The Whole Cancer Genome Sequencing Project initiated in Japan has led to the accumulation of large-scale whole-genome data. However, to elucidate mutations and structural abnormalities in non-coding regions, which are expected to be newly discovered by whole-genome analysis, it is essential to understand functional genomic regions such as enhancers, transcriptional regulators, and long non-coding RNAs. Methods such as ChIP-seq and ATACseq, which assess chromatin status, have been incorporated into clinical samples, and the epigenomic status of the entire cancer genome is being clarified through allele-specific methylation analysis by long-read analysis and full-length transcriptome sequencing. In this session, we will focus on new research areas that integrate epigenomic and whole-g

In recent years, it has been reported that chemotherapy drugs such as CDK4/6 inhibitors and radiotherapy induce cellular senescence in cancer and stromal cells, which contributes to cancer treatment resistance and recurrence. Furthermore, senescent cells are involved in the development and malignancy of various cancers via senescence-associated secretory phenotype (SASP). Therefore, understanding the roles of senescent cells and SASP in the cancer microenvironment is expected to lead to control of the increase in cancer incidence with aging and the malignancy of cancer. Development of senolytic drugs targeting senescent cells and senomorphic drugs regulating SASP derived from senescent cells is actively underway for cancer prevention and treatment. In this session, we will discuss novel cancer treatment strategies targeting senescent cells and SASP in the cancer microenvironment.

Recent studies showed that gene expression is regulated by multiple layers of a dynamic coordination of regulatory factors at certain genomic loci. In many types of cancers, genetic alterations are found in such factors, especially epigenetic regulators, RNA splicing factors, and RNA binding proteins, indicating the crucial properties of these factors during carcinogenesis. Epigenetic regulators and other associated proteins in many important nuclear processes was shown to engage in multilayer cooperative interactions that dynamically regulate not only cancer cells but also the cells composing tumor microenvironment including different types of immune cells. These findings may raise a possibility of novel drug targets for cancer treatment. In this session, researchers from Asian counties discuss an emerging perspective of gene regulatory network, which contributes to establish tumor cells and their microenvironmental heterogeneity.

Dynamic interactions of cancer cells with their microenvironment consisting of stromal cells and extracellular matrix components play important roles in the evolution of cancer cells. Components of tumor stroma, including tumor vessels, cancer associate fibroblasts and immune cells, are also affected by cancer cells and communicate with them. Increasing lines of evidence have suggested that these mutual interaction between cancer cells and tumor stroma alter the tumor microenvironment, which leads to cancer progression and metastasis. Therefore, understanding the underlying cellular and molecular mechanisms governing these interactions can be used as a novel strategy to disrupt cancer cell interplay and contribute to the development of efficient therapeutic strategies to fight cancer. In this symposium, leading scientists in the field of tumor microenvironment will introduce the recent progress in their fields, and discuss how to develop effective and safe cancer therapies by targeting the tumor microenvironment.

As represented by cancer genome therapy, comprehensive omics analysis and its medical application have been remarkably conducted and tried in cancer field. Many issues are, however, yet to be solved such as development of accurate cancer risk prediction and prevention, detailed stratification of treatment and recurrence prediction, and novel therapeutic agents for recurrent and refractory tumors. While cells are exposed to various carcinogenic factors and microenvironments, they adapt and evolve their genome structures and epigenome modifications in various ways from precancerous stages accumulating cancer risks to development of cancer, during progression and metastasis, or acquiring resistance to treatment during recurrence. Through various analytic approaches such as three-dimensional chromatin structure, spatial transcriptome, and single-cell analysis, elucidation of such genome/epigenome adaptation of cancer cells in their lifetime and development of medical strategies are comprehensively conducted in Japan and Asia. We will discuss on frontier studies in this field and disseminate cutting-edge information in this session.

On one hand, multistep carcinogenesis bears a high degree of similarity to Darwin's definition of evolution because it is characterized by heterogeneous cells with the ability to self-renew and by selection pressure from the microenvironment. On the other hand, it clearly differs from biological evolution in that cancer evolution is initiated by a genome that is already complex from the start, and epigenetic effects promote cancer evolution. Indeed, some tumors develop with minimal genetic changes, while cellular plasticity contributes to both tumor development and progression. However, an evolutionary theory capable of explaining these features of the carcinogenic process has not yet been established. Therefore, in this session, we call for theoretical and experimental studies to understand cancer evolution and to enable evolutionary-based cancer diagnosis and treatment strategies. Specifically, this includes single-cell analysis of cancer tissue, spontaneous carcinogenesis from non-human species, and studies focusing on the contribution of cell lineage-specific genes to carcinogenesis. In addition, proposals for new theories specific to cancer evolution and research on therapeutic strategies based on cancer evolutionary theory are also welcome.

