Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0268596 (EMA)
 2,520 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Clinical investigations with imaging- and endoscopic techniques in order to identify the primary tumor sites in patients with CUP syndrome generally entail a significant diagnostic effort. If costs exceed <euro> 800.00, a financial loss ensues for German hospitals, as public health insurance companies do not reimburse above this amount. Combined cytological/immunocytochemical investigation of metastatic cancer cells represents a cost-effective, minimally invasive procedure to identify the probable primary cancer site that can be applied on an outpatient basis. We report on 85 fine needle aspiration biopsies of metastases to the liver, 30 to the lymph nodes and over 180 serous effusions and/or ascites with metastatic cancer cells in CUP. After conventional microscopic inspection, a routine panel of six monoclonal antibodies was applied (CK 5/6, CK 7, CK 20, Cdx 2, TTF 1 and CA 125). We were thus able to correctly identify the primary tumor sites in 90.3%, 92.0% and 85.1%, respectively, within three days. In total, 23 primary hepatocellular carcinomas could all be classified correctly, applying the antibodies HepPar 1, BerEp 4, AFP, CD 31, CD 68 and Ki 67. In addition, 141 malignant epithelial mesotheliomas were typed correctly in 97.1%, using the antibodies BerEp 4, Calretinin, Mesothelin, EMA and WT. Therefore, immunocytochemical investigation of metastatic cancer cells from fine needle aspiration biopsies or in serous effusions offers an efficient, cost-effective diagnostic alternative to imaging and endoscopic techniques in the workup of patients with CUP syndrome.
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PMID:[Immunocytochemical identification of carcinomas of unknown primaries on fine-needle-aspiration-biopsies]. 1975 20

The proper display of transmembrane receptors on the leading edge of migrating cells and cell extensions is essential for their response to guidance cues. We previously discovered that MADD-4, which is an ADAMTSL secreted by motor neurons in Caenorhabditis elegans, interacts with an UNC-40/EVA-1 co-receptor complex on muscles to attract plasma membrane extensions called muscle arms. In nematodes, the muscle arm termini harbor the post-synaptic elements of the neuromuscular junction. Through a forward genetic screen for mutants with disrupted muscle arm extension, we discovered that a LAMMER kinase, which we call MADD-3, is required for the proper display of the EVA-1 receptor on the muscle's plasma membrane. Without MADD-3, EVA-1 levels decrease concomitantly with a reduction of the late-endosomal marker RAB-7. Through a genetic suppressor screen, we found that the levels of EVA-1 and RAB-7 can be restored in madd-3 mutants by eliminating the function of a p38 MAP kinase pathway. We also found that EVA-1 and RAB-7 will accumulate in madd-3 mutants upon disrupting CUP-5, which is a mucolipin ortholog required for proper lysosome function. Together, our data suggests that the MADD-3 LAMMER kinase antagonizes the p38-mediated endosomal trafficking of EVA-1 to the lysosome. In this way, MADD-3 ensures that sufficient levels of EVA-1 are present to guide muscle arm extension towards the source of the MADD-4 guidance cue.
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PMID:The MADD-3 LAMMER Kinase Interacts with a p38 MAP Kinase Pathway to Regulate the Display of the EVA-1 Guidance Receptor in Caenorhabditis elegans. 2712 83