Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0019621 (Langerhans cell histiocytosis)
 3,250 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Using a modified method of Con A, LCH or PHA-E affinity crossed-line immunoelectrophoresis, we studied AFP subfractions in 78 sera including 58 from patients with primary hepatoma, 11 from patients with hepatic metastasis of gastric cancer and 9 from patients with germ cell tumors of the gonads (yolk sac tumor, immature solid teratoma or mature solid teratoma). It was found that AFP in primary hepatoma, metastatic hepatoma or germ cell tumors of the gonads were differently glycosylated, and different patterns of AFP subfractions identified by Con A, LCH or PHA-E affinity crossed-line immunoelectrophoresis facilitated a differential diagnosis of such AFP related malignancies.
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PMID:[Serum AFP subfractions in patients with hepatic cancer or germ cell tumor of the gonads]. 241 63

Using a modified method of concanavalin A (Con A), lentil lectin (LCH) or phytohemagglutinin-E (PHA-E) affinity crossed-line immunoelectrophoresis (ACIE), we studied alpha-fetoprotein (AFP) subfractions in 69 sera, including 58 from patients with primary liver cancer and 11 from patients with hepatic metastasis of gastric cancer. We found that Con A non-reactive subfraction (type b) or LCH weakly-reactive subfraction (type B) was more frequently detected in metastatic liver cancer, as compared with liver cancer hepatoma. The amount of Con A non-reactive subfraction (type b) or of PHA-E reactive subfraction (type X) was significantly higher in case of metastatic liver cancer than in primary liver cancer. Since different affinities between AFP and lectins are due to the microheterogeneity in AFP sugar chain, our findings suggest that AFP in primary liver cancer and metastatic liver cancer is glycosylated in a different manner. It is also indicated that different patterns of AFP subfractions identified by the combination of Con A, LCH or PHA-E ACIE facilitate a differential diagnosis of these hepatic malignancies.
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PMID:Serum alpha-fetoprotein subfractions in hepatic malignancies identified by different reactivities with concanavalin A, lentil lectin or phytohemagglutinin-E. 242 Oct 34

Alpha-fetoprotein (AFP) subfractions were studied in 38 sera including 34 patients with primary hepatoma and 4 from patients with hepatic metastasis of gastric cancer. Fractionation of AFP was carried out by concanavalin A (Con A) or lentil lectin (LCH) crossed-line affinity immunoelectrophoresis. With use of Con A, fetal-liver-originated subfraction (peak a) was commonly found in both primary hepatoma and metastatic liver cancer, while yolk-sac-originated subfraction (peak b) was detected in 7 of 34 (20.6%) primary hepatomas and 4 of 4 (100%) metastatic liver cancers. With use of LCH, fetal-liver-originated subfractions (peaks A and/or C) were commonly found in both primary hepatoma and hepatic metastasis of gastric cancer, while yolk-sac-originated subfraction (peak B) was found only in metastatic liver cancer. These findings suggest that glycosylation of AFP in primary hepatoma differs from that in hepatic metastasis of gastric cancer. It is also suggested that AFP synthesized in hepatic cancers and fetal liver are differently glycosylated and AFP synthesis of hepatic malignancies are not always retrogenetically expressed, as in case of the fetal liver. Clinically, different patterns of AFP subfraction identified by Con A or LCH crossed-line affinity immunoelectrophoresis facilitate a differential diagnosis of primary hepatoma and hepatic metastasis of gastric cancer, in cases of elevated serum AFP levels. In the current study, attention was also given to the retrogenetic expression of AFP synthesis in hepatic metastasis of gastric cancer.
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PMID:Serum alpha-fetoprotein subfractions in patients with primary hepatoma or hepatic metastasis of gastric cancer. 257 79

P21-activated kinase 4 (PAK4), a serine/threonine protein kinase, has involved in the regulation of cytoskeletal reorganization, cell proliferation, gene transcription, oncogenic transformation and cell invasion. Moreover, PAK4 overexpression, genetic amplification and mutations were detected in a variety of human tumors, which make it potential therapeutic target. In this paper we found that LCH-7749944, a novel and potent PAK4 inhibitor, effectively suppressed the proliferation of human gastric cancer cells through downregulation of PAK4/c-Src/EGFR/cyclin D1 pathway. In addition, LCH-7749944 significantly inhibited the migration and invasion of human gastric cancer cells in conjunction with concomitant blockage of PAK4/LIMK1/cofilin and PAK4/MEK-1/ERK1/2/MMP2 pathways. Interestingly, LCH-7749944 also inhibited the formation of filopodia and induced cell elongation in SGC7901 cells. Importantly, LCH-7749944 caused successful inhibition of EGFR activity due to its inhibitory effect on PAK4. Taken together, these results provided novel insights into the development of PAK4 inhibitor and potential therapeutic strategies for gastric cancer.
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PMID:LCH-7749944, a novel and potent p21-activated kinase 4 inhibitor, suppresses proliferation and invasion in human gastric cancer cells. 2208 92

Superior cervical ganglia 10 (SCG10), as a microtubule (MT) destabilizer, maintains MT homeostasis and has a critical role in neuronal development, but its function in tumorigenesis has not been characterized. In the present study, we demonstrated that p21-activated kinase 4 (PAK4)-mediated SCG10 phosphorylation regulates MT homeostasis in metastatic gastric cancer. Our results indicate that SCG10 is a physiological substrate of PAK4, which is phosphorylated on serine 50 (Ser50) in a PAK4-dependent manner. Phosphorylated SCG10 regulated MT dynamics to promote gastric cancer cell migration and invasion in vitro and metastasis in a xenograft mouse models. Inhibiting PAK4, either by LCH-7749944 or RNA interference, resulted in the inhibition of Ser50 phosphorylation and a blockade to cell invasion, suggesting that PAK4-SCG10 signaling occurs in gastric cancer cell invasion. Moreover, we demonstrated a strong positive correlation between PAK4 and phospho-Ser50 SCG10 expression in gastric cancer samples. We also showed that high expression of SCG10 phospho-Ser50 is highly correlated to an aggressive phenotype of clinical gastric cancer. These findings revealed a novel function of SCG10 in promoting invasive potential of gastric cancer cells, suggesting that blocking PAK4-mediated SCG10 phosphorylation might be a potential therapeutic strategy for metastasis of gastric cancer.
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PMID:PAK4 kinase-mediated SCG10 phosphorylation involved in gastric cancer metastasis. 2389 40