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Your search keyword '"Receptor Protein-Tyrosine Kinase"' showing total 3 results
Start Over Descriptor "Receptor Protein-Tyrosine Kinase" Publisher elsevier
3 results on '"Receptor Protein-Tyrosine Kinase"'

1. Anti-angiogenic agents for the treatment of solid tumors: Potential pathways, therapy and current strategies – A review

Author

Ahmed M. Al-Abd, Abdulmohsin J. Alamoudi, Ashraf B. Abdel-Naim, Thikryat A. Neamatallah, and Osama M. Ashour

Subjects
Angiogenesis inhibitors, Receptor protein-tyrosine kinase, Tumor microenvironment, Natural products, Medicine (General), R5-920, Science (General), Q1-390
Abstract

Recent strategies for the treatment of cancer, other than just tumor cell killing have been under intensive development, such as anti-angiogenic therapeutic approach. Angiogenesis inhibition is an important strategy for the treatment of solid tumors, which basically depends on cutting off the blood supply to tumor micro-regions, resulting in pan-hypoxia and pan-necrosis within solid tumor tissues. The differential activation of angiogenesis between normal and tumor tissues makes this process an attractive strategic target for anti-tumor drug discovery. The principles of anti-angiogenic treatment for solid tumors were originally proposed in 1972, and ever since, it has become a putative target for therapies directed against solid tumors. In the early twenty first century, the FDA approved anti-angiogenic drugs, such as bevacizumab and sorafenib for the treatment of several solid tumors. Over the past two decades, researches have continued to improve the performance of anti-angiogenic drugs, describe their drug interaction potential, and uncover possible reasons for potential treatment resistance. Herein, we present an update to the pre-clinical and clinical situations of anti-angiogenic agents and discuss the most recent trends in this field.

Published
2017
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2. Titin antibodies in 'seronegative' myasthenia gravis - A new role for an old antigen

Author

Stergiou, C., Lazaridis, K., Zouvelou, V., Tzartos, J., Mantegazza, R., Antozzi, C., Andreetta, F., Evoli Stampanoni-B, Amelia, Deymeer, F., Saruhan Direskeneli, G., Durmus, H., Brenner, T., Vaknin, A., Berrih Aknin, S., Behin, A., Sharshar, T., De Baets, M., Losen, M., Martinez Martinez, P., Kleopa, K. A., Zamba Papanicolaou, E., Kyriakides, T., Kostera Pruszczyk, A., Szczudlik, P., Szyluk, B., Lavrnic, D., Basta, I., Peric, S., Tallaksen, C., Maniaol, A., Gilhus, N. E., Casasnovas Pons, C., Pitha, J., Jakubíkova, M., Hanisch, F., Bogomolovas, J., Labeit, D., Labeit, S., Tzartos, S. J., Evoli, Amelia (ORCID:0000-0003-0282-8787), Stergiou, C., Lazaridis, K., Zouvelou, V., Tzartos, J., Mantegazza, R., Antozzi, C., Andreetta, F., Evoli Stampanoni-B, Amelia, Deymeer, F., Saruhan Direskeneli, G., Durmus, H., Brenner, T., Vaknin, A., Berrih Aknin, S., Behin, A., Sharshar, T., De Baets, M., Losen, M., Martinez Martinez, P., Kleopa, K. A., Zamba Papanicolaou, E., Kyriakides, T., Kostera Pruszczyk, A., Szczudlik, P