This symposium highlights recent advances in basic p53 research while also showcasing the development of clinical studies targeting p53, including therapies focused on the MDM2-p53 pathway.

Organoids can recapitulate the in vivo characteristics of cells and significantly contribute to elucidating the molecular mechanisms involved in the development and progression of cancer. Cancer progression is influenced by diverse factors in the microenvironment, such as inflammation, immune reaction, extracellular matrix remodeling, energy metabolism, and hypoxia. However, most of the molecular mechanisms promoting malignant progression remain unknown. Functional analysis using state-of-the-art technologies such as imaging, omics analysis, and novel devices in organoid culture systems has made it possible to analyze fundamental processes that take place in the microenvironment. Also, manipulating gene functions utilizing various genetic approaches in organoids has uncovered many novel gene functions that regulate differentiation, cell proliferation, and drug responses. In addition, constructing a library of patient-derived organoids and the stratification of cancers according to their responsiveness to cancer drugs or niche factors promote personalized medicine. Such analyses have provided new insights regarding cancer stem cells, cell plasticity, and the interactions between cancer cells and the immune system. These efforts will lead to identifying new therapeutic targets and establishing new therapies to cure malignant cancers for which no treatment is available. In this symposium, we will discuss the cutting edge of organoid research and the future direction.

Owing to the next-generation sequencing technology, gut microbiota research has recently advanced, revealing that gut bacteria are associated with various human diseases. This session will focus on recent cutting-edge topics, particularly the relationship between cancer and gut microbiota. We will discuss the relationship between colorectal cancer and E. coli positive for the mutagenic bacterial toxin, colibactin, as well as the analysis of the hereditary colorectal tumors and the gut microbiota. Additionally, this session will cover the involvement of bacterial species present within tumors in cancer progression, which has been recently elucidated. Furthermore, we will discuss the bacterial species that enhance the efficacy of immune checkpoint inhibitors (ICIs) and the potential of phage therapy targeting specific causative bacteria. We are also accepting one presentation from the public.

Animal models are essential tools for cancer research. To date, attempts have been made to develop animal models that faithfully recapitulate the molecular etiology and pathophysiology of human cancer, such as syngeneic/xenogeneic tumor-bearing mouse models, patient-derived xenografted mouse models, humanized mouse models and genetically modified mouse models. Furthermore, over the past two decades, the NIH/NIC in the USA has led the development of novel animal models using naturally occurring tumors in pet dogs, known as the “Comparative Oncology Project”, and has successfully accumulated critical knowledge through the biological studies including genome and informatics analysis. Moreover, the canine tumor models are now used to evaluate immunotherapy for rare cancers as the “Cancer Moonshot Project” in the United States, which is being promoted around the world. The aim of this symposium is to provide the basics from the cutting-edge mouse models to naturally occurring canine tumor models, as well as their practical application in future research. These approaches will greatly contribute to the innovative cancer research and therapeutic strategy.

In recent years, expectations for artificial intelligence (AI) technology have been increasing due to the rapid progress of machine learning, centered around deep learning. Since the development of Transformer in 2017, there has been significant progress in the field of generative AI, including large language models (LLMs), and AI is now being used in various fields of social life, as well as being a research tool. The medical field is no exception, and AI is being introduced into a wide range of medical research, from basic research to clinical research. According to the latest data from the US FDA, there are over 950 AI-equipped medical devices that have been approved by the FDA and are actually being used in clinical practice. Under these circumstances, this symposium will be held in collaboration with the Japanese Association for Medical Artificial Intelligence to present the results of cancer research using cutting-edge AI, from basic research to clinical applications, and to discuss future directions and issues.

Recent studies have demonstrated that the tumor angiogenesis is a highly complex and heterogenous process. Over 20 angiogenic factors are known to be secreted by cancer cells of different origins. Moreover, additional cytokines/growth factors produced by immune cells and cancer-associated fibroblasts induce structural alterations of tumor blood vessels. As a result, tumor vasculatures are quite different among many cancer types, and phenotypic alterations of endothelial cells affect the biological behavior of cancer cells. Nevertheless, there is no doubt that tumor angiogenesis is a key process for metastasis and an important target of the therapy.
To get better insights into tumor angiogenesis and to develop innovative anti-angiogenic therapies, we would like to present recent advances in tumor angiogenesis research. Invited speakers will introduce unique model systems that cover both in vitro and in vivo studies using novel imaging, tissue engineering and molecular dissections. We will expect constructive and fruitful discussions to defeat cancer angiogenesis and to suppress cancer progression.

