Outline of our study

Outline of our study

Outline of our study

Our aims

In Japan, one in two people will develop cancers, and one in four people will die of these malignant diseases. Because of the expansion of the aging population, cancer incidence and mortality are expected to increase further. Thus, further understanding of cancer biology and applying our knowledge to improve early diagnosis and treatment efficacy is becoming increasingly critical. In spite of  significant progress in medical science and cancer therapy, major challenges remain, which include cancers with difficulties in early diagnosis, therapeutic resistance, recurrence, and metastasis.

Cancer development, or tumorigenesis, is driven by dynamic interactions between environmental factors and genetic diversities/abnormalities. Technological advances, such as next generation sequencing, have enormously expanded our understanding of cancer biology. However, key questions persist: How do normal cells, precancerous and cancer cells respond intrinsic and extrinsic selection pressures during malignant transformation? How is cell fate determined, and what govens these selection processes? Recent evidence suggests that cancer cells adapt to their environment and evade cancer surveillance mechanisms through epigenetic reprogramming at the very early stages of malignant transformation, enabling their survival and sustained proliferation. To tackle these issues, we aim to explore the pathophysiology of cancer through the lenses of environmental response and epigenetic regulation, ultimately identifying novel therapeutic targets and diagnostic markers for prevention and treatment.

Epigenetics refers to “stably heritable phenotype resulting from changes in a chromosome without alterations in the DNA sequence”, encompassing the modifications of DNA binding proteins (e.g. histones), DNA, RNA, and noncoding RNAs. Growing evidence strongly highlights the role of epigenetics in shaping biological properties of cancer cells from their very early to later stages of proliferation. Thus, in order to develop an innovative strategy for cancer prevention and treatment, we need deeper understandings of the regulatory mechanisms governing cellular responses to intrinsic and extrinsic changes in vivo. To address these questions, we mainly employ genetically modified mouse models and cultured cells to study their phenotypic alterations through epigenomic, cell biological, biochemical approaches and imaging approaches. Furthermore, we are expanding our research into aging biology to uncover potential routes for cancer prevention.