Is the radial groove a myth? Is the radial nerve in direct contact with the posterior humerus?

BACKGROUND: The radial groove is known as a sulcus on the posterior humerus and protects the radial nerve from adjacent muscle and soft tissue. In the literature, there exists heterogeneity regarding the presence of an actual radial groove and the radial nerve's interaction with the periosteum of the humerus. This study aimed to determine if there is a real radial groove, "sulcus," and define the relationship between the radial nerve and the periosteum of the posterior humerus. METHODS: Eighteen fresh-frozen cadaveric specimens were dissected using a posterior triceps splitting approach. The radial nerve's interaction with the periosteum of the humerus was determined. The presence of a visible and palpable radial groove was also examined. RESULTS: In 56% of specimens, the radial nerve was directly seated over the periosteum of the posterior humerus (direct contact between the nerve and bone). In comparison, 44% of specimens had a layer of the medial head of the triceps brachii muscle fibers interposition between the nerve and bone. 89% of specimens had no visible or palpable radial groove. In 11% of specimens, there was mild palpable depression. CONCLUSION: This study shows that the radial groove may not exist and is probably not a true anatomical structure. In addition, the nerve is in direct contact with the posterior periosteum of the humerus in most specimens. These anatomic relationships and findings add to the anatomical understanding of the radial nerve, which helps during operative approaches and fixation of the humerus.

Loss of tumor suppressor WWOX accelerates pancreatic cancer development through promotion of TGFß/BMP2 signaling.

Pancreatic cancer is one of the most lethal cancers, owing to its late diagnosis and resistance to chemotherapy. The tumor suppressor WW domain-containing oxidoreductase (WWOX), one of the most active fragile sites in the human genome (FRA16D), is commonly altered in pancreatic cancer. However, the direct contribution of WWOX loss to pancreatic cancer development and progression remains largely unknown. Here, we report that combined conditional deletion of Wwox and activation of KRasG12D in Ptf1a-CreER-expressing mice results in accelerated formation of precursor lesions and pancreatic carcinoma. At the molecular level, we found that WWOX physically interacts with SMAD3 and BMP2, which are known activators of the TGF-ß signaling pathway. In the absence of WWOX, TGFß/BMPs signaling was enhanced, leading to increased macrophage infiltration and enhanced cancer stemness. Finally, overexpression of WWOX in patient-derived xenografts led to diminished aggressiveness both in vitro and in vivo. Overall, our findings reveal an essential role of WWOX in pancreatic cancer development and progression and underscore its role as a bona fide tumor suppressor.