Abstract Introduction Invariant natural killer T (iNKT) cells are a unique subset of T lymphocytes that recognize glycolipid antigens presented by CD1d. As key liver-resident immune cells, they contribute to the pathogenesis of liver diseases such as autoimmune hepatitis. Understanding mechanisms regulating iNKT cell development and function may uncover therapeutic targets. N6-methyladenosine (m6A), the most abundant eukaryotic RNA modification, controls mRNA stability and translation, primarily via the m6A reader YTHDF2. While YTHDF2 is known to regulate immune cell functions, its role in iNKT cells and liver disease remains unclear. Methods We generated Ythdf2 conditional knockout (cKO) mice and assessed iNKT cell development in thymus, spleen, and liver by flow cytometry. Thymic iNKT cells from Ythdf2 cKO and controls underwent scRNA-seq. α-GalCer- and Con A-induced liver injury models were used to evaluate YTHDF2 function. Liver iNKT cells post-α-GalCer treatment were analyzed by bulk RNA-seq. Results Ythdf2 cKO mice showed markedly reduced iNKT cell numbers in thymus, liver, and spleen, with a significant loss of stage 3 thymic iNKT cells. YTHDF2 was dispensable for differentiation into NKT1, NKT2, and NKT17 subsets. scRNA-seq analysis identified transcription factor Bach2 as a potential YTHDF2 target during iNKT cell development. Loss of YTHDF2 in iNKT cells exacerbated α-GalCer- and Con A-induced acute liver injury. Ythdf2 cKO mice displayed elevated serum TNF-α levels compared to controls; however, TNF-α was mainly secreted by monocyte-derived macrophages rather than iNKT cells. Bulk RNA-seq of liver iNKT cells revealed that Csf1 (macrophage colony-stimulating factor), a key cytokine for macrophage differentiation, survival, migration, and function, is likely regulated by YTHDF2 in iNKT cells. Conclusion YTHDF2 is essential for iNKT cell development and modulates iNKT cell-mediated liver injury. Further studies are needed to define underlying mechanisms. Funding Source NIH Topic Categories Immune Response Regulation: Molecular Mechanisms (IRM)

Abstract Introduction Innate lymphoid cells (ILCs) represent a highly diverse family of lymphocytes that play pivotal roles in tissue homeostasis, inflammation, and cancer immunity. Despite growing evidence of their plasticity and functional heterogeneity, a comprehensive understanding of human ILC diversity across pathological contexts remains limited. Methods We performed large-scale single-cell RNA sequencing (scRNA-seq) analysis of 3,322 human samples spanning 60 physiological and pathological conditions. Results By integrating and harmonizing ILC transcriptomes across tissues and diseases, we systematically characterized the cellular states, transcriptional regulators, and disease-specific adaptations of ILC subsets. Our atlas reveals both conserved and disease-specific transcriptional programs of ILCs. Pathological conditions induce profound compositional and phenotypic shifts in ILC subsets. Comparative analyses between TCF7+ ILC1 and ZNF683+ NK-derived IFNG+ ILC1 populations highlight distinct transcription factor dependencies and microenvironmental stimuli shaping their effector programs. Notably, GZMB+ ILC2 cells, enriched in multiple cancer types, were associated with improved patient prognosis, suggesting a potential cytotoxic role. In contrast, NR4A1+ ILC3 cells within NCR⁻ ILC3 clusters were preferentially enriched in tumors and inflammatory diseases, correlating with poor prognosis and resistance to immunotherapy. Conclusion This comprehensive single-cell atlas delineates the dynamic landscape of human ILCs across diseases. Funding Source n/a Topic Categories Computational and Systems Immunology (COMP)

Chimeric antigen receptor (CAR) T-cell therapy enables potent, antigen-specific immune responses and has demonstrated success in treating hematologic malignancies. However, conventional ex vivo CAR T manufacturing remains costly, individualized, and logistically complex, posing significant barriers to accessibility and scalability. In vivo CAR T-cell engineering offers a transformative alternative by reprogramming endogenous T cells within the patient, bypassing the need for cell harvesting and expansion. This review focuses on current in vivo CAR T delivery strategies, including viral vectors (such as lentiviruses, γ-retroviruses, adeno-associated viruses, and viral-like particles) and nonviral systems (such as lipid nanoparticles and polymer-based carriers), with a focus on how these platforms are engineered to achieve efficient, specific, and safe CAR transgene transfer. We also discuss the design principles of vector tropism, membrane modifications, and targeting ligands, as well as translational studies in both preclinical and clinical settings. Finally, the review explores delivery-related challenges and future perspectives for optimizing vector stability, enhancing T-cell targeting, and reducing immunogenicity to advance in vivo CAR T therapy toward broader clinical applications.

