There is increasing evidence for the importance of events that govern and influence the interaction between the transformed cell and its host being ultimately responsible for the establishment of the cancer phenotype. To derive an animal model that will allow us to define some of these phenomena at the molecular level, we have chosen to induce the expression of a viral oncogene in all tissue types, with the hope of identifying sites that are more susceptible to malignant transformation. When the gene for simian virus 40 large tumor antigen (T antigen) was placed under the control of a major histocompatibility complex class I gene enhancer, the resulting transgenic mice not only developed choroid plexus papillomas, as seen with wild-type simian virus 40, but also lymphoid hyperplasia and multiple endocrine neoplasias. The development of lymphoid hyperplasia was preceded by an elevated level of expression of T antigen in these tissues at an early age. Surprisingly, the striking thymic hyperplasia has not been observed to progress toward malignancy. The multiple endocrine neoplasias developed later in life and involved the pancreas, pituitary, thyroid, adrenals, and testes. While not preceded by an elevated level of expression of T antigen, once endocrine tumors appeared they quickly progressed toward malignant growth. Although other tissues also exhibited a basal level of expression of the viral oncogene similar to that detected in endocrine tissues, they rarely developed tumors. This transgenic mouse model seems particularly suitable for a molecular understanding of events responsible for certain tissue types being so much more susceptible to neoplastic conversion, with others being so refractory.
Background Residency programs are increasingly being asked to defend their quality, and that of the residents they produce. Yet “residency quality” is a construct that has not been well defined, with no accepted standards other than meeting accreditation standards. In 2009, the Association of Family Medicine Residency Directors developed a strategic plan that included the goal of raising the quality of family medicine training. Objective We describe the development of this quality improvement tool, which we called the residency performance index (RPI), and its first year of use by family medicine residency programs. We describe the use of the tool as a “dashboard” to facilitate program self-improvement. Intervention Using program metrics specific to family medicine training, and benchmark criteria for these metrics, the RPI was launched in 2012 to help programs identify strengths and areas for improvement in their educational activities and resident clinical experiences that could be tracked and reviewed as part of the annual program evaluation. Results Approximately 100 program directors began using the tool and 70 finished the process, and were provided aggregate data. Initial review of this experience revealed difficulties with collecting data, and lack of information on graduates' scope of practice. It also showed the potential usefulness of the tool as a program improvement mechanism. Conclusions The RPI is a new quality improvement tool for family medicine residency programs. Although some initial challenges need to be addressed, it has the promise to aid family medicine residency in its internal improvement efforts.
could consistently occur simultaneously with efforts to support the core content requirements of the family medicine clerkship, exportable teaching models for use in dispersed clinical settings may emerge. The differences in the number of FTE's devoted to support medical student education varied greatly in the ADFM Quick Hitter Survey with the differences appearing not attributable to class size. The survey reveals responses concerning a variety of tracts for medical student learning to include rural, urban, and underserved, global/international health, research, and community/integrative health. Although these tracts may have unique importance for individual departments, the implication of these activities on the ability to deliver required family medicine teaching experiences consistent with national norms is unknown. Departments must carefully balance their practice transformational activities with the dynamic changes that come with evolving standardization of required family medicine teaching experiences occurring mostly in stand-alone family medicine clerkships as well as department-specifi c elective and selective activities.
Cancer may be thought of as an immunological disorder that arises because certain 'transformed' cells, endowed with the propensity to divide, have learned to evade detection by the immune system. The prospect of intervention by 'immunotherapy' depends very much on our ability to either [1] render cancer cells more recognizable to the immune system, or [2] potentiate the immune system towards a more effective recognition of cancer cells. There is now direct evidence that suppression of the major histocompatibility complex class I antigens, a family of cell-surface glycoproteins required for the presentation of cancer cells to the immune system, is directly responsible for the ability of tumor cells to escape immune surveillance. It has been shown that cancer cells can be made immunogenic either by the expression of an exogenous class I gene introduced by DNA-mediated gene transfer, or by the derepression of endogenous class I genes with interferon; these cells are efficiently rejected by the immune system. Even more interesting is the finding that the immune system can be potentiated to reject tumors by immunization with homologous tumor cells that have been manipulated to express normal levels of class I antigens. Since increasing numbers of human tumors have been found to have greatly reduced levels of class I antigens, these findings suggest a direct route to immunotherapy that involves debulking of the tumor mass, raising the level of class I antigens in a small number of explanted tumor cells, and re-immunizing the host.
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