Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:2.7.10.1 (ERK)
95,504 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The cellular and humoral immune responses of CF1 and C57BL/6 mice with schistosomiasis mansoni were evaluated before and after chemotherapeutic cure of their infections by praziquantel. Mice were infected for either 10 or 20 weeks prior to treatment and followed until 10 weeks after treatment. Peripheral blood eosinophilia, without concomitant general leukocytosis, was observed within 3 days of treatment and persisted for up to 4 weeks. By 6 and 10 weeks after treatment schistosomal-associated hepatosplenomegaly had greatly decreased. Delayed-type hypersensitivity to a soluble adult worm extract (SWAP) was modulated over 20 weeks of infection, and in C57BL/6 mice this modulation was alleviated by cure. In parallel studies of pulmonary egg granuloma formation, granuloma modulation was not effectively reversed. Antibodies against egg (SEA), cercarial (CAP) and adult worm (SWAP) extracts generally decreased by 10 weeks after chemotherapy of mice that were previously infected for 10 weeks. Mice infected for 20 weeks and then treated, generated increased levels of antibodies to SWAP and CAP by 10 weeks after treatment. Immunoglobulin isotypic analyses largely reflected the results of total antibody studies. These data demonstrate that the duration of infection prior to treatment is a determining factor in subsequent expression of immune reactivity, and provide the immunological background for experiments on resistance following chemotherapy of experimental murine schistosomiasis mansoni.
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PMID:Effects of anti-schistosomal chemotherapy on immune responses, protection and immunity. I. Changes in cellular and humoral responses. 308 Sep 12

Eosinophil count, delayed intradermal test and lymphoblast transformation test (LTT) using SEA, have been used to study the correlation of eosinophilia with CMI in patients with schistosomiasis mansoni. Only a weak positive correlation was found between the eosinophil count and both in vivo and in vitro manifestations of CMI. When IgE serum level was correlated with eosinophil count, a positive correlation was only found in cases with hepato-splenic disease (those with increased CMI).
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PMID:Study of eosinophilia in relation to serum IgE level and cell mediated immunity (CMI) to soluble egg antigen (SEA) in human schistosomiasis mansoni. 316 9

An unusual hematologic neoplasia has been described recently in which the predominant clinical features include T-cell lymphoma, myeloid hyperplasia, and eosinophilia. The multilineage involvement in this disorder suggests transformation of a primitive stem cell. Abnormal karyotypes have been described in three such cases, including one case with t(8;13)(p11.2;q12) and a second case with t(8;13)(p23;q14). We report translocation of chromosomes 8 and 13 in lymph node karyotypes from two patients with this syndrome. Fluorescence in situ hybridization confirmed an identical translocation, t(8;13)(p11;q11-12), in lymphoma cells from each patient. The translocation breakpoints are of particular interest because the FLT3 receptor tyrosine kinase gene has been mapped 13q12. FLT3 is expressed highly in hematopoietic progenitor cells and in myeloid and lymphoid acute leukemias.
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PMID:Translocation t(8;13)(p11;q11-12) in stem cell leukemia/lymphoma of T-cell and myeloid lineages. 753 88

Specific IgA assays by ELISA technique for schistosomal cases of school age children (12-14 years), were performed before and 3 months after praziquantel treatment. Sera of the resistant cases (non-reinfected after chemotherapeutic cure) showed a significant higher titres of anti-soluble egg antigen (anti-SEA) and anti-soluble worm antigen preparation (anti-SWAP) IgA antibodies than that of reinfected schistosomal cases before and 3 months after treatment. Praziquantel therapy insignificantly (P > 0.05) increased anti-SEA and anti-SWAP IgA antibodies in the sera of schistosomal cases and 3 months after treatment. Anti-SEA IgA & IgE anti-SWAP IgA & IgE were correlated positively with each other among schistosomal cases either resistant or reinfected while anti-SEA and anti-SWAP IgA antibody levels of schistosomal cases with eosinophilia were significantly higher than that with normal eosinophilic counts. Anti-SEA IgA antibody titres of schistosomal cases were correlated negatively, before treatment, with intensity of infection but anti-SWAP IgA titres were not, which might indicates that anti-SEA IgA antibodies inhibit schistosomes for egg laying and subsequently pathological complications due to granuloma formation. The higher titres of specific IgA antibody of resistant cases, its positive correlation with IgE and its negative correlation with intensity of infection might support the role of IgA as an essential component of acquired (resistance) immunity to share with IgE in protection of cured schistosomal cases against reinfection.
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PMID:Human resistance to reinfection with schistosomes. II. Specific IgA titres before & 3 months after praziquantel treatment. 784 15

Three hundred children with hepatomegaly were selected. They were subjected to full clinical and laboratory examinations. Also serum samples were examined to detect IgG using ELISA against SEA, chromatography purified hydatid cyst antigen, commercially available Toxoplasma antigen, partially purified adult Fasciola antigen and second-stage larvae Toxocara canis antigen. IFAT was used to detect IgG against Toxoplasma and T. canis. A commercially available IHAT kit for leishmaniasis was used. Based on immunological assays, 125 cases were suffering from various parasitic infections. Thirty cases with schistosomiasis (10%), 26 cases fascioliasis (8.7%), 18 toxocariasis (6%), 35 toxoplasmosis (11.7%), 3 cases hydatidosis (1%) and 13 cases mixed parasitic infections. No parasitic causes could be found in 175 cases (58.3%). Moderate or marked hepatomegaly favours the presence of schistosomiasis. Whereas, most cases with other parasites and those with non-parasitic infections fall in the category of mild hepatic enlargement. There was no associated splenomegaly in cases with Fasciola, Toxocara, hydatid disease and/or the non-parasitic group. Most of hepatomegalic cases with non-parasitic causes were found to be associated with fever (88.5%). Fever was found in nearly 50% of cases with either Toxoplasma or Toxocara infections. Mild eosinophilia was found in all cases with parasitic causes. Only 24 cases of non-parasitic group (13.7%) had easinophilia. Moderate and high eosinophilia were found in cases with fascioliasis and toxocariasis. Cases with fascioliasis had a statistically significant increase in enzymes activities specially alkaline phosphatase. It was concluded that parasitic infections should be considered as an important cause of liver enlargement in children. Serological methods using purified antigenic fractions are an important tool for diagnosis.
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PMID:Parasitic causes of hepatomegaly in children. 872 Dec 39

Chromosomal abnormalities involving the short arm of chromosome 12 have been frequently observed in a broad spectrum of hematological malignancies. Recently, a gene located in this chromosomal region and implicated in leukemogenesis was identified. The gene, called ETV6 (previously known as TEL) is a new member of the ETS family, a group of genes thought to act as transcriptional activators. The gene spans 240 kb and consists of eight exons coding for a helix-loop-helix (HLH) and a DNA-binding domain. ETV6 was originally identified in a t(5;12)(q33;p13) occurring in a chronic myelomonocytic leukemia (CMML). Recent reports, however, show its involvement in a growing number of translocations associated with myeloid as well as lymphoid leukemias. At the molecular level fusions of ETV6 with PDGFRB (5q33), ABL (9q34), MNI(22q11) and AML1(21q22) have already been identified. Analysis of these chimeric proteins indicates that distinct domains of ETV6 can be involved in different fusion products, thus ETV6 can provide transcriptional and dimerization properties for partner genes, or the gene itself can act as an altered transcriptional factor. At least two clinico-pathological entities associated with ETV6 rearrangements have emerged as distinct disorders. The first one is a chronic myeloid malignancy characterized by t(5;12)(q33;p13), monocytosis and/or eosinophilia. The second entity is a type of childhood acute lymphoblastic leukemia (ALL) hallmarked by t(12;21)(p13;q22), and is shown to be the most frequent but cytogenetically largely undetectable chromosomal anomaly in childhood ALL.
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PMID:ETV6 gene rearrangements in hematopoietic malignant disorders. 903 Nov 9

Chromosome 8p11-12 is the site of a recurrent breakpoint in a myeloproliferative disorder that involves lymphoid (T- or B-cell), myeloid hyperplasia and eosinophilia, and evolves toward acute leukemia. This multilineage involvement suggests the malignant transformation of a primitive hematopoietic stem cell. In this disorder, the 8p11-12 region is associated with three different partners 6q27, 9q33, and 13q12. We describe here the molecular characterization of the t(8;13) translocation that involves the FGFR1 gene from 8p12, encoding a tyrosine kinase receptor for members of the fibroblast growth factor family, and a gene from 13q12, tentatively named FIM (Fused In Myeloproliferative disorders). FIM is related to DXS6673E, a candidate gene for X-linked mental retardation in Xq13.1; this defines a gene family involved in different human pathologies. The two reciprocal fusion transcripts, FIM/FGFR1 and FGFR1/FIM are expressed in the malignant cells. The FIM/FGFR1 fusion protein contains the FIM putative zinc finger motifs and the catalytic domain of FGFR1. We show that it has a constitutive tyrosine kinase activity.
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PMID:Fibroblast growth factor receptor 1 is fused to FIM in stem-cell myeloproliferative disorder with t(8;13). 957 49

In patients with an atypical stem-cell myeloproliferative disorder with lymphoma (B or T cell), myeloid hyperplasia, and eosinophilia, the chromosome 8p11-12 region is the site of a recurrent breakpoint that can be associated with three different partners, 6q27, 9q32-34, and 13q12. Rearrangements are supposed to affect a pluripotent stem cell capable of myeloid and lymphoid differentiation and to involve the same 8p11-12 gene. The t(8;13) translocation has recently been shown to result in a fusion between the FGFR1 gene that encodes a tyrosine kinase receptor for fibroblast growth factors and a novel gene, FIM (also called RAMP or ZNF198), belonging to a novel family of zinc finger genes. In the present study, we have cloned the t(6;8)(q27;p11) translocation in two patients and found a fusion between FGFR1 and a novel gene, FOP (FGFR1 Oncogene Partner), located on chromosome band 6q27. This gene is alternatively spliced and ubiquitously expressed. It encodes a protein containing two regions of putative leucine-rich repeats putatively folding in alpha-helices and separated by a hydrophobic spacer. The two reciprocal fusion transcripts were evidenced by reverse transcription-polymerase chain reaction in the tumoral cells of the patients. The predicted chimeric FOP-FGFR1 protein contains the FOP N-terminus leucine-rich region fused to the catalytic domain of FGFR1. It may promote hematopoietic stem cell proliferation and leukemogenesis through a constitutive phosphorylation and activation of the downstream pathway of FGFR1.
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PMID:The t(6;8)(q27;p11) translocation in a stem cell myeloproliferative disorder fuses a novel gene, FOP, to fibroblast growth factor receptor 1. 994 82

A 40-year-old male patient presented with leukocytosis and mild splenomegaly. Bone marrow aspirate showed myeloid hyperplasia and eosinophilia resembling chronic myelogenous leukemia in the chronic phase. Cytogenetic examination of bone marrow cells revealed an unusual karyotype, t(8;13)(p11;q12), in 20/20 metaphases. Not the BCR/ABL, but the ZNF198/FGFR1 chimeric mRNA was detected by reverse transcription-polymerase chain reaction. Since 1992, 12 patients with a similar atypical myeloproliferative disorder with T-cell non-Hodgkin's lymphoma or eosinophilia, associated with a t(8;13) translocation in both bone marrow and lymph node specimens, have been described. The present case is an additional one that should be classified into this new clinicopathologic entity.
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PMID:A chronic myelogenous leukemia-like myeloproliferative disorder accompanied by T-cell lymphoblastic lymphoma with chromosome translocation t(8;13)(p11;q12): a Japanese case. 1064 54

Two distinct clinical syndromes have been associated with the p11.12 region of the short arm of chromosome 8: stem-cell myeloproliferative disorder (B-or T-cell lymphoblastic leukemia/lymphoma with myeloid hyperplasia and peripheral blood eosinophilia) and acute myeloid leukemia (myelomonocytic or monocytic with erythrophagocytosis). The FGFR1 and MOZ genes are rearranged in these diseases and encode one of the four fibroblast growth factor receptors and a member of a novel histone acetyltransferase family, respectively. The predicted fusion proteins that are putatively oncogenic - FOP-FGFR1, CEP110-FGFR1, and FIM-FGFR1 - and - MOZ-CBP, MOZ-p300, and MOZ-TIF2 - lead to tumorigenesis through distinct pathways. The constitutive kinase activity triggered by dimerization mediated by the protein-protein interaction motifs of the FGFR1 protein partner regardless of external stimuli and the delocalization of the fusion proteins compared to their normal counterparts may lead to tumorigenesis presumably by inducing inappropriate recruitment in the cytoplasm of signaling substrates. Currently, little is known about the precise role of MOZ in the regulation of gene transcription. However, all the aberrant proteins described to date retain the MOZ histone acetyltransferase domain fused to that of the transcription coactivators CBP, p300, and TIF2. The fusion of two acetyltransferases whose activity may be mistargetted or misregulated could be a critical event in leukemogenesis. The increasing number of translocations affecting FGFR1 and MOZ strongly suggest their involvement in oncogenic processes and point to these proteins as potential therapeutical targets.
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PMID:[FGFR1 and MOZ, two key genes involved in malignant hemopathies linked to rearrangements within the chromosomal region 8p11-12]. 1117 18


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