N6-methyladenosine (m6A) RNA modification has emerged as a pivotal epitranscriptomic mark shaping RNA metabolism and cellular programs. Among the diverse m6A reader proteins, YTHDF2 has garnered significant attention as a key regulator of RNA stability. Recent studies highlight the multifaceted roles of YTHDF2 in orchestrating hematopoietic stem cell self-renewal and differentiation, fine-tuning immune cell development and function, and modulating tumor-immune interactions within the tumor microenvironment. YTHDF2 has also been shown to function as a reader for RNA 5-methylcytosine (m5C) modification. By linking m6A- and/or m5C-dependent RNA dynamics to hemato-immune homeostasis, YTHDF2 functions as a central epitranscriptomic integrator linking intrinsic genetic programs to developmental and environmental cues. Here, we summarize current advances in understanding YTHDF2-mediated RNA regulation across physiological and pathological contexts, discuss its potential as a therapeutic target in immune-related diseases and cancers, and highlight future directions in the field.

Abstract Introduction Innate lymphoid cells (ILCs) represent a highly diverse family of lymphocytes that play pivotal roles in tissue homeostasis, inflammation, and cancer immunity. Despite growing evidence of their plasticity and functional heterogeneity, a comprehensive understanding of human ILC diversity across pathological contexts remains limited. Methods We performed large-scale single-cell RNA sequencing (scRNA-seq) analysis of 3,322 human samples spanning 60 physiological and pathological conditions. Results By integrating and harmonizing ILC transcriptomes across tissues and diseases, we systematically characterized the cellular states, transcriptional regulators, and disease-specific adaptations of ILC subsets. Our atlas reveals both conserved and disease-specific transcriptional programs of ILCs. Pathological conditions induce profound compositional and phenotypic shifts in ILC subsets. Comparative analyses between TCF7+ ILC1 and ZNF683+ NK-derived IFNG+ ILC1 populations highlight distinct transcription factor dependencies and microenvironmental stimuli shaping their effector programs. Notably, GZMB+ ILC2 cells, enriched in multiple cancer types, were associated with improved patient prognosis, suggesting a potential cytotoxic role. In contrast, NR4A1+ ILC3 cells within NCR⁻ ILC3 clusters were preferentially enriched in tumors and inflammatory diseases, correlating with poor prognosis and resistance to immunotherapy. Conclusion This comprehensive single-cell atlas delineates the dynamic landscape of human ILCs across diseases. Funding Source n/a Topic Categories Computational and Systems Immunology (COMP)

CD4+ T cells differentiate into various subsets, including T helper 1 (Th1), Th2, Th9, Th17 and regulatory T (Treg) cells, which are essential for immune responses and cancer immunotherapy. However, the role of RNA N6-methyladenosine (m6A) modification in this differentiation is unclear. Here we show that YTHDF2, an important m6A reader protein known to destabilize m6A-modified mRNA, negatively regulates Th9 cell differentiation. Ablation of Ythdf2 in both mouse and human naive CD4+ T cells promotes Th9 differentiation by stabilizing Gata3 and Smad3 mRNA under interleukin-4 (IL-4) and transforming growth factor β (TGF-β) signaling, respectively. Ythdf2-deficient Th9 cells produce increased amounts of IL-9 and IL-21, leading to increased tumor infiltration and cytotoxicity by CD8+ T cells and natural killer (NK) cells, thereby improving antitumor activity compared with wild-type Th9 cells. Moreover, YTHDF2 depletion in CAR-Th9 cells enhances their immune activation, reduces their terminal differentiation and augments their antitumor efficacy. Targeting YTHDF2 is thereby a promising strategy to enhance Th9 and CAR-Th9 cell-based cancer immunotherapies. The authors show that the m6A reader protein YTHDF2 negatively regulates Th9 cell differentiation and function. Ablation of YTHDF2 promotes antigen-specific Th9 cell and CAR-Th9 cell antitumor activity in solid tumors.