With the development of various omics analysis technologies in recent years, multi-omics analysis research is being actively conducted around the world, which can further develop the results of mature cancer genomics research. In particular, in the field of proteogenomics analysis research that integrates genomics and proteomics, The International Cancer Proteogenome Consortium (ICPC), in which 14 countries participate, was established in 2016 under the leadership of the Cancer Moonshot Project in the United States. In this framework, many important findings have been reported, including new cancer stratification and discovery of therapeutic targets based on proteogenomics. Moreover, further important discoveries are expected to be made in this field, from basic cancer biology to findings that will lead to clinical applications under global research collaborations and AI-assisted big data infrastructure. In this session, we would like to provide an opportunity to learn about the new possibilities offered by proteogenomics analysis by inviting researchers with distinguished achievements and leadership in Asian countries.

Large-scale genomic analyses of cancer have shown that genomic instability is closely linked to cancer initiation, progression and drug resistance. It is also becoming clear how genomic instability arises at the cellular level and how it affects the properties of cancer cells. Furthermore, there is a growing trend to view genomic instability as a weakness of cancer cells and as a new therapeutic target. This International Session will discuss the latest findings on genomic instability in cancer at the cellular level, which complement large-scale genomic analyses of cancer and may lead to new therapeutic opportunities.

It has been a long time since “molecular epidemiology” was introduced into the field of cancer epidemiology. Initially, hypothesis-based research using functional single nucleotide polymorphisms (SNPs) was mainly conducted but various approaches using a SNP-chip along with advance in genotyping technic have emerged such as whole-genome association analysis, mendelian randomization analysis, and development of polygenic risk score. Although primary aim of epidemiology is to prevent cancer, application to preventive measures has been challenge due to limited evidence considering environmental factors in many large-scale studies. Against this background, the aim of this session is to present the latest approaches in cancer molecular epidemiology by researchers representing the Asian region, and to promote future collaboration in cancer molecular epidemiology in Asia.

The focus of this session is to create a forum on new trends in radiation therapy and radiobiology in cancer researcher’s community. Radiation therapy has been established as a standard therapy against cancer and widely applied to treatment for various cancers. Recently, new radiation therapies have emerged; proton beam therapy, heavy ion therapy, boron neutron capture therapy, targeted alpha therapy and so on. These radiotherapeutic modalities impact on oncology not only in Europe and the United States, but also in Asia and Oceania. In order to accelerate these trends and further develop next generation radiation therapy, the contribution of radiobiology is fully expected. Radiobiology has so far made a great contribution not only to radiation oncology but also life sciences including cancer research. However, there are many challenging issues to be addressed, especially the biological or biophysical effects on living body after irradiation. New findings and technical advances in radiobiology will lead to the innovation of radiation therapy. In this session, we will invite cutting-edge researchers and radiation oncologists in Asia and Oceania to share our future on radiation therapy and radiobiology.

Advances in cancer research and in vivo model engineering are intricately linked and have grown hand in hand. The contribution of current models in the discovery of the new diagnostics and therapeutics is noteworthy. However, there exist large discrepancies between the actual clinical pathology and existing animal models, and new models that address these differences will further advance this field. Recent novel technological development enables researchers and clinicians not only to engineer new animal models, but also to re-purpose/re-engineer existing animal models such as zebrafish or fruit flies that have been utilized for a longtime. Due to limitations of existing animal models and increasing ethical regulations, the usage of these lower organism models will play important roles in both understanding of pathophysiological elucidation and developing new diagnostic and therapeutic strategies. In this session, we aim to discuss various emerging animal models that is likely to have a profound impact in the years to come.

Recently, emerging evidences suggest that certain commensal bacteria are associated with cancers. Abnormal bacteria and their metabolites affect eithersystemic or local immune responses, which contribute to cancer progression and therapeutic outcomes. Consequently, new approaches that target gut microbiota have been clinically applied to cancer detection and treatment. In this syposium, we will primarily discuss the mechanism how microbiota modulates tumor immunity. We will also discuss recent advances and challenges using microbiota-modulating therapies such as fecal transplantation, prebiotics, or probiotics. We encourage the application and participation of young researchers.

