Percutaneous transhepatic use of rigid bronchial forceps as bailout in difficult biliary stent retrieval.

Endoscopic retrieval of embedded, proximally migrated, or fractured plastic biliary stents may be technically challenging and sometimes unsuccessful. Percutaneous transhepatic techniques have previously been described to assist in such challenging cases. Here in, we describe a difficult case in which all commonly described endoscopic and percutaneous techniques failed to retrieve a proximally migrated, fractured, and looped plastic biliary stent. We finally successfully retrieved the plastic forceps after off-label utilization of rigid bronchial forceps via a percutaneous transhepatic approach. We describe the technique utilized in detail and this appears to be the first description of this off-label use in this challenging scenario.

Radiation-induced insufficiency fracture of the femur 18 years after radiation therapy.

Advances in oncologic treatment have improved survival rates, allowing late effects of radiotherapy to become more prevalent. Our patient, an 82-year-old woman with a remote history of right thigh basal cell carcinoma treated with resection and radiation therapy 18 years prior, presented with severe right thigh pain and inability to bear weight as she had suffered a femur fracture after a fall from standing. Initial imaging was suspicious for pathologic fracture secondary to malignancy due to imaging findings and because radiation-induced fractures have rarely been reported beyond 44 months from treatment. However, upon further imaging, evidence pointed to radiation-induced osteonecrosis as the mechanism for her insufficiency fracture. This case highlights the permanent deleterious effects of radiation therapy on bone, and the prudence of considering radiation-induced osteonecrosis as a mechanism of injury in low-energy trauma even long after radiation therapy. In addition, the case serves to review the natural history of irradiated bone injury and pertinent imaging findings.

Somatic Trp53 mutations differentially drive breast cancer and evolution of metastases.

TP53 mutations are the most frequent genetic alterations in breast cancer and are associated with more aggressive disease and worse overall survival. We have created two conditional mutant Trp53 alleles in the mouse that allow expression of Trp53R172H or Trp53R245W missense mutations in single cells surrounded by a normal stroma and immune system. Mice with Trp53 mutations in a few breast epithelial cells develop breast cancers with high similarity to human breast cancer including triple negative. p53R245W tumors are the most aggressive and exhibit metastases to lung and liver. Development of p53R172H breast tumors with some metastases requires additional hits. Sequencing of primary tumors and metastases shows p53R245W drives a parallel evolutionary pattern of metastases. These in vivo models most closely simulate the genesis of human breast cancer and will thus be invaluable in testing novel therapeutic options.