Exosomes, cancer's little army.

In an attempt to conceptualize the process of cancer formation, Hanahan and Weinberg [2000] have outlined six universal characteristics of tumorigenesis, and labelled them as the "hallmarks of cancer". These hallmarks include; unlimited proliferation, evading growth suppressors, resisting cell death, replicative immortality, inducing angiogenesis, initiating invasion and metastasis. Cancer cell signalling is crucial for initiating and controlling cellular pathways that are involved in these hallmarks. The intricate network of communication between cancer cells and other cancer or non-cancer cells is still being investigated, and is yet to be fully understood. Initially it was proposed that the main form of communication between cells within the tumour microenvironment are soluble growth factors, and gap junctions. Then, researchers reported another form of cell-to-cell communication, through the release of spherical particles called exosomes. It is believed that these exosomes enable communication through the transfer of active components from the releasing cell, and off-loading it into the recipient cell. As researchers continue to examine the development of the cancer hallmarks and the pathways involved, it became evident that cancer cell-derived exosomes play a major role in almost all of them. This review will examine the role played by cancer cell-derived exosomes in development of cancer.

Thrombolytic therapy in a patient with inferolateral myocardial infarction after carbon monoxide poisoning.

INTRODUCTION: ST segment elevation myocardial infarction (STEMI) due to coronary artery occlusion caused by intracoronary thrombosis in the setting of acute carbon monoxide (CO) poisoning is a very rare presentation. We present a case of intracoronary large and mobile thrombus formation after CO poisoning. CASE PRESENTATION: A previously healthy 50-year-old woman was referred for CO poisoning. She had chest pain after exposure to CO. Her initial mental status was preoccupied with chest pain. Her initial CO fraction was 28.1%, and initial laboratory data showed creatine kinase-myocardial isoenzyme of 134 U/L (upper limit 25 U/L) and troponin I of >50 ng/mL (upper limit 0.06 ng/mL). Electrocardiography was carried out on admission, revealing an ST segment elevation in the inferolateral leads. After initial evaluation, coronary angiography was performed and an intracoronary large mobile thrombus was seen in the proximal left anterior descending (LAD) artery with no significant stenosis. We administered tenecteplase with heparin. After the thrombolytic therapy, ST elevation in the inferolateral leads resolved. Repeat angiography was performed after 24 h; the thrombus in LAD had resolved. The patient was discharged after 5 days, with persistent Q wave in the inferior leads and mild hypokinesia of the inferoposterior wall suggesting myocardial injury. CONCLUSION: We describe intracoronary thrombus formation induced by CO poisoning. Because intracoronary thrombus can result in myocardial infarction, its consideration following CO poisoning is important. Patients with CO poisoning who have symptoms of STEMI should be carefully evaluated with serial electrocardiograms, cardiac biomarkers, and an echocardiogram. When there is evidence of acute myocardial injury, a primer in coronary angiography can determine which patients could benefit from intervention.

Misuse of fentanyl transdermal patch mixed with acute coronary syndrome.

Fentanyl transdermal patches have long been used in the palliative care of patients with chronic pain with a favorable safety profile. However, intoxications secondary to intentional and unintentional misuse have been widely reported. In this study, we report an otherwise healthy woman presented to emergency department who used three patches of fentanyl to alleviate her knee pain and with a picture mimicking acute coronary syndrome.