Natural killer (NK) cells are emerging as a promising tool for cancer immunotherapy due to their innate ability to selectively recognize and eliminate cancer cells. Over the past 3 decades, strategies to harness NK cells have included cytokines, small molecules, antibodies, and the adoptive transfer of autologous or allogeneic NK cells, both unmodified and genetically engineered. Despite favorable safety profiles in clinical trials, challenges such as limited in vivo persistence, exhaustion, and the suppressive tumor microenvironment continue to hinder their efficacy and durability. This review categorizes NK cell-based therapies into 3 major approaches: (i) cellular therapies, including unmodified and chimeric antigen receptor-engineered NK cells; (ii) cytokine-based strategies such as interleukin-2 and interleukin-15 derivatives; and (iii) antibody-based therapies, including immune checkpoint inhibitors and NK cell engagers. We highlight these advancements, discuss current limitations, and propose strategies to optimize NK cell-based therapies for improved cancer treatment outcomes.

N6-methyladenosine (m6A) modification plays pivotal roles in myriad biological processes. The YTH domain family protein YTHDF2, recognized as an m6A "reader" protein, is primarily associated with the canonical function of facilitating RNA degradation. Nevertheless, the intricate non-decay regulatory mechanism exerted by YTHDF2 remains enigmatic. Here, using ovarian cancer as a model, we demonstrate that YTHDF2 forms a tangible interaction with the eukaryotic translation initiation factor eIF3F and the RNA helicase DDX1, thereby enhancing protein synthesis in tumor cells. Instead of promoting RNA degradation, YTHDF2 facilitates the translation of m6A-modified mRNAs encoding microtubule-associated proteins, which drives cancer progression and reduces the chemosensitivity of cancer cells to paclitaxel, a commonly used chemotherapy drug. Notably, through virtual screening, we identified a YTHDF2-specific small-molecule inhibitor. Therapeutic targeting of YTHDF2 with this inhibitor effectively suppresses protein translation in tumor cells and reverses paclitaxel resistance.

N6-methyladenosine (m6A) is a key mRNA modification influencing mRNA stability and translation. YTHDF2, a major m6A 'reader', was initially recognized for promoting mRNA decay but is now also known to enhance translation by binding to methylated mRNAs. YTHDF2 maintains the function of immune suppressive cells, including tumor-associated macrophages (TAMs), myeloid-derived suppressor cells (MDSCs), and regulatory T cells (Tregs), while also supporting cytotoxic immune cells, including natural killer (NK) and CD8+ T cells. Additionally, YTHDF2 acts as a tumor-intrinsic regulator orchestrating tumor immune evasion. Its multifaceted roles in tumor immunity make YTHDF2 a promising yet challenging therapeutic target. This review explores the complex roles and mechanisms of YTHDF2 in cancers, immune regulation, and tumor immune evasion and highlights emerging therapeutic strategies that target YTHDF2.

Natural killer (NK) cells are innate lymphocytes that play central roles in immune surveillance, tissue homeostasis, and the regulation of adaptive immunity. While traditionally studied in the context of viral infection and cancer, it is now clear that NK cells also influence the pathogenesis and outcomes of a wide range of non-malignant conditions. Growing evidence links NK cell activity to autoimmune diseases, transplantation tolerance or rejection, neurodegenerative disorders, and chronic infections. At the same time, advances in cellular engineering and immunotherapy have expanded opportunities to harness NK cells as therapeutic agents in these settings. In this review, we summarize recent progress in understanding how NK cells contribute to the development and regulation of non-malignant diseases, and highlight emerging strategies to harness NK cells for therapeutic benefit. By integrating findings across diverse fields, we aim to provide a comprehensive perspective on NK cell biology beyond cancer, emphasizing their dual potential as both drivers of pathology and tools for intervention. Ultimately, a deeper understanding of NK cell function in these contexts will open new avenues for precision immunotherapy and improve outcomes for patients with non-malignant diseases.