Chimeric Antigen Receptor T-cell (CAR-T) therapy has achieved remarkable success in the treatment of hematological malignancies. However, significant challenges persist in the context of solid tumors, necessitating further innovation. In particular, the tumor microenvironment—characterized by an abundance of cancer stem cells and fibroblasts—as well as the antigenic heterogeneity and loss unique to solid tumors, underscore the limitations of current therapeutic approaches. Overcoming these obstacles requires the development of novel treatment strategies that go beyond conventional CAR-T therapies. This proposal aims to unlock the potential of "next-generation designer cell therapies powered by RNA science" by harnessing precise genomic information and state-of-the-art nucleic acid technologies. Recent advances in RNA modification measurement and profiling have not only paved the way for precision medicine in cancer treatment but have also expanded the potential of nucleic acid-based therapeutics. Specifically, we seek to address antigenic diversity through epitope broadening, regulate immune memory, and develop therapeutic strategies targeting cells beyond T cells, utilizing innovative models that accurately recapitulate human pathophysiology. Additionally, this initiative promotes groundbreaking technological advancements by young researchers, fostering transformative studies that aspire to pioneer the next generation of cancer therapies.

Alterations in lipid metabolism in cancer are understandable. The phospholipids that make up the cell membrane need to increase significantly due to the larger size of cancer cells. Increased cell proliferation also requires increased lipid synthesis.
These may be regarded as requirements for oncogenesis.
On the other hand, in recent years, accumulated studies revealed that changes in lipid metabolism actively drive oncogenesis. For example, the phospholipid hydrolysing enzyme sPLA2, which is essential in lymphomagenesis, is produced by tumour-associated macrophages (TAMs), suggesting that it is involved in oncogenesis through active alterations in lipid metabolism. In hepatocellular carcinoma, lipid accumulation by palmitic acid upregulates PD-L1 expression, suggesting that it induces aggressive tumour cell immune deviation.
In this symposium, we hope to stimulate active discussion and deepen our understanding of oncogenesis actively driven by such changes in lipid metabolism.

Research on lung cancer is progressing rapidly. Recent advances in whole-genome analysis technology are beginning to elucidate the entire picture of genomic abnormalities in lung cancer. Furthermore, with the advent of immune checkpoint inhibitors, molecular target drugs, antibody-drug conjugates, and bispecific antibodies, the perioperative treatment of lung cancer and the treatment of advanced stage cancers are undergoing dramatic changes. There is a feeling that bispecific antibodies will lead to a paradigm shift in the treatment of small cell lung cancer, where no major changes have been seen in treatment. In this symposium, we would like to share cutting-edge information on research into lung cancer. We are looking forward to many participants.

Brain tumors are notoriously refractory to treatment and are associated with dismal prognoses, underscoring the critical need for the development of novel therapies. In recent years, intensive research efforts have led to a rapid expansion of molecular understanding in brain tumors, leading to personalized medicine based on molecular abnormality and induction of molecularly targeted therapies. As well as primary brain tumors, the advancement of understanding of systemic cancers has enabled us to induce personalized therapies for metastatic brain tumors based on the molecular characteristics of the primary organ. However, these therapies contribute to the limited number of patients, with the remaining patients with dismal prognoses yet. This session will focus on recent advances in basic and translational research on malignant and metastatic brain tumors, highlighting the latest insights to understand brain tumor pathogenesis and advance novel therapeutic development. The program welcomes early-career investigators and graduate students and calls for abstracts from younger researchers and clinicians.

Cell division is the basis of cell proliferation and has long been expected to provide promising targets for cancer therapy. A number of agents that inhibit microtubule dynamics, mitotic kinases and motors have therefore been clinically tested; however, their efficacy has been limited in practice, primarily because mitosis is a fundamental process for all cells and its disruption damages normal proliferating cells. How can we circumvent this narrow therapeutic window and find out means to selectively suppress the proliferation of cancer cells? One potential approach involves the identification of cancer-specific vulnerabilities, by figuring out the differences in the regulation of mitotic cell cycle between cancer and normal cells. In this symposium, we will highlight recent studies devising unique approaches on the basis of cancer-specific cellular responses. Recent progress in the understanding of cell cycle regulation and in technologies including CRISPR screening has allowed us to identify cancer-specific vulnerabilities in the regulation of cell division or chromosome dynamics, thereby revealed possible intervening points. Although we are still in early phases of the development, deep understandings of these processes in both physiological and pathological contexts should pave the way for innovative anti-cancer therapeutics targeting the mitotic cell cycle.

The intricate interplay among iron, sulfur, and oxygen represents a fundamental yet often overlooked aspect of cancer biology. This triangular redox dynamics provides a fresh perspective on how oxidative and reductive forces shape tumor development and progression. Iron, a double-edged sword in cellular metabolism, fuels oxidative stress through the Fenton reaction, generating reactive oxygen species (ROS) that induce DNA damage and genomic instability. Oxygen, while essential for cellular respiration, also amplifies oxidative stress under dysregulated conditions, exacerbating cancer risk. In contrast, sulfur-containing compounds, such as glutathione and persulfides, counteract this oxidative burden by maintaining a reductive environment and supporting antioxidant defense mechanisms.
Understanding the balance among these three elements is critical, as it dictates cancer cell survival, proliferation, and therapeutic resistance. Emerging concepts such as ferroptosis, a form of iron-dependent cell death, and the role of sulfur metabolism in redox regulation, offer promising avenues for intervention. By targeting iron metabolism, modulating sulfur pathways, and controlling oxidative stress, novel strategies for cancer prevention and therapy may be developed, opening new frontiers in redox-based oncology.

