Sysmex Scientific Seminar
Outline
47th (2025) Sysmex Scientific Seminar
Genomic Variations Associated with Aging and the Origin of Cancer
| Date/Time | May 31st, 2025 10:00am–4:10pm (JST) |
|---|---|
| Format | Webinar（Live） |
Are All Our Body Cells the Same?
We all start from a single fertilized egg, growing through countless cell divisions. However, the DNA sequences in our cells don't remain identical throughout our lives. As we age, errors (mutations) can occur during cell division. If these errors aren't repaired, they result in a mix of normal and mutated cells. This phenomenon is likened to a mosaic art and is called "somatic mosaicism".
This isn't just about genetics. Factors like UV radiation, inflammation, lifestyle habits (i.e., drinking, smoking, stress, and lack of sleep), and the natural decline of repair mechanisms with age can accelerate the mosaicism of our body cells.
When Somatic Cells Become a Mosaic...
Research has revealed that genetic mutations can increase the risk of cancer, heart disease, and even mental disorders. Heart disease, a leading cause of death worldwide, can be particularly severe when mutated blood cells infiltrate the arteries and heart, worsening the condition.
With advancements in detection technologies, uncovering the realities of somatic mosaicism could bring groundbreaking insights across various fields. Why not take this opportunity to dive into the fascinating world of somatic mosaicism?
Interview with Seishi Ogawa
(Planner, 47th Sysmex Scientific Seminar)
Program / Abstracts
| Time*JST | Agenda |
|---|---|
| 10:00-10:05 |
Opening Address
Yutaka Yatomi, M.D., Ph.D. Chairperson of Sysmex Scientific Seminar Planning Committe |
| 10:05-10:35 |
Abstract / Curriculum Vitae
AbstractOur bodies are made up of approximately 40 trillion cells. The blueprint of these cells is recorded in the cell nucleus as a DNA sequence, which is continuously and accurately copied at each cell division throughout the life cycle. Recent breakthroughs in genome analysis technology have revealed that even normal cells accumulate genetic mutations little by little with each cell division. In the body, cells compete with each other for proliferation speed, and among the various types of cells created by genetic mutations, cells that have acquired a specific genetic mutation often proliferate more than the surrounding cells. This population of cells (gene mutated clones) increases with age and external influences and can rebuild various organs and eventually lead to cancer and chronic diseases. This presentation will introduce the latest findings on somatic cell mosaicism, which overturns the conventional notion that genetic information remains unchanged throughout the life cycle. Curriculum Vitae
|
| 10:35-11:25 |
Abstract / Curriculum Vitae
AbstractRecently, it has been reported that genomic abnormalities accumulate not only in cancer but also in normal tissues due to aging and exposure to various environmental factors, resulting in clonal expansion of cells that have acquired driver mutations for cancer. We reported that in normal esophageal epithelium, clonal expansion of esophageal cancer driver mutations is caused by alcohol consumption and smoking, in addition to aging. The oral cavity, pharynx, and esophagus are commonly composed of squamous epithelium. Drinking and smoking are common risk factors for carcinogenesis in these three organs, and it is known that multiple cancers in the same region can cause field carcinogenesis, and it is assumed that epithelial remodeling by driver mutant clones occurs not only in the esophagus but also in the pharynx and buccal mucosa. Therefore, we attempted to evaluate the degree of exposure to esophageal cancer risk factors such as alcohol consumption and smoking by detecting gene mutation clones in the buccal mucosa. Because the clone size of driver mutations in buccal swabs is small compared to the observed area and conventional sequencing is not sensitive enough to detect them, we used the latest sequencing technology called error-corrected sequencing (ECS) to identify the mutated clones with high sensitivity. We will present our recent research results including clonal expansion of the buccal mucosa as well as clonal expansion of the esophagus and pharynx. Curriculum Vitae
|
| 11:25-11:35 |
QA
|
| 11:35-12:50 |
Lunch Break
|
| 12:50-13:40 |
Abstract / Curriculum Vitae
AbstractCancer is a disease caused by the accumulation of mutations in DNA. To understand the mechanism of carcinogenesis, it is necessary to clarify the process of DNA alterations in normal cells leading to tumorigenesis. Recently, genome analysis using next-generation sequencers has revealed that somatic mutations of cancer-related genes occur during the aging process in various normal tissues and that cells derived from mutant clones are widely present. Some studies have reported that somatic mutations in cancer-related genes occur in normal cells years to decades before carcinogenesis. In other words, cells with somatic mutations in cancer-related genes are thought to coexist with other cells for a long period of time without becoming cancerous. Morphological characteristics of tissues may be involved in the mechanism of accumulation and proliferation of cell clones with cancer-related gene mutations in the three-dimensional space of tissues. The speaker will introduce the genomic analysis of normal endometrium that they are working on. Curriculum Vitae
|
| 13:40-13:50 |
QA
|
