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INTRODUCTION: This case raises awareness of the diagnosis of sternal fracture during labor and obviates the need for lengthy, expense-consuming workup. This report identifies a subset of women who may be at higher risk for this pathology. METHODS: Upon diagnosing and treating a patient who spontaneously fractured her sternum during labor, we reviewed previously reported cases and highlight key points of this entity. RESULTS: We report the third case of sternal fracture during labor in a healthy primigravida with female athlete triad. After 12 h of labor, the woman underwent epidural placement. By 16 h, the cervix was fully dilated. During the second push in the chin-to-chest position, a healthy baby was delivered, but the mother experienced acute anterior chest pain. Tenderness persisted for three weeks. Plain radiographs confirmed the presence of the fracture, which healed spontaneously. CONCLUSION: While chest pain during labor often results from serious causes including pulmonary embolism, myocardial infarction, and spontaneous pneumothorax, hyperflexion sternal fracture can occur, particularly in a woman with female athlete triad.
RESUMO
NUT midline carcinoma (NMC) is an aggressive type of squamous cell carcinoma that is defined by the presence of BRD-NUT fusion oncogenes, which encode chimeric proteins that block differentiation and maintain tumor growth. BRD-NUT oncoproteins contain two bromodomains whose binding to acetylated histones is required for the blockade of differentiation in NMC, but the mechanisms by which BRD-NUT act remain uncertain. Here, we provide evidence that MYC is a key downstream target of BRD4-NUT. Expression profiling of NMCs shows that the set of genes whose expression is maintained by BRD4-NUT is highly enriched for MYC upregulated genes, and MYC and BRD4-NUT protein expression is strongly correlated in primary NMCs. More directly, we find that BRD4-NUT associates with the MYC promoter and is required to maintain MYC expression in NMC cell lines. Moreover, both siRNA knockdown of MYC and a dominant-negative form of MYC, omomyc, induce differentiation of NMC cells. Conversely, differentiation of NMC cells induced by knockdown of BRD4-NUT is abrogated by enforced expression of MYC. Together, these findings suggest that MYC is a downstream target of BRD4-NUT that is required for maintenance of NMC cells in an undifferentiated, proliferative state. Our findings support a model in which dysregulation of MYC by BRD-NUT fusion proteins has a central role in the pathogenesis of NMC.
