RESUMEN
Blunt and penetrating vascular injuries to the neck represent a significant burden of mortality and disability among trauma patients. Blunt cerebrovascular injury can present with signs of stroke either immediately or in a delayed fashion. Most injuries are detected with computed tomography angiogram and managed by antiplatelet agents or unfractionated heparin. In contrast, for patients presenting with penetrating neck injuries, assessment for hard signs of vascular and aerodigestive injury should be done and prompt emergent surgical consultation if present. Overall management priorities for penetrating neck injuries focus on airway management, hemorrhage control, and damage control resuscitation before definitive surgical repair.
Asunto(s)
Traumatismos del Cuello , Heridas no Penetrantes , Heridas Penetrantes , Humanos , Heparina , Traumatismos del Cuello/diagnóstico , Traumatismos del Cuello/terapia , Heridas Penetrantes/diagnóstico , Heridas Penetrantes/terapia , Cuello , Heridas no Penetrantes/diagnóstico , Heridas no Penetrantes/terapia , Dolor en el PechoRESUMEN
The tumor microenvironment (TME) is an important mediator of breast cancer progression. Cancer-associated fibroblasts constitute a major component of the TME and may originate from tissue-associated fibroblasts or infiltrating mesenchymal stromal cells (MSCs). The mechanisms by which cancer cells activate fibroblasts and recruit MSCs to the TME are largely unknown, but likely include deposition of a pro-tumorigenic secretome. The secreted embryonic protein NODAL is clinically associated with breast cancer stage and promotes tumor growth, metastasis, and vascularization. Herein, we show that NODAL expression correlates with the presence of activated fibroblasts in human triple-negative breast cancers and that it directly induces Cancer-associated fibroblasts phenotypes. We further show that NODAL reprograms cancer cell secretomes by simultaneously altering levels of chemokines (e.g., CXCL1), cytokines (e.g., IL-6) and growth factors (e.g., PDGFRA), leading to alterations in MSC chemotaxis. We therefore demonstrate a hitherto unappreciated mechanism underlying the dynamic regulation of the TME.