| 13:50-14:40 |
Abstract / Curriculum Vitae
AbstractThere are still many unknowns about the carcinogenic mechanism of breast cancer, especially changes in the early stages of carcinogenesis. We examined genetic mutations in normal mammary cells and obtained results suggesting that the accumulation of mutations in the mammary gland is influenced by life events specific to women, such as menopause and childbirth, in addition to aging. We also focused on breast cancer with surrounding precancerous lesions and succeeded in tracing the evolutionary history of cancer in detail from the early stages of carcinogenesis by analyzing the genomes of cancerous and noncancerous epithelium, respectively. The results showed that der(1;16) translocation, a driver mutation, was acquired around puberty in der(1;16)-positive breast cancer, that the non-cancerous clones that acquired the der(1;16) translocation expanded by several centimeters, and that multiple clonal evolutions occurred among these expanded clones, some of which led to carcinogenesis. The results showed that the noncancerous clones that acquired translocations expanded by several centimeters. These results reveal one aspect of the characteristic carcinogenic mode of der(1;16)-positive breast cancer, which accounts for about 20% of breast cancers, and are expected to lead to the elucidation of the carcinogenic mechanism of breast cancer. Curriculum Vitae
|
| 14:40-14:50 |
QA
|
| 14:50-15:05 |
Break
|
| 15:05-15:55 |
Abstract / Curriculum Vitae
AbstractRecent genome analysis has revealed that normal cells continuously acquire somatic mutations from the fertilized egg stage, resulting in a mosaic state in each tissue and clonal proliferation associated with the acquisition of driver mutations, leading to future carcinogenesis. In normal bronchial epithelium, mutations accumulate with aging, and smoking has been shown to increase the number of mutations by several thousand per cell. In addition, driver mutations in genes such as TP53, which are frequently observed in lung cancer, also increased, and were thought to be associated with the development of lung cancer. On the other hand, in individuals with a history of smoking, especially in former smokers who had smoked in the past, the number of mutations was found to be close to normal in a small number of cells, suggesting that environmental factors such as smoking may be causing dynamic clonal competition. This talk will review somatic mosaicism in bronchial epithelium and its relationship to smoking. Curriculum Vitae
|
| 15:55-16:05 |
QA
|
| 16:05-16:10 |
Closing Address
Seishi Ogawa, M.D., Ph.D. Planner of the 47th Sysmex Scientific Seminar |
About
Sysmex Scientific Seminar is an annual seminar held by Sysmex Corporation, with the aim of contributing to medical care.
In recent years, basic, laboratory, and clinical medicine have come closer together, and the speed of change has been accelerating.
In line with this change, the seminar has been focusing on medical research that is closely related to our business domain of clinical testing.
A wide range of topics is covered in the seminar, including bone marrow medical science, autoimmune diseases, genetic testing, regenerative medicine, and more.
We will continue our efforts to provide up-to-date information that will enable you to experience the progress of today's medical science.
Sysmex Scientific Seminar is a purely academic seminar devoid of corporate PR.
Over the past 46 years, more than 55,000 people have participated in the event, which has also been live-streamed overseas.
People from 21 countries have watched the event, and a total of approximately 3,500 people have participated, both domestically and internationally (as of 2022).
Archives
On the Sysmex Scientific Seminar Member's page, you can watch videos of past Sysmex Scientific Seminars and download PDF versions of the texts.
If you wish to view the videos, please click "seminar videos and PDF texts" to proceed to the registration form.
46th (2024) Sysmex Scientific Seminar
Highlight of the 46th Sysmex Scientific Seminar
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- Plenary Lecture: Future Prospects for Cardiovascular Disease Research
- Speaker:Yutaka Yatomi, M.D., Ph.D.
(Chairperson of Sysmex Scientific Seminar planning committee)
- Lecture 1: The Future of Cardiovascular Medicine
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Speaker:Issei Komuro, M.D., Ph.D.
(Vice President, International University of Health and Welfare, Specially Appointed Professor, Graduate School of Medicine, The University of Tokyo)
- Lecture 2: How Can We Prevent Cardiovascular Aging?
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Speaker: Tohru Minamino, M.D., Ph.D.
(Professor and Chairman, Department of Cardiovascular Biology and Medicine, Juntendo University Graduate School of Medicine)
- Lecture 3: Precision Medicine for Primary Dyslipidemias and Atherosclerotic Cardiovascular Diseases
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Speaker: Hayato Tada, M.D., Ph.D.
(Assistant Professor, Department of Cardiology, Kanazawa University Hospital)
- Lecture 4: Addressing Unmet Needs in the Cardiovascular Area by Industry-Academia Collaboration: Establishment of a Novel Method to Assess HDL Functionality
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Speaker: Ryuji Toh, M.D., Ph.D.
(Associate Professor, Division of Evidence-based Laboratory Medicine, Kobe University Graduate School of Medicine)