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Objectives Immediate clip migration following breast biopsy is not a rare condition but its impact on future cancer management can be profound. However, there is limited knowledge on what causes the phenomenon and how to prevent it. Methods A systematic search was performed to identify articles discussing factors associated with clip migration, and a meta-analysis for each risk factor was conducted to determine the risk ratio. Results The most significant risk factor for immediate clip migration is globally fatty breast (RR = 2.00 [1.43-2.80], P<0.00001), while local heterogeneity has a moderate but insignificant protective effect (RR=0.68 [0.45-1.04], P=0.07). Clips with bioabsorbable carriers and biopsy along the superior/inferior breast axis do not change the rate of clip migration. Conclusion Intrinsic breast composition is the most important determinant for accurate clip placement. Further research to identify potentially modifiable factors, such as clip design and biopsy techniques, is needed. Advances in knowledge Fatty breast composition has the highest risk of clip migration. Research on potentially modifiable factors such as clip design and biopsy techniques is needed.

Testicular cancer (TC) is a rare malignancy worldwide and is the most common malignancy in males aged 15–44 years. The Wnt/β-catenin signaling pathway mediates numerous essential cellular functions and has potentially important effects on tumorigenesis and cancer progression. The search for drugs to inhibit this pathway has identified a small molecule, PNU-74654, as an inhibitor of the β-catenin/TCF4 interaction. We evaluated the therapeutic role of PNU-74654 in two TC cell lines, NCCIT and NTERA2, by measuring cell viability, cell cycle transition and cell death. Potential pathways were evaluated by protein arrays and Western blots. PNU-74654 decreased cell viability and induced apoptosis of TC cells, with significant increases in the sub G1, Hoechst-stained, Annexin V-PI-positive rates. PNU-74654 treatment of both TC cell lines inhibited the TNFR1/IKB alpha/p65 pathway and the execution phase of apoptosis. Our findings demonstrate that PNU-74654 can induce apoptosis in TC cells through mechanisms involving the execution phase of apoptosis and inhibition of TNFR1/IKB alpha/p65 signaling. Therefore, small molecules such as PNU-74654 may identify potential new treatment strategies for TC.

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