Recent advancements in spatial single-cell analysis have enabled high-resolution mapping of cellular organization and interactions within tissues. These technologies provide unprecedented insights into the cellular heterogeneity and spatial architecture of various biological systems, offering new perspectives on disease mechanisms, tumor microenvironments, and immune responses. By integrating spatial transcriptomics, proteomics, and machine learning-based analysis, researchers can now explore complex cellular ecosystems with greater precision, driving innovations in biomarker discovery and therapeutic development.
This session will bring together leading experts to discuss the latest advancements, applications, and challenges in spatial single-cell analysis. By examining cutting-edge technologies and their translational potential, we aim to foster interdisciplinary discussions on how these methods can bridge the gap between fundamental research and clinical practice. The session will highlight key developments in data integration, computational modeling, and clinical validation, providing insights into how spatial single-cell analysis can enhance disease diagnosis, treatment strategies, and precision medicine approaches.
Through this exchange, we hope to identify opportunities for collaboration and innovation, ultimately contributing to the broader implementation of spatial single-cell technologies in biomedical research and clinical applications.

Translational Research (TR) is crucial to the development of cancer therapy, as it enables medical discoveries and new technologies to be applied clinically. This session will focus on extracellular vesicles (EVs, exosomes), which are attracting attention as a new modality. EVs transport various cellular constituents such as miRNA, mRNA, DNA, lipids, and proteins over long distances and affect many physiological and pathological states including cancer microenvironment. Interestingly, vesicles with EVs-like activities like those in humans have been identified in plants and bacteria. Various clinical applications of these plant-derived EVs are also in progress. EVs also play a crucial role in intracellular signal transduction in cancer therapy, making them promising candidates for therapeutic agents, drug delivery systems（DDS）, and cancer biomarkers for Lquid biopsy. Therefore, in this session, we would like to focus on various types of EVs and introduce clinical applications of EVs in cancer TR research. We hope that this session will lead to suggestions for new cancer therapy.

Cell division is the basis of cell proliferation and has long been expected to provide promising targets for cancer therapy. A number of agents that inhibit microtubule dynamics, mitotic kinases and motors have therefore been clinically tested; however, their efficacy has been limited in practice, primarily because mitosis is a fundamental process for all cells and its disruption damages normal proliferating cells. How can we circumvent this narrow therapeutic window and find out means to selectively suppress the proliferation of cancer cells? One potential approach involves the identification of cancer-specific vulnerabilities, by figuring out the differences in the regulation of mitotic cell cycle between cancer and normal cells. In this symposium, we will highlight recent studies devising unique approaches on the basis of cancer-specific cellular responses. Recent progress in the understanding of cell cycle regulation and in technologies including CRISPR screening has allowed us to identify cancer-specific vulnerabilities in the regulation of cell division or chromosome dynamics, thereby revealed possible intervening points. Although we are still in early phases of the development, deep understandings of these processes in both physiological and pathological contexts should pave the way for innovative anti-cancer therapeutics targeting the mitotic cell cycle.

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Epstein-Barr virus (EBV) is a virus that infects nearly every human worldwide. While most individuals coexist with EBV without experiencing health issues, in some, it contributes to the development of life-threatening malignancies. What determines this difference? The answer lies not only in the virus but also in the host.
This symposium explores the critical role of host factors in EBV-induced carcinogenesis. Although EBV-related malignancies are found globally, they are particularly prevalent in Asia, underscoring the need for close collaboration and knowledge sharing among researchers in this region. To foster a multidisciplinary approach, we have invited leading experts from diverse fields, including hematology, pediatrics, otolaryngology, genomics, and regenerative medicine. Together, they will examine how genetic predisposition, immune response, and microenvironmental factors drive EBV-associated carcinogenesis.
How do EBV-infected cells evade host immunity and undergo malignant transformation? Can we predict, prevent, or even overcome EBV-related malignancies? Through cutting-edge research and dynamic discussions, we aim to uncover the answers. Tackling these challenges requires large-scale, longitudinal studies, and international collaboration will be key to accelerating progress.
We welcome both established experts and those new to the field to join this discussion, which may redefine our understanding of EBV and its role in malignancies. Together, let us explore the complex interplay between EBV and its host.

In recent years, rapid advances in high-resolution omics technologies—such as single-cell and spatial transcriptomics—have ushered in an era where comprehensive molecular profiling can illuminate the heterogeneity of cancer tissues both within and between tumors. At the same time, the growing complexity of these datasets has driven the development of diverse analytical methods—including deep learning, probabilistic modeling, and mathematical modeling—to extract meaningful insights. These approaches enable the identification of gene programs associated with clinical features, tracing the differentiation trajectories of cancer cells, and characterizing the population structures within tumor microenvironments. As a result, these computational strategies have become essential for elucidating and interpreting tumor heterogeneity in cancer biology.
This symposium will bring together researchers who develop and apply a variety of computational methods to explore cutting-edge techniques and findings that deepen our understanding of tumor heterogeneity through the analysis of high-resolution omics data. Through this exchange, we aim to envision the future of computational analyses in high-resolution omics and to investigate the transformative impact these sophisticated approaches can have on cancer biology.