Tumors evade attacks from the immune system through various mechanisms. Here, we identify a component of tumor immune evasion mediated by YTH domain–containing family protein 2 (YTHDF2), a reader protein that usually destabilizes m 6 A-modified mRNA. Loss of tumoral YTHDF2 inhibits tumor growth and prolongs survival in immunocompetent tumor models. Mechanistically, tumoral YTHDF2 deficiency promotes the recruitment of macrophages via CX3CL1 and enhances mitochondrial respiration of CD8 + T cells by impairing tumor glycolysis metabolism. Tumoral YTHDF2 deficiency promotes inflammatory macrophage polarization and antigen presentation in the presence of IFN-γ. In addition, IFN-γ induces autophagic degradation of tumoral YTHDF2, thereby sensitizing tumor cells to CD8 + T cell–mediated cytotoxicity. Last, we identified a small molecule compound that preferentially induces YTHDF2 degradation, which shows a potent antitumor effect alone but a better effect when combined with anti–PD-L1 or anti–PD-1 antibodies. Collectively, YTHDF2 appears to be a tumor-intrinsic regulator that orchestrates immune evasion, representing a promising target for enhancing cancer immunotherapy.

AbstractBackgroundIn a previously reported Phase I trial, we observed therapy‐associated declines in circulating myeloid‐derived suppressor cells (MDSCs) with the administration of white button mushroom (WBM) tablets in prostate cancer (PCa) patients. These observations led us to hypothesise that WBM could mitigate PCa progression by suppressing MDSCs.MethodsWe performed bidirectional translational research to examine the immunomodulatory effects of WBM consumption in both syngeneic murine PCa models and patients with PCa participating in an ongoing randomised Phase II trial (NCT04519879).ResultsIn murine models, WBM treatment significantly suppressed tumour growth with a reduction in both the number and function of MDSCs, which in turn promoted antitumour immune responses mediated by T cells and natural killer (NK) cells. In patients, after consumption of WBM tablets for 3 months, we observed a decline in circulating polymorphonuclear MDSCs (PMN‐MDSCs), along with an increase in cytotoxic CD8+ T and NK cells. Furthermore, single immune cell profiling of peripheral blood from WBM‐treated patients showed suppressed STAT3/IRF1 and TGFβ signalling in circulating PMN‐MDSCs. Subclusters of PMN‐MDSCs presented transcriptional profiles associated with responsiveness to fungi, neutrophil chemotaxis, leukocyte aggregation, and regulation of inflammatory response. Finally, in mouse models of PCa, we found that WBM consumption enhanced the anticancer activity of anti‐PD‐1 antibodies, indicating that WBM may be used as an adjuvant therapy with immune checkpoint inhibitors.ConclusionOur results from PCa murine models and patients provide mechanistic insights into the immunomodulatory effects of WBM and provide a scientific foundation for WBM as a nutraceutical intervention to delay or prevent PCa progression.Highlights White button mushroom (WBM) treatment resulted in a reduction in pro‐tumoural MDSCs, notably polymorphonuclear MDSCs (PMN‐MDSCs), along with activation of anti‐tumoural T and NK cells. Human single immune cell gene expression profiling shed light on the molecular alterations induced by WBM, specifically on PMN‐MDSCs. A proof‐of‐concept study combining WBM with PD‐1 blockade in murine models revealed an additive effect on tumour regression and survival outcomes, highlighting the clinical relevance of WBM in cancer management.

Chronic graft-versus-host disease (cGVHD), characterized by chronic tissue inflammation and fibrosis involving multiple organs, remains a major complication after allogeneic hematopoietic stem cell transplantation (allo-HSCT). Dimethyl fumarate (DMF) is an anti-inflammatory drug approved for the treatment of multiple sclerosis and psoriasis. We previously reported that DMF effectively inhibits acute GVHD (aGVHD) while preserving the graft-versus-leukemia effect. However, the role of DMF in cGVHD progression remains unknown. Here, we found that DMF administration significantly suppresses follicular helper T cell (Tfh) differentiation, and germinal center formation and alleviates disease severity in different murine cGVHD models. Mechanistically, DMF treatment downregulates IL-21 transcription by activation of Nrf2, thus orchestrating Tfh-related gene programs both in mice and humans. The inhibitory role of DMF on Tfh cell differentiation was diminished in Nrf2 deficient T cells. Importantly, the therapeutic potential of DMF in clinical cGVHD has been validated in human data whereby DMF effectively reduces IL-21 production and Tfh cell generation in peripheral blood mononuclear cells from active cGVHD patients and further attenuates xenograft GVHD. Collectively, our findings reveal that DMF potently inhibits cGVHD development by repressing Tfh cell differentiation via Nrf2, paving the way for the treatment of cGVHD in the clinic.

