Delineating Extramammary Findings at Breast MR Imaging.

Breast magnetic resonance (MR) imaging is the only breast imaging modality that consistently encompasses extramammary structures in the thorax and upper abdomen. Incidental extramammary findings on breast MR images of patients with a history of breast cancer or other malignancies are significantly more likely to be malignant and may affect staging and treatment. An understanding of the frequency, distribution, and context of extramammary findings on breast MR images and a familiarity with common and uncommon sites of breast cancer metastasis inform the differential diagnosis and prompt the appropriate diagnostic next step, to differentiate benign from malignant findings. High-yield organ systems on breast MR images, as reflected by a high positive predictive value for malignancy, are correlated with known distant sites of breast cancer metastasis in the bone, lung, liver, and lymph nodes. Staging is considered when disease involves the skin and chest wall. Unusual sites of breast cancer metastasis from invasive lobular carcinoma are discussed, including the gastrointestinal tract, peritoneum, and adrenal glands. Nonmalignant clinically important findings involving the cardiovascular and gastrointestinal systems are reviewed, and potential pitfalls in diagnosis and interpretation are highlighted. A consistently systematic diagnostic approach is emphasized for identifying extramammary abnormalities on breast MR images. All things considered, the radiologist should be able to improve diagnostic sensitivity and specificity while interpreting extramammary findings on breast MR images. ©RSNA, 2017.

Lung Adenocarcinoma: Correlation of Quantitative CT Findings with Pathologic Findings.

Purpose To identify the ability of computer-derived three-dimensional (3D) computed tomographic (CT) segmentation techniques to help differentiate lung adenocarcinoma subtypes. Materials and Methods This study had institutional research board approval and was HIPAA compliant. Pathologically classified resected lung adenocarcinomas (n = 41) with thin-section CT data were identified. Two readers independently placed over-inclusive volumes around nodules from which automated computer measurements were generated: mass (total mass) and volume (total volume) of the nodule and of any solid portion, in addition to the solid percentage of the nodule volume (percentage solid volume) or mass (percentage solid mass). Interobserver agreement and differences in measurements among pathologic entities were evaluated by using t tests. A multinomial logistic regression model was used to differentiate the probability of three diagnoses: invasive non-lepidic-predominant adenocarcinoma (INV), lepidic-predominant adenocarcinoma (LPA), and adenocarcinoma in situ (AIS)/minimally invasive adenocarcinoma (MIA). Results Mean percentage solid volume of INV was 35.4% (95% confidence interval [CI]: 26.2%, 44.5%)-higher than the 14.5% (95% CI: 10.3%, 18.7%) for LPA (P = .002). Mean percentage solid volume of AIS/MIA was 8.2% (95% CI: 2.7%, 13.7%) and had a trend toward being lower than that for LPA (P = .051). Accuracy of the model based on total volume and percentage solid volume was 73.2%; accuracy of the model based on total mass and percentage solid mass was 75.6%. Conclusion Computer-assisted 3D measurement of nodules at CT had good reproducibility and helped differentiate among subtypes of lung adenocarcinoma. (©) RSNA, 2016.

PTEN has tumor-promoting properties in the setting of gain-of-function p53 mutations.

We show, for the first time, that the tumor suppressor PTEN can have tumor-promoting properties. We show that PTEN acquires these unexpected properties by enhancing gain-of-function mutant p53 (mut-p53) protein levels. We find that PTEN restoration to cells harboring mut-p53 leads to induction of G(1)-S cell cycle progression and cell proliferation and to inhibition of cell death. Conversely, PTEN inhibition in cells expressing wild-type PTEN and mut-p53 leads to inhibition of cell proliferation and inhibition of in vivo tumor growth. We show the dependency of the tumor-promoting effects of PTEN on mut-p53 by showing that knockdown of mut-p53 expression inhibits or reverses the tumor-promoting effects of PTEN. Mechanistically, we show that PTEN expression enhances mut-p53 protein levels via inhibition of mut-p53 degradation by Mdm2 and possibly also via direct protein binding. These findings describe a novel function of PTEN and have important implications for experimental and therapeutic strategies that aim at manipulating PTEN or p53 in human tumors. They suggest that the mutational status of PTEN and p53 should be considered to achieve favorable therapeutic outcomes. The findings also provide an explanation for the low frequency of simultaneous mutations of PTEN and p53 in human cancer.