The 85th Annual Meeting of the Japanese Cancer Association

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Despite advances in development of cancer genomic medicine, it is still necessary to elucidate the molecular basis of carcinogenesis from various approaches and develop new therapeutic strategies. The mechanisms of epigenetic driver activation, including enhancer hijacking caused by genomic structural abnormalities e.g. translocations and inversions, super-enhancer (SE) formation, CTCF binding site mutations, and more recently, the amplification of oncogenes and SEs due to extrachromosomal DNA (ecDNA) formation, are particularly anticipated for elucidation and medical application. Various researches on epigenetic remodeling that leads to enhancer dysregulation and cancer gene activation, as well as druggable epigenetic abnormalities, are comprehensively conducted in Japan and Asia, and there is great significance in discussing and disseminating such cutting-edge information in this session.

This session delves into the multifaceted roles of mitochondria in oncology beyond simple energy production. We explore how mitochondrial genome instability drives tumor evolution and how metabolic reprogramming within cancer cell mitochondria supports survival under stress. Furthermore, we highlight the critical influence of mitochondrial dynamics in immune cells, determining their activation and anti-tumor efficacy. A key focus will be the emerging phenomenon of intercellular mitochondrial transfer, where the "transfer" of these organelles between cells shapes the tumor microenvironment. By integrating these perspectives, we aim to redefine cancer as a systemic mitochondrial disease and identify novel therapeutic vulnerabilities.

Cellular senescence functions as an important tumor-suppressive mechanism during the early stages of tumorigenesis. However, accumulating evidence indicates that senescent cells can also promote cancer initiation and progression through the senescence-associated secretory phenotype (SASP). Elucidating the molecular mechanisms underlying SASP is therefore expected to provide new strategies to control malignant phenotypes in cancer cells. Recent studies have shown that chemotherapeutic agents as well as radiation therapy, can induce senescence in both cancer cells and stromal cells, which may contribute to therapy resistance and tumor recurrence. Moreover, SASP factors can remodel the tumor microenvironment and impair immune cell function. Consequently, controlling the diverse functions of senescent cells within the tumor microenvironment may offer promising strategies for cancer prevention and improved therapeutic outcomes. This session will discuss the multifaceted roles of cellular senescence in cancer initiation and progression.

CAR-T cell therapy is now expanding into solid tumors, as several clinical trials have reported encouraging results. Recent studies have identified key mechanisms underlying therapeutic resistance, including heterogeneity in antigen expression and molecular drivers of T-cell dysfunction. Intensive efforts are underway to further engineer T cells genetically to overcome these limitations.
Beyond improving T-cell fitness, the successful development of cellular therapies requires a deeper understanding of tumor cells and their microenvironment, as well as greater insight into other therapeutic modalities to achieve synergistic effects. In this symposium, we aim to invite internationally leading researchers in these fields to provide an overview of recent advances and discuss future directions.

Research on ubiquitination has yielded a vast number of findings over the past 40 years. In contrast, research on the control of deubiquitination has intensified over the last 20 years, particularly in the past decade. As the modification of proteins with ubiquitin is critically regulated by the balance between these processes, this session will focus on controlling cancer malignancy through them. The session will also discuss new therapeutic strategies based on a deeper understanding of ubiquitination and the subsequent proteasome-mediated degradation.

Theranostics has emerged as a key paradigm in next-generation cancer medicine by integrating molecular diagnostic imaging and targeted therapy. Advances in molecular imaging technologies now enable highly sensitive visualization of tumor biology, allowing the same molecular targets to be used for both diagnosis and therapy. This symposium will highlight recent progress in theranostics research, including novel radiopharmaceuticals, molecular imaging biomarkers, and targeted radionuclide therapy using alpha- and beta-emitting isotopes. Through these presentations, the session aims to provide an overview of cutting-edge developments and discuss future clinical translation in precision oncology and personalized cancer medicine driven by theranostics.

Cancer metastasis is profoundly influenced by the dynamic plasticity of the tumor microenvironment. Reciprocal interactions between cancer cells and stromal components—including endothelial cells, fibroblasts, immune cells, and extracellular matrix—govern invasion, dissemination, and metastatic colonization. Increasing evidence indicates that stromal cells actively regulate metastatic progression through phenotypic and functional changes that create permissive niches for cancer cells. Recent advances in imaging technologies, together with molecular and genetic approaches, have enabled the visualization and analysis of tumor–stroma interactions in living tissues. This session will highlight recent studies on how microenvironmental plasticity regulates metastasis and discuss emerging concepts and therapeutic opportunities targeting the tumor microenvironment.

In this session, we introduce the launch of a cancer spatial analysis consortium, ASTRA (Asia–Pacific Spatial Translational Research Alliance). ASTRA is a regional initiative intended to standardize sampling, clinical metadata, spatial transcriptomic and proteomic assays, analytical workflows and capacity development efforts. In its initial phase, the Alliance will develop a spatial atlas comprising approximately 2,000 clinically annotated tumor specimens from varied populations and tumor types. This work defines key priorities and milestones to link spatial characteristics to clinical outcomes, identify actionable targets, and encourage robust cross-cohort comparisons to advance patient stratification and expedite translational research.

Tissue stem cells are responsible for the formation, maintenance, repair, and homeostasis of tissues, and those present in cancer tissues are referred to as cancer stem cells. Advances in stem cell biology have revealed the presence of complex factors, including stem cell plasticity, dedifferentiation, and heterogeneity. Recent progress in cutting edge technologies such as single cell analysis has enabled detailed characterization of stem cell properties within tissues, deepening our understanding of the fundamental mechanisms underlying the development of both normal and cancerous tissues. In this session, we will discuss the nature of cancer stem cells and their potential as therapeutic targets in the pursuit of cancer eradication.

A substantial gap persists between scientific evidence and public policy regarding alcohol and cancer prevention. Alcohol is a Group 1 carcinogen and a major contributor to the global cancer burden, yet its carcinogenicity is not consistently reflected in risk communication, guidelines, or regulatory strategies. This session brings together experts in epidemiology, prevention science, and public health policy to present the current state of knowledge and existing policy approaches from multiple perspectives. By placing scientific findings alongside policy realities, the session aims to clarify where and why discrepancies remain, and to encourage participants to reconsider priorities and future directions in evidence-informed cancer control.