COE Study Abroad Project Report


Report on Cold Spring Harbor Laboratory Summer School.

Takako Maeda , Master's course student

I attended the meeting course gstem cellh which was held for 2 weeks at Cold Spring Harbor Laboratory on July 29- August 11, 2004.

(outline of the course and brief comments)
This two-week lecture and discussion course were covered a series of subjects including the cells of the early embryo, the nature of germ cells, the mechanisms that control the number of stem cells, their stability, transformation into other cell types and clinical potential of stem cell technology. It brought leading researchers in the stem cell field. The courses had approximately 20 students from all over the world that range in experience from graduate students to faculty.

This was a lecture course and most days were split into 3 parts, Morning (9 AM), Afternoon (2 PM) and Evening (7:30 PM).
The Morning and Afternoon sessions were devoted to a single topic.
The first hour was an introduction to the topic.
The second hour was a research seminar based on current work.
The Evening sessions were either open-ended discussions on subjects of interest or focused on specific topics.
We often had informal discussion about lectures and subject of our study over break, lunch and dinner.

I think it was to provide participants with a great opportunity to achieve an advanced understanding of the scientific and clinical importance of stem cells. And it was very impressive for me to get lectures by Dr. Austin Smith, Dr. Azim Surani, Dr. Anne MacLaren because I am interested in the mechanisms to self-renewal of stem sell, maintenance of pluripotency and origin of primordial germ cell.

I learned various stem cells and become more intrigued with stem cells in this course. Of particular interest to me is tumor stem cell. Dr. Wicha hypothesizes that mammary stem cells or their immediate progeny are targets for transformation during carcinogenesis. One of the key events in carcinogenesis may involve disregulation of self-renewal pathways of normal mammary stem cells. Consistent with this model, they have found that breast tumors isolated from different patients contain a small sub-population of tumorigenic cells with the cell-surface phenotype ESA+CD44+CD24-/low Lineage that have properties of tumor stem cells. As few as 200 of these cells are able to consistently generate tumors in NOD/SCID mice, while the vast majority of cells in these tumors that lack this phenotype are incapable of tumor formation even when tens of thousands of cells are injected mice. The identification of tumor stem cells in situ may have diagnostic and prognostic significance. Furthermore, if tumors arise through mutations in stem sell and progenitor cells, it will be most important to identify and develop strategies to eliminate this cell population. An alternative strategy involves the development of agents which induce irreversible differentiation of these population. Current therapies developed by virtue of their ability to induce tumor regression may selectively target more differentiated cells in tumor, while leaving the tumor stem cell population intact. Tumor stem cells may then regenerate the tumor, contributing to relapse. More effective therapies, therefore, will require the targeting and elimination of tumor stem cell populations in breast cancer patients.

I would like to strive to make use of what I has learned at this course in my research.