A method of beam-couch intersection detection

At the time of treatment planning it would be useful to know whether part of the treatment beam passes through the patient/couch support assembly before it passes through the patient. In the previous work of Yorke, the range of gantry angles leading to beam-couch intersection was found as a function of couch translation for symmetric field sizes and for zero couch rotation. Yorke's method has been extended to include couch rotation, dual independent jaws, and multi-leaf collimator (MLC) field shapes. In addition, the new method is also applicable in the situation of the couch top located above the isocenter. For a clinically treatable, 20 x 20 cm field configuration in a linac, the range of gantry angles leading to beam-couch intersection are different by 6.7 degrees for a couch rotation angle of 25 degrees when compared to no couch rotation. The new method agrees with data within the setup and measurement uncertainties for a variety of field sizes including an oval shaped MLC field, and various couch locations, couch, and collimator rotation angles.     

Humanized C3 Mouse: A Novel Accelerated Model of C3 Glomerulopathy

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Brk is coamplified with ErbB2 to promote proliferation in breast cancer

Amplification of the receptor tyrosine kinase ErbB2 is frequently observed in breast cancer. Amplification of erbB2 is also associated with multiple genomic gains and losses; however, the importance of these associated changes is largely unknown. We demonstrate that Brk, a cytoplasmic tyrosine kinase, is coamplified and coexpressed with ErbB2 in human breast cancers. ErbB2 interacts with Brk and increases its intrinsic kinase activity. Expression of Brk enhances the ErbB2-induced activation of Ras/MAPK signaling and cyclin E/cdk2 activity to induce cell proliferation of mammary 3-dimensional acini in culture. In a murine model of breast cancer, expression of Brk was found to shorten the latency of ErbB2-induced tumors by promoting cell proliferation, with no effect on protection from apoptosis. Furthermore, overexpression of Brk conferred resistance to the ability of Lapatinib, an ErbB2 kinase inhibitor, to inhibit ErbB2-induced proliferation. Thus, we identified Brk as a drug target for ErbB2-positive cancers.