Fifty adult cadavers have been dissected bilateraly. Judged from our anatomical study, the site of division of the radial nerve into its superficial terminal and posterior interosseous branches is above the lateral humeral epicondyle in 96％. Usually, the brachialis, brachioradialis, and extensor carpi radialis longus and brevis all receive several muscular branches, which stem from different portions of the radial nerve. Muscular branch for ECRB arising from the superficial radial nerve of one side amounts to 25％.Two arcades are found to be situated along the radial side of the anterior cubital region, one being formed from the proximal tendinous margin of the ECRB muscle, and the other from the proximal edge of the superficial portion of the supinator. The lateral half of the ECRB arch, which covers that of the supinator arch, is definite and sharp and is crossed by the posterior interosseous nerve (PIN) obliquely. Its medial half coincides with the corresponding half of the supinator arch, but occassionally they may fuse together. The supinator arch may be divided into loop or circular types, with its longitudinal and transverse diameters of nearly 1～1.2 cm. Those which are tendinous in nature (arcade of Frohse)amount to 18％.There are 28 sides of PIN being compressed by the ECRB arch during passive supination, while 18 sides by the supinator arch (Frohse' arch in 2) during passive pronation. For this reason, in addition to their close relationship and position on the radial side, they are preferred to be combined and named as the cubital radial arch.

Metastasis is the leading cause of human cancer deaths. Unfortunately, no approved drugs are available for anti-metastatic treatment. In our study, high-throughput sequencing-based high-throughput screening (HTS) and a breast cancer lung metastasis (BCLM)-associated gene signature were combined to discover anti-metastatic drugs. After screening of thousands of compounds, we identified Ponatinib as a BCLM inhibitor. Ponatinib significantly inhibited the migration and mammosphere formation of breast cancer cells in vitro and blocked BCLM in multiple mouse models. Mechanistically, Ponatinib represses the expression of BCLM-associated genes mainly through the ERK/c-Jun signaling pathway by inhibiting the transcription of JUN and accelerating the degradation of c-Jun protein. Notably, JUN expression levels were positively correlated with BCLM-associated gene expression and lung metastases in breast cancer patients. Collectively, we established a novel approach for the discovery of anti-metastatic drugs, identified Ponatinib as a new drug to inhibit BCLM and revealed c-Jun as a crucial factor and potential drug target for BCLM. Our study may facilitate the therapeutic treatment of BCLM as well as other metastases.