Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0079731 (B-cell lymphoma)
 16,671 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We analysed the subcellular distribution of p210(BCR-ABL) protein using a junction-specific anti-BCR-ABL monoclonal antibody and confocal laser scanning microscopy (CLSM). Our studies have shown that p210(BCR-ABL) is arranged in discrete foci in the cytoplasm of cell lines and primary CD34(+) cells but not mononuclear cells suggesting the foci may be a feature of immature chronic myeloid leukaemia cells. We have devised a strategy to score the foci and found the mean number of foci varies between the cell types. The number of foci per cell is directly related to the level of p210(BCR-ABL) expression. CLSM was also used to analyse the distribution and colocalization of CT10 regulator-like (CRKL) p210(BCR-ABL). CRKL-p210(BCR-ABL) foci were completely or partially associated, touching or separate in different regions of the same cell. We also analysed the distribution of phosphorylated CRKL (pCRKL) with p210(BCR-ABL) and unexpectedly found only a small proportion of pCRKL in complex with p210(BCR-ABL). The foci distribution and high levels of uncomplexed p210(BCR-ABL), pCRKL and CRKL protein suggested the possibility of a dynamic equilibrium. Imatinib promoted nuclear transport of p210(BCR-ABL)-positive foci. It also disrupted complex formation between p210(BCR-ABL) and casitas B-cell lymphoma and CRKL but not between p210(BCR-ABL) and GRB2. Our observations of the CRKL and p210(BCR-ABL) complex may be important for understanding the function of CRKL.
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PMID:Subcellular distribution of p210(BCR-ABL) in CML cell lines and primary CD34+ CML cells. 1805 81

The v-Crk avian sarcoma virus CT10 oncogene homolog-like (CRKL) protein is important in cancer progression. However, its expression pattern and biological roles in human endometrial carcinoma remain unexplored. The potential mechanism of CRKL-induced cancer progression is still unclear. The present study aimed to explore the expression pattern and biological roles of CRKL in human endometrial carcinoma. Using immunohistochemistry, it was observed that the CRKL protein was overexpressed in 50.5% (44/87) of endometrial carcinoma tissues. Plasmid transfection of CRKL into Ishikawa cells was performed, and CRKL overexpression promoted cell proliferation, colony formation and cell cycle transition in the transfected cells. In addition, CRKL overexpression inhibited cell apoptosis in Ishikawa cells treated with cisplatin, with decreased caspase-3 and caspase-9 cleavage. Further analysis revealed that CRKL upregulated the expression of cyclin D1, cyclin E, B cell lymphoma (Bcl)-2 and survivin, and downregulated Bcl-2 associated X protein expression. In conclusion, the present study demonstrated that CRKL overexpression in endometrial carcinoma contributes to malignant cell growth and resistance to apoptosis, possibly through Bcl-2.
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PMID:CRKL overexpression promotes cell proliferation and inhibits apoptosis in endometrial carcinoma. 2812 21