The Tyranny of Content: "Content Coverage" as a Barrier to Evidence-Based Teaching Approaches and Ways to Overcome It.

Instructors have inherited a model for conscientious instruction that suggests they must cover all the material outlined in their syllabus, and yet this model frequently diverts time away from allowing students to engage meaningfully with the content during class. We outline the historical forces that may have conditioned this teacher-centered model as well as the disciplinary pressures that inadvertently reward it. As a way to guide course revision and move to a learner-centered teaching approach, we propose three evidence-based strategies that instructors can adopt: 1) identify the core concepts and competencies for your course; 2) create an organizing framework for the core concepts and competencies; and 3) teach students how to learn in your discipline.

Hyaluronan mediates adhesion of metastatic colon carcinoma cells.

Background: Hyaluronan (HA) is a cell-surface glycosaminoglycan that has been implicated in cancer progression. Cells isolated from metastatic colon carcinoma (SW620) produce greater amounts of pericellular HA than cells isolated from a primary tumor (SW480). Inhibition of hyaluronan synthases (HAS) by transfection with antisense cDNA decreases HA production.

Melanoma chondroitin sulfate proteoglycan enhances FAK and ERK activation by distinct mechanisms.

Melanoma chondroitin sulfate proteoglycan (MCSP) is an early cell surface melanoma progression marker implicated in stimulating tumor cell proliferation, migration, and invasion. Focal adhesion kinase (FAK) plays a pivotal role in integrating growth factor and adhesion-related signaling pathways, facilitating cell spreading and migration. Extracellular signal-regulated kinase (ERK) 1 and 2, implicated in tumor growth and survival, has also been linked to clinical melanoma progression.

Hyaluronan synthase-3 is upregulated in metastatic colon carcinoma cells and manipulation of expression alters matrix retention and cellular growth.

HA is a glycosaminoglycan that is synthesized on the inner surface of the plasma membrane and secreted into the pericellular matrix. HA and its biosynthetic enzymes (HAS1, HAS2 and HAS3) are thought to participate in tumor growth and cancer progression. In our study, colon carcinoma cells isolated from a lymph node metastasis (SW620) produced more pericellular HA and expressed higher levels of HAS3 mRNA compared to cells isolated from a primary colon carcinoma (SW480).

Insulin-like growth factor I-stimulated melanoma cell migration requires phosphoinositide 3-kinase but not extracellular-regulated kinase activation.

Dysregulated signaling contributes to altered cellular growth, motility, and survival during cancer progression. We have evaluated the ability of several factors to stimulate migration in WM1341D, a cell line derived from an invasive human vertical growth phase melanoma. Basic fibroblast growth factor, hepatocyte growth factor, interleukin-8, and CCL27 each slightly increased migration.