ABSTRACT
To investigate a potential role for galectins as biomarkers that enable diagnosis or prognostication of breast or non-small cell lung cancer, the serum levels of galectins -1, -3, -7, -8, and -9 of cancer patients determined by ELISA assays were compared to the mutation status of 50 known cancer-critical genes, which were determined using multiplex PCR in tumors of the same patients. Mutations in the KIT proto-oncogene, which codes for the c-Kit protein, a receptor tyrosine kinase, correlated with higher levels of galectins -1, -3, -8, and -9 in breast cancer patients and galectin-1 in non-small cell lung cancer patients. Mutations in the KIT gene were more likely found in brain metastases from both of these primary cancers. The most common KIT mutation in our panel was p.M541L, a missense mutation in the transmembrane domain of the c-Kit protein. These results demonstrate an association between KIT oncogenic signaling and elevated serum galectins in patients with metastatic disease. Changes in protein trafficking and the glycocalyx composition of cancer cells may explain the observed alterations in galectin expression. This study can be useful for the targeted selection of receptor tyrosine kinase and galectin inhibitor anti-cancer treatments.
ABSTRACT
BACKGROUND: Many pancreatic pseudocysts spontaneously resolve, but larger or symptomatic pseudocysts may require procedural management. Though endoscopic ultrasound guided approaches are standard of care and have high success rates, complications can include bleeding, infection, and splenic perforation. This patient case report details an unusual series of complications of endoscopic cystogastrostomy that should encourage clinicians to evaluate for anatomic disruptions caused by mass effects of pancreatic pseudocysts prior to endoscopic pseudocyst drainage. CASE PRESENTATION: A 53-year-old African American male with a past medical history notable for alcohol use disorder, chronic pancreatitis, and insulin dependent diabetes presented with a 4-day history of left upper quadrant abdominal pain. Computed tomography imaging with contrast revealed enlargement of a known pancreatic pseudocyst to 15.9 × 10.4 cm. Due to pseudocyst size and the patient's symptoms, endoscopic cystogastrostomy stent placement was performed. However, postprocedurally, he developed leukocytosis to 19,800 cells/m3 (from 14,100 cells/m3 preoperatively) as well as acute hypoxemic respiratory failure with a large left pleural effusion. Postprocedural computed tomography with contrast demonstrated a new large subcapsular splenic hematoma in communication with a new subdiaphragmatic fluid collection. Due to suspicion of endoscopic procedural complication, he underwent open laparotomy which revealed grade 4 splenic laceration, septic splenic hematoma, and a subdiaphragmatic abscess. CONCLUSIONS: While endoscopic drainage of pancreatic pseudocyst was technically successful, this case demonstrates complications from mass effect of a large pancreatic pseudocyst which putatively tore the splenorenal ligament, leading to excessive separation of the left kidney and spleen. If anatomic disruptions caused by mass effect from a pancreatic pseudocyst are recognized through preprocedural abdominal imaging, such cases may be considered for early open repair versus cystogastrostomy.