Abstract YTHDF2 is a well-known m6A reader protein that binds and destabilizes m6A-modified mRNA. We have identified YTHDF2 as a novel regulator of antitumoral polarization in tumor-associated macrophages (TAMs). However, whether YTHDF2 regulates tumor immune evasion remains unknown. Here, we found that loss of YTHDF2 inhibited tumor growth and prolonged survival in syngeneic B16-OVA melanoma and MC38 colon cancer mouse models. Mechanistically, Ythdf2 deficiency-mediated immune remolding was multifactorial, involving promoting the recruitment and polarization of TAMs via chemoattractant CX3CL1, as well as impairing the tumor glycolysis metabolism and enhancing the mitochondrial respiration of tumor-infiltrating CD8+ T cells, thereby enhancing CD8+ T cell effector functions. We screened a small compound that can target YTHDF2 and promote its degradation. YTHDF2 degrader showed a potent anti-tumor effect and better efficacy when combined with anti-PD-L1 antibody therapy. Collectively, YTHDF2 is implicated as a regulator that orchestrates immune evasion and is a promising target to enhance cancer immunotherapy.

Abstract We described previously a human natural killer (NK) cell population that upregulates PD-L1 expression upon recognizing and reacting to tumor cells or exposure to a combination of IL12, IL18, and IL15. Here, to investigate the safety and efficacy of tumor-reactive and cytokine-activated (TRACK) NK cells, human NK cells from umbilical cord blood were expanded, transduced with a retroviral vector encoding soluble (s) IL15, and further cytokine activated to induce PD-L1 expression. Our results show cryopreserved and thawed sIL15_TRACK NK cells had significantly improved cytotoxicity against non–small cell lung cancer (NSCLC) in vitro when compared with non-transduced (NT) NK cells, PD-L1+ NK cells lacking sIL15 expression (NT_TRACK NK), or NK cells expressing sIL15 without further cytokine activation (sIL15 NK cells). Intravenous injection of sIL15_TRACK NK cells into immunodeficient mice with NSCLC significantly slowed tumor growth and improved survival when compared with NT NK and sIL15 NK cells. The addition of the anti-PD-L1 atezolizumab further improved control of NSCLC growth by sIL15_TRACK NK cells in vivo. Moreover, a dose-dependent efficacy was assessed for sIL15_TRACK NK cells without observed toxicity. These experiments indicate that the administration of frozen, off-the-shelf allogeneic sIL15_TRACK NK cells is safe in preclinical models of human NSCLC and has potent antitumor activity without and with the administration of atezolizumab. A phase I clinical trial modeled after this preclinical study using sIL15_TRACK NK cells alone or with atezolizumab for relapsed or refractory NSCLC is currently underway (NCT05334329).

B-cell acute lymphoblastic leukemia (B-ALL) is an aggressive malignancy characterized by the aberrant accumulation of immature and dysfunctional B cells in bone marrow (BM). Although chemotherapy and other therapies have been widely applied, some patients such as relapsed or drug-refractory (R/R) B-ALL patients exhibit limited response. YT521-B homologous domain-containing protein 1 (YTHDC1) is a nuclear reader of N6-methyladenosine (m6A) RNA modification, which has been implicated in different malignancies including leukemia. In the current study, we show that YTHDC1 is highly expressed in B-ALL cells. YTHDC1 knockdown attenuated B-ALL cell proliferation and cell cycle progression in vitro, and prolonged survival of mice in the human B-ALL xenograft model in vivo attributable to compromised leukemogenesis. Mechanistically, YTHDC1 knockdown significantly increased the accumulation of endogenous and chemotherapeutic agents-induced DNA damage in B-ALL cells. Furthermore, we identified that YTHDC1 binds to and stabilizes m6A-modified KMT2C mRNA. KMT2C is a key enzyme catalyzing histone H3K4 methylation required for the expression of DNA damage response (DDR)-related genes, implying that YTHDC1 inhibitors might improve chemotherapy by attenuating DDR via reducing KMT2C. Indeed, with molecular docking and biochemical experiments, we identified EPZ-5676 as a YTHDC1 inhibitor, and combination of EPZ-5676 with Cytarabine (Ara-c) significantly improved the efficacy of chemotherapy in B-ALL mouse models using YTHDC1high primary and lined B-ALL cells. Collectively, YTHDC1 is required for DDR in B-ALL cells by upregulating DDR-related gene expression via stabilizing m6A-modified KMT2C mRNA, thereby leading to increased histone H3K4 methylation, and targeted inhibition of YTHDC1 is a potentially new therapeutic strategy against B-ALL, especially YTHDC1high B-ALL.

Lung cancer remains the most common cause of cancer death. Given the continued research into new drugs and combination therapies, outcomes in lung cancer have been improved, and clinical benefits have been expanded to a broader patient population. However, the overall cure and survival rates for lung cancer patients remain low, especially in metastatic cases. Among the available lung cancer treatment options, such as surgery, radiation therapy, chemotherapy, targeted therapies, and alternative therapies, immunotherapy has shown to be the most promising. The exponential progress in immuno-oncology research and recent advancements made in the field of immunotherapy will further increase the survival and quality of life for lung cancer patients. Substantial progress has been made in targeted therapies using tyrosine kinase inhibitors and monoclonal antibody immune checkpoint inhibitors with many US Food And Drug Administration (FDA)-approved drugs targeting the programmed cell death ligand-1 protein (e.g., durvalumab, atezolizumab), the programmed cell death-1 receptor (e.g., nivolumab, pembrolizumab), and cytotoxic T-lymphocyte-associated antigen 4 (e.g., tremelimumab, ipilimumab). Cytokines, cancer vaccines, adoptive T cell therapies, and Natural killer cell mono- and combinational therapies are rapidly being studied, yet to date, there are currently none that are FDA-approved for the treatment of lung cancer. In this review, we discuss the current lung cancer therapies with an emphasis on immunotherapy, including the challenges for future research and clinical applications.

Abstract Frequent consumption of edible mushrooms, such as white button mushrooms (WBM), has been associated with a lower risk of prostate cancer [1]. Our laboratory at City of Hope has over 20 years of collective experience in defining the anticancer mechanisms of WBM [2, 3]. Previous studies have indicated that WBM consumption has anti-androgenic activities in prostate cancers in both preclinical models [4] and clinical trials [5]. In our first-in-human phase 1 trial on prostate cancer patients, we ensured the safety of consuming WBM in humans. In addition to observing a therapeutic-responsive decline in prostate-specific antigen (PSA), the levels of myeloid-derived suppressor cells (MDSCs) reduced in responders to WBM treatments [5]. These observations led us to hypothesize that WBM may mitigate the progression of prostate cancer in part by modulating the immune response. In the current study, we conducted translational research in syngeneic murine models and in prostate cancer patients from an ongoing phase 2 trial, aiming to define the immunomodulatory activity and mechanisms of WBM. We confirmed that WBM consumption in mouse models altered the number and function of immunosuppressive cells (MDSCs) and anti-tumor immune cells (T & NK cells), ultimately enhancing the intratumor and systemic immune responses. At a bulk-transcriptional level, we observed the elevated expression of programmed cell death protein 1 (PD-1) in xenograft tumors. In our single immune cell profiling of patients’ blood specimens following 3 months of WBM consumption in freeze-dried tablets form, we investigated the transcriptional landscape of circulating immune cells in response to WBM interventions. The level of circulating neutrophil-associated PMN-MDSCs decreased, and the remaining cells showed transcriptional profiles associated with "neutrophil chemotaxis", "leukocyte aggregation", and "regulation of inflammatory response", as functions associated with enhanced anti-tumor activity. Lastly, we also showed in a mouse model that WBM consumption synergistically enhances the anticancer activity of anti-PD1 drugs, indicating that WBM may be used as adjuvant therapy with immune checkpoint inhibitors. In summary, our results from prostate cancer patients and murine models show the immunomodulatory effects of WBM consumption and provide a scientific foundation for the application of WBM in alleviating prostate cancer progression. References 1, Zhang S., et al. Int. J. Cancer. 2019; 146:2712-2720. 2, Chen S., et al. Cancer Res. 2006; 66:12026-12034. 3, Adams L.S., et al. Nutr. Cancer. 2008; 60:744-756. 4, Wang X., et al. J. Nutr. Biochem. 2021; 89:108580.5, Twardowski P., et al. Cancer. 2015; 121:2942-2950. Citation Format: Xiaoqiang Wang, Shoubao Ma, Przemyslaw Twardowski, Clayton Lau, Yin Chan, Kelly Wong, Jinhui Wang, Xiwei Wu, Paul Frankel, Timothy G. Wilson, Timothy W. Synold, Cary Presant, Jianhua Yu, Shiuan Chen. Reduction of PMN-MDSC level/activity following the consumption of white button mushroom in prostate cancer murine models and patients: A translational study to mitigate cancer progression [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 1831.