Gene regulation is fundamental to cell activity and malignant transformation, in which a manifestation of changes in gene expression facilitate the growth and spread of cancer cells into foreign niches. Recent advances in cancer research have highlighted that alterations in multiple layers of RNA regulation, including transcription, RNA splicing, RNA editing and modification, RNA 3’-end processing, non-coding RNA regulation, and biomolecular condensate regulation, are widespread in cancer cells beyond genomic alterations, contributing to cancer hallmarks and cancer diversity, and further opening a new avenue for cancer treatment. As understanding of the basic mechanisms of RNA regulation has continued to grow in recent years, the spectrum of RNA dysregulation also interplays with genetic, epigenetic, and translational mechanisms to shape altered gene expression programs in cancer. In addition, technological advances in RNA biology, such as bioinformatics, next-generation sequencing, genome/RNA engineering, and single cell analysis, have elaborated system-level understanding of RNA dysregulation in cancer and identified novel targets for therapeutic development. This symposium will connect domestic and foreign researchers and discuss the cutting edge and future of RNA research in cancer biology.

Due to the inability to model cancer in a living human body, researchers have developed various cancer models to simulate and investigate aspects of cancer in the laboratory, including mechanisms of cancer development, progression and drug sensitivity. Such models now encompass a panoply of in vitro, in vivo and computational models, with each model having its own strength and weakness. Although these model systems have provided significant insights into cancer biology, each model is in part self-contained and perhaps being used in its own research culture and community, hampering translational and transinstitutional effort toward the same goal of understanding cancer for human well-being. The use of cancer models that involve human tissues requires an adjustment of ethical issues, which also should not be overlooked. In this symposium, we would like to share our exciting insights obtained from a variety of cutting-edge cancer models. Through active discussion, we aspire not only to deepen our fundamental understanding of cancer biology but also to facilitate collaborative research through mutual recognition of each model and expertise.

Recent studies have made remarkable strides in elucidating the pathogenesis of cancer. Specifically, determining the key signaling pathways involved in carcinogenesis has been pivotal in understanding the mechanisms underlying cancer development and progression. Moreover, the identification of novel therapeutic targets has significantly promoted the development of anti-cancer drugs. In these studies, various screening technologies have contributed to delineating previously unappreciated genes governing cancers. For example, genome-wide genetic approaches in organoids and whole animals have unveiled essential genes implicated in cancer development, progression, and therapy resistance. This symposium invites six speakers who will present their cutting-edge achievements in various domains, including cancer initiation and progression. Sharing and discussing the latest methodologies and findings should open up new avenues for accelerating cancer research.

Expectations for artificial intelligence (AI) are rising with rapid advances in machine learning technology, particularly deep learning. AI is currently being introduced in various areas of society, and the medical field is no exception, with AI-based medical devices already in use not only at the research level but also in clinical practice. In cancer research, AI is beginning to be actively utilized in a wide range of fields, including analysis of medical images such as endoscopic images, pathological images, and radiological images, omics analysis, and drug discovery. In particular, recent cancer research requires analysis of large-scale data such as whole genome data and multimodal analysis of data from various modalities, and AI-based cancer research is expected to become increasingly important in the future. Therefore, this symposium will be held to present the latest results of AI-based cancer research and to help participants understand the current status of AI-based cancer research.

Most of cancer-related death is caused by metastasis, thus it is important to understand the molecular mechanism of metastasis to develop novel therapeutic strategy. Recent genome analysis demonstrated that accumulation of driver mutations is confirmed in the primary cancer tissues, and the metastasis-specific genetic alterations are rarely found. On the other hand, there have been shown to be novel biological mechanisms that include extracellular vesicle-led premetastatic niche generation, education of tumor-promoting stromal cells for survival of disseminated tumor cells, cell cluster migration and polyclonal metastasis, and stemness-regulated dormancy of the drug-resistant cells, etc. In this symposium, we would like to discuss about such novel biological mechanisms to expand our knowledge about metastasis development.

Cancer immunotherapies such as monoclonal antibodies against PD-1/PD-L1 or CTLA-4 have been approved in the treatment for various types of cancer, leading to a paradigm shift in cancer treatment. However, their efficacies are unsatisfactory as monotherapies. It is essential to understand the mechanisms of treatment sensitivity and resistance in the tumor microenvironment (TME) to increase efficacy. Various novel technologies including single-cell sequencing and imaging system have made it possible for us to elucidate the TME in detail. In addition, new insights into the tumor metabolic environment, the molecular mechanisms of immune checkpoints, and the balance between immunogenicity and oncogenic function of gene mutations have been uncovered. In this symposium, six presenters will show novel insights about the TME based on their latest findings.