Stem cell migration: a quintessential stepping stone to successful therapy.

Migration is an innate and fundamental cellular function that enables hematopoietic stem cells (HSCs) and endothelial progenitors (EPCs) to leave the bone marrow, relocate to distant tissue, and to return to the bone marrow. An increasing number of studies demonstrate the widening scope of the therapeutic potential of both HSCs and endothelial cells. Therapeutic success however not only relies upon their ability to repair damaged tissue, but is also fundamentally dependent on the migration to these areas.

Tumor immune escape mechanisms: impact of the neuroendocrine system.

Tumor cells act upon, and react to both their proximate and more distant environment, the mechanisms by which this is achieved being both autocrine and paracrine in nature. This interaction, however, takes place not only between adjacent malignant cells, but also non-malignant cells such as those of the immune system, the latter also partaking in the modeling of the tumor environment. Although tumor cells descend from normal tissue cells and thus bear in classical immunological terms 'self signals', it is evident that the immune system is able to recognize tumor cells as a harassment for the body and in consequence tries to eliminate these cells.

Differential effects of culture conditions on the migration pattern of stromal cell-derived factor-stimulated hematopoietic stem cells.

Evidence is mounting that hematopoietic stem cells (HSCs) play a critical role in bone marrow regeneration and tissue renewal, for which migration is an obvious prerequisite. Computer-aided analysis and a three-dimensional collagen matrix assay enabled us to analyze single-cell migratory characteristics of stromal cell-derived factor-1 alpha (SDF-1 alpha)-stimulated cord blood-derived HSCs. We defined and resolved specific migratory parameters in spontaneous and SDF-1 alpha-induced migration of these cells.

Tumor cell locomotion: differential dynamics of spontaneous and induced migration in a 3D collagen matrix.

Although great strides have recently been made in elucidating the factors initiating tumor cell migration and the relevant cellular pathways involved, the constituent components of migratory dynamics for individual tumor cell motion have still not been resolved. Utilizing a three-dimensional (3D) collagen assay and computer-assisted, continuous single cell tracking, we investigated the basic parameters for both the spontaneous and norepinephrine-induced migration of highly metastatic MBA-MB-468 breast, PC-3 prostate, and SW 480 colon carcinoma cells. We show that tumor cells do not migrate with uniform migrational structure and speed as previously thought, but rather, the induction of locomotion elicits significant increases in speed, break frequency, and total cell displacement, but decreases in break length and no change in the recruitment of nonlocomotory cells.