### Total Build Time: 49 ms 39.860 KB
CONCEPT_NAME gt=1 ms Completed: 1 ms rowSize= 330 bytes
CONCEPT_SOLR_HIT_STATS gt=0 Completed: 0 ms rowSize= 14 bytes
CONCEPT_DEFINITION gt=0 Completed: 0 ms rowSize= 594 bytes
- Skipping details on:
CONCEPT_SYNONYM gt=NONE 0 Completed: 0 ms rowSize= 0 bytes
- Skipping details on:
CONCEPT_TEXT gt=NONE 0 Completed: 0 ms rowSize= 0 bytes
CONCEPT_SEMANTIC_TYPE gt=1 ms Completed: 1 ms rowSize= 14 bytes
- Skipping details on:
CONCEPT_NAMESPACE gt=NONE 0 Completed: 0 ms rowSize= 0 bytes
CONCEPT_PARENTS gt=0 Completed: 0 ms rowSize= 7 bytes
CONCEPT_CHILDREN gt=0 Completed: 0 ms rowSize= 8 bytes
CONCEPT_ANCESTRAL_ROOTS gt=0 Completed: 0 ms rowSize= 15 bytes
CONCEPT_RELATIONSHIPS gt=8 ms Completed: 8 ms rowSize= 13.972 KB
CONCEPT_GENES gt=27 ms Completed: 27 ms rowSize= 23.766 KB
CONCEPT_XREFS gt=11 ms Completed: 11 ms rowSize= 1.150 KB
CONCEPT_ANCILLARY gt=1 ms Completed: 1 ms rowSize= 14 bytes
human : 15
|Human||TCL1A||8115||T-cell leukemia/lymphoma 1A|
The TCL1 locus on chromosome 14 band q32.1 is frequently involved in the chromosomal translocations and inversions with the T-cell receptor genes observed in several T-cell tumors, including T-prolymphocytic leukemias, acute and chronic leukemias associated with the immunodeficiency syndrome ataxia-telangiectasia, and adult T-cell leukemia.
A role for ATM in the development of sporadic T-cell chronic leukemias is supported by the finding of loss of heterozygosity at 11q22-23 and ATM mutations in leukemias carrying TCL-1 rearrangements.
|Human||TNF||7124||tumor necrosis factor|
Polymorphisms associated with control of gene expression and protein levels were not associated with occurrence of chronic idiopaathic leukemia in adults and were not responsible for the increased cytokines
|Human||TFRC||7037||transferrin receptor (p90, CD71)|
Combined assessments of TfR and Ki-67 expression revealed a Ki-67- TfR- phenotype in 82% of chronic leukemias, compared with 28% of acute type, and a Ki-67+ TfR+ pattern was found in 27% of acute proliferations but not in any case of chronic leukemia.
To estimate the extent of the TRG gamma variable (V) gene repertoire used in human T cell ontogeny, we have analyzed the variety of V gamma gene rearrangements in a large series of T and non-T acute and chronic leukemias.
|Human||SRC||6714||v-src avian sarcoma (Schmidt-Ruppin A-2) viral oncogene homolog|
Curcumin treatment inhibited v-src gene expression in K562 chronic leukaemia cells
|Human||ABCB4||5244||ATP-binding cassette, sub-family B (MDR/TAP), member 4|
Expression of the MDR1 and MDR3 gene products in acute and chronic leukemias.
We determined the expression levels of the mdr1 and mdr3 multidrug-resistance genes (also known as PGY1 and PGY3, respectively) in peripheral blood cells from 69 adult patients with acute and chronic leukemias, using an RNase protection assay.
Expression of mdr1 and mdr3 multidrug-resistance genes in human acute and chronic leukemias and association with stimulation of drug accumulation by cyclosporine.
It may be speculated that precytotoxic agents induced mdr1 and mdr3 P-gp expression in acute leukemia; however, in chronic leukemia, both P-gps were expressed independently of exposure to precytotoxic agents.
Of 23 patients with chronic leukemia (CLL and GLPD), 10 (37%) were positive for mdr1 P-gp and 12 (44%) for mdr3 P-gp.
The results of this study may have implications for clinical therapy for acute or chronic leukemias expressing the mdr1 or mdr3 gene, in particular, treatment with combinations of cytotoxic drugs plus agents that reverse multidrug resistance.
In the 27 patients with chronic leukemia (CLL and GLPD), mdr1 and mdr3 P-gp expression did not correlate to exposure to precytotoxic agents, nor did mdr1 P-gp expression correlate to mdr3 P-gp expression.
We performed immunocytochemistry to detect mdr1 and mdr3 P-glycoproteins (P-gps) in 81 patients with acute and chronic leukemia, using the mdr1 P-gp-specific monoclonal antibody (MoAb) MRK16, and the mdr3 P-gp-specific MDR3M.
|Human||NPM1||4869||nucleophosmin (nucleolar phosphoprotein B23, numatrin)|
Fusion tyrosine kinases (FTKs) such as BCR/ABL, TEL/ABL, TEL/JAK2, TEL/PDGF beta R, TEL/TRKC(L), and NPM/ALK arise from reciprocal chromosomal translocations and cause acute and chronic leukemias and non-Hodgkin;s lymphoma.
The clinical spectrum of normocytic hypoplastic anemia, leukocytosis, thrombocytopenia, and abnormal blood cell forms led to diagnoses of congenital infection, myelodysplastic syndromes, or chronic leukemia in these patients before recognition of mevalonate kinase deficiency.
In addition to containing the gag, pol, and env genes of the chronic leukemia viruses, the genome of HTLV-I contains a long open reading frame (LOR) located between the 3; end of the envelope gene and the 3; long terminal repeat sequence (LTR).
|Human||JAK2||3717||Janus kinase 2|
Fusion tyrosine kinases (FTKs) such as BCR/ABL, TEL/ABL, TEL/JAK2, TEL/PDGF beta R, TEL/TRKC(L), and NPM/ALK arise from reciprocal chromosomal translocations and cause acute and chronic leukemias and non-Hodgkins lymphoma.
Curcumin treatment inhibited Jak2 mRNA expression in K562 chronic leukaemia cells
To gain insights into the patterns of activation of this gene during hematopoietic differentiation, we have examined HOXA10 expression in CD34+ and CD34- subfractions of normal marrow and normal peripheral blood, as well as samples from patients with a variety of acute and chronic leukemias.
|Human||GATA1||2623||GATA binding protein 1 (globin transcription factor 1)|
findings suggest that GATA1 mutations are not frequent occurrences in the evolution of blast crisis from chronic myeloid leukaemia chronic phase
|Human||FLT3||2322||fms-related tyrosine kinase 3|
Identified FLT3 internal tandem duplication mutations in a subset of human chronic myelonomocytic leukemia
Curcumin treatment inhibited cyclin D1 mRNA expression in K562 chronic leukaemia cells
APOE genotype influences chronic lymhocytic leukemia outcome and response to therapy, it does not alter susceptibility to developing this disease