Mammography and MRI manifestations of breast angiosarcoma.

BACKGROUND: Breast angiosarcoma is rare and previous studies only focus on its pathology. This study aimed to summarize its imaging features. METHODS: Overall 17 patients pathologically confirmed with breast angiosarcoma were recruited. Eight patients underwent preoperative mammography, and 13 received preoperative MRI scan. The mammography and MRI findings were classified according to the ACR-BI-RADS-mammography/MR lexicon. RESULTS: Mammography showed that 3 cases developed diffuse asymmetry occupying two or more quadrants of the affected breast and that 5 patients had lobulated or oval masses. The 13 patients' lesions presented as diffuse and slightly/significantly high homogeneous or heterogeneous signals on T1-weighted images, while the necrotic and cystic parts had relatively low signals. The hemorrhagic lesions in 7 cases had high signals on both T1- and T2-weighted images. A hemosiderin ring at the edge of an old hemorrhagic lesion had long and short signals on the T1- and T2-weighted images, respectively. Contrast-enhanced MRI revealed that the 13 patients' lesions had significant heterogeneous enhancement. Significant enhancement was observed in the early phase, and varying degrees of concentric enhancement was seen in the delayed phase. CONCLUSIONS: The mammography findings are nonspecific. MRI scan is helpful in determining the malignancy of the lesions. Breast angiosarcoma usually shows heterogeneous signals on both T1-weighted and T2-weighted images. Due to their incomplete lumens and lack of thrombocytes, patients with angiosarcoma have a higher incidence of bleeding (nearly 50% in this study) than those with other malignant tumors. The pattern of the enhancement curve helps to distinguish this disease from the typical types of breast cancer.

The Design, Synthesis and Preliminary Pharmacokinetic Evaluation of d3-Poziotinib Hydrochloride.

To establish a synthetic route to d3-poziotinib hydrochloride. Treatment of 4-chloro-7-hydroxyquinazolin-6-yl pivalate (1) with d3-methyliodide afforded the etherization product, which reacted with 3,4-dichloro-2-fluoroaniline to generate the key intermediate d3-4-(3,4-dichloro-2-fluorophenylamino)-7-methoxyquinazolin-6-yl pivalate (3). Followed the de-protection reaction, the nucleophilic substitution (SN2) reaction with tert-butyl 4-(tosyloxy)piperidine-1-carboxylate (TSP), and the de-protection reaction of t-butoxycarbonyl (Boc) group, and the amide formation reaction with acrylyl chloride, d3-poziotinib was obtained, which was converted to hydrochloride salt by treatment with concentrated hydrochloric acid (HCl). Starting from a known compound 4-chloro-7-hydroxyquinazolin-6-yl pivalate (1), after 7 steps transformation, d3-poziotinib hydrochloride was obtained with a total yield of 9.02%. The structure of d3-poziotinib hydrochloride was confirmed by 1H-NMR, 13C-NMR, and high resolution (HR)-MS. Meanwhile, the in vitro microsomal stability experiment showed that d3-poziotinib had a longer half time (t1/2 = 4.6 h) than poziotinib (t1/2 = 3.5 h).