases treatment related side effects. While breakthroughs in radiotherapy and immunotherapy have resulted in precision cancer care, chemotherapies given with radiotherapy remain non-targeted drugs. We propose a precision oncology strategy by replacing classical chemotherapies with a targeted antibody drug conjugate, tisotumab-vedotin. In this proposal, we will perform key translational studies necessary for clinical trial testing of tisotumab-vedotin with radiotherapy and immunotherapy for women with cervical cancer.

Cervical Cancer

The standard of care treatment for locally advanced cervical cancer remains combined radiotherapy with cisplatin. Although patients have improved outcomes with chemo-radiotherapy, tumor recurrence remains a problem. Moreover, combining chemotherapy with radiotherapy increases treatment related side effects. 

Exploiting tissue factor expression for precision therapy of advanced cervical cancer

Colorectal cancer is the second-leading cause of cancer deaths in the US and expected to kill more than 53,000 people in 2024. The CRC incidence is rising sharply among people younger than 50 and these cases are often diagnosed at more aggressive stages where the current standard treatments are inadequate. Seren Bio is developing a first-in-class drug that specifically kills cancer cells without harming normal cells based on the fact that all cancer cells consume a large amount of glucose, called glycolysis, to survive and propagate in contrast to normal cells. Our drug will induce a large oxidative burst in cells mainly dependent on glycolysis such as cancer cells, which leads to their demise. We demonstrated a proof of this concept in animals already and now we are working
on improving the efficacy of a potential drug candidate. Because our technology exploits the cellular trait shared by all cancer cells, our success will save a large population of not only colorectal cancer patients who don’t respond to the conventional therapies but also benefit many patients suffering from other types of cancer.

“We discovered the cellular target, a natural ligand, and the mechanism by which in principle we can eliminate all cancer cells without harming normal cells, the holy grail of cancer treatment. We are currently testing newly designed synthetic ligands for improved efficacy and pharmacology. The Curebound funding will accelerate our efforts to advance this endeavor as we currently operate in a small budget of the pre-seed investment.” – Jongdae Lee, PhD

Colorectal Cancer

Colorectal cancer is the second-leading cause of cancer deaths in the US and expected to kill more than 53,000 people in 2024. The CRC incidence is rising sharply among people younger than 50 and these cases are often diagnosed at more aggressive stages where the current standard treatments are inadequate.

Seren Bio: Development of DMGV analogs as a first-in-class, small molecule therapy for colorectal cancer

Annually, approximately 250,000 people worldwide succumb to glioblastoma (GBM), with a median survival time of just 15 months post-diagnosis, despite treatment. The disease’s complexity leads to near-inevitable recurrence and a dismal 5-year survival rate of 5-7%. Moreover, GBM progressively impairs neurological functions, severely affecting quality of life. Resolute Science is advancing RS-5 and RS-8, two first-in-class therapeutics that leverage our Macrophage-Targeted- Conjugates (MAC-TACs) delivery platform. The most promising candidate will be selected for clinical trials targeting glioblastoma. We anticipate that successful validation of either RS-5 or RS-8 could introduce a groundbreaking treatment option for GBM, offering a safer, and more effective therapeutic to patients who are currently without options.

“Resolute Science’s goal is to provide cancer cures for more people. We are extremely grateful for Curebound’s support & funding, which will allow us to accelerate our preclinical research into brain tumors and GBM specifically.” – Faith Barnett, MD, PhD

Glioblastoma

Annually, approximately 250,000 people worldwide succumb to glioblastoma (GBM), with a median survival time of just 15 months post-diagnosis, despite treatment.

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