Serial computed tomographic (CT) scans of 200 patients with malignant testicular teratomas were reviewed. Of the 200 patients, 120 were treated with chemotherapy for metastatic disease; 80 patients with no evidence of metastases (stage I disease) received no treatment and served as a control group. CT was performed at regular intervals for ongoing follow-up in both groups. Thymic enlargement occurred 3-14 months after initiation of treatment in 14 of the 120 patients (11.6%) who received chemotherapy but in only one patient in the control group. Histologic examination in one patient who received chemotherapy revealed that the thymic enlargement represented true hyperplasia. Thirteen of the 14 patients (93%) with thymic enlargement after chemotherapy were well and disease free on mean follow-up of 45 months, compared with 78% of the group that did not show thymic enlargement after chemotherapy (P less than .02). Rebound thymic hyperplasia in adults after chemotherapy for metastatic testicular teratoma may be a good prognostic feature and should be considered when an anterior mediastinal mass develops after chemotherapy for metastatic malignancy.

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Four cases of focal sparing in otherwise diffuse fatty infiltration of the liver are reported. The characteristic features are described as shown at sonography, computed tomography (CT) and scintigraphy. It is emphasised that, with ultrasound, if the increased echogenicity of the majority of the liver is not appreciated, then the area of normal hepatic parenchyma may be misinterpreted as a pathological hypoechoic lesion.

Purpose To assess whether individual reader performance with digital breast tomosynthesis (DBT) and two-dimensional (2D) mammography varies with number of years of experience or volume of 2D mammograms read. Materials and Methods After written informed consent was obtained, 8869 women (age range, 29-85 years; mean age, 56 years) were recruited into the TOMMY trial (A Comparison of Tomosynthesis with Digital Mammography in the UK National Health Service Breast Screening Program), an ethically approved, multicenter, multireader, retrospective reading study, between July 2011 and March 2013. Each case was read prospectively for clinical assessment and to establish ground truth. A retrospective reading data set of 7060 cases was created and randomly allocated for independent blinded review of (a) 2D mammograms, (b) DBT images and 2D mammograms, and (c) synthetic 2D mammograms and DBT images, without access to previous examinations. Readers (19 radiologists, three advanced practitioner radiographers, and two breast clinicians) who had 3-25 (median, 10) years of experience in the U.K. National Health Service Breast Screening Program and read 5000-13 000 (median, 8000) cases per annum were included in this study. Specificity was analyzed according to reader type and years and volume of experience, and then both specificity and sensitivity were analyzed by matched inference. The median duration of experience (10 years) was used as the cutoff point for comparison of reader performance. Results Specificity improved with the addition of DBT for all readers. This was significant for all staff groups (56% vs 68% and 49% vs 67% [P < .0001] for radiologists and advanced practitioner radiographers, respectively; 46% vs 55% [P = .02] for breast clinicians). Sensitivity was improved for 19 of 24 (79%) readers and was significantly higher for those with less than 10 years of experience (91% vs 86%; P = .03) and those with total mammographic experience of fewer than 80 000 cases (88% vs 86%; P = .03). Conclusion The addition of DBT to conventional 2D screening mammography improved specificity for all readers, but the gain in sensitivity was greater for readers with less than 10 years of experience.

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Twenty-five years after its first description the p53 protein has been shown to play a key role in both cancer and ageing. The p53 protein is activated by many different stress pathways, including oncogene action and DNA damage. The elucidation of the p53 response, which is aberrant in most cancers (including breast, lung, stomach and colorectal cancer), has provided many new targets for drug development and p53 gene therapy is now approved in China. In tumours where p53 is mutant small molecules may be able to restore its function. In many tumours the wild-type p53 gene remains intact but its function is compromised by loss of upstream signalling pathways or downstream effectors. A key regulator is Mdm2, an E3 ubiquitin ligase, that binds and ubiquitinates p53 and directs its degradation via the proteosome. Small potent peptides that can block the p53 Mdm2 interaction and activate the p53 response have been described. Growing selections of lead small molecules that mimic the action of these peptides have also been recently discovered. Cell-based screens have revealed that inhibitors of nuclear export and inhibitors of transcription (one of which is in clinical trial) can also activate the p53 response therapeutically. The pharmaceutical regulation of the p53 pathway offers great hope for improved treatment of human cancer.

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