Compliance with the commission on cancer quality of breast cancer care measures: self-evaluation advised.

To provide evaluations of cancer care quality, the Commission on Cancer and the National Quality Forum (NQF) established three breast cancer treatment quality measures. Programs that submit data to the National Cancer Data Base (NCDB) can receive feedback on their compliance with these quality measures, and perform comparisons with other member institutions. Data received by a county hospital from the NCDB revealed poor compliance. The purpose of this study was to evaluate the accuracy of submitted data, identify contributing factors and initiate processes to improve. Reported 2004 NCDB quality measure compliance was 26% for radiation, 61.4% for chemotherapy, and 21.3% for hormonal therapy. Retrospective treatment review was performed. Data collected included: patient demographics, pathology, final surgical intervention, adjuvant treatment, and quality measure compliance. Sources included two electronic records, an electronic results depository, two paper charts, a pharmacy data base, and a "shadow chart." Applicability of and compliance with these quality measures was noted. Of 540 records reviewed, 132 met final study criteria. Actual compliance differed significantly from NCDB rates and were found to be 97% for radiation, 98% for chemotherapy, and 88% for hormonal therapy. Process analysis revealed the need for tumor registry staff to evaluate all sources of data. A significant problem was neo-adjuvant chemotherapy and the requirement to submit NCDB data within 6 months of initial diagnosis. Processes and education initiated for tumor registry staff, medical records personnel, physicians, and other care providers resulted in significantly improved 2007 compliance of data submitted to the NCDB. Prior to public reporting, institutions should perform NQF quality measure compliance assessments, confirm accuracy, and initiate educational processes/imperatives.

Neurog2 is a direct downstream target of the Ptf1a-Rbpj transcription complex in dorsal spinal cord.

PTF1-J is a trimeric transcription factor complex essential for generating the correct balance of GABAergic and glutamatergic interneurons in multiple regions of the nervous system, including the dorsal horn of the spinal cord and the cerebellum. Although the components of PTF1-J have been identified as the basic helix-loop-helix (bHLH) factor Ptf1a, its heterodimeric E-protein partner, and Rbpj, no neural targets are known for this transcription factor complex. Here we identify the neuronal differentiation gene Neurog2 (Ngn2, Math4A, neurogenin 2) as a direct target of PTF1-J. A Neurog2 dorsal neural tube enhancer localized 3' of the Neurog2 coding sequence was identified that requires a PTF1-J binding site for dorsal activity in mouse and chick neural tube. Gain and loss of Ptf1a function in vivo demonstrate its role in Neurog2 enhancer activity. Furthermore, chromatin immunoprecipitation from neural tube tissue demonstrates that Ptf1a is bound to the Neurog2 enhancer. Thus, Neurog2 expression is directly regulated by the PTF1-J complex, identifying Neurog2 as the first neural target of Ptf1a and revealing a bHLH transcription factor cascade functioning in the specification of GABAergic neurons in the dorsal spinal cord and cerebellum.

Manipulating Robo expression in vivo perturbs commissural axon pathfinding in the chick spinal cord.

In vertebrate embryos, most spinal commissural axons cross the ventral midline (VM) and project either alongside or significant distances away from the floor plate (FP). The upregulation of repulsive Robo1/2 receptors on postcrossing commissural axons, in mammals, presumably allows these axons to respond to the midline-associated repellents, Slit1-3, facilitating their expulsion from, and prohibiting their reentry into, the FP. Compelling data suggest that Robo3 represses Robo1/2 function on precrossing axons and that Robo1/2 inhibit attractive guidance receptors on postcrossing axons, thereby ensuring that decussated axons are selectively responsive to midline Slits. However, whether Robo1/2 expel decussated commissural axons from the VM and/or prevent their reentry into the FP has not been explicitly established in vivo. Furthermore, some commissural axons do not require Robo1/2 to elaborate appropriate contralateral projections in the mouse spinal cord. Here, we use unilateral in ovo electroporation together with Atoh1 and Neurog1 enhancer elements to visualize, and assess the consequences of manipulating Robo expression on, dl1 and dl2 chick commissural axons. In response to misexpressing a cytoplasmic truncation of Robo1 and/or Robo2, which should block all Robo-ligand interactions, postcrossing commissural axons extend alongside, but do not project away from or reenter the FP. In contrast, misexpression of full-length Robo2 prevents many commissural axons from crossing the VM. Together, these findings support key and selective in vivo roles for Robo receptors in presumably altering the responsiveness of decussated commissural axons and facilitating their expulsion from the VM within the chick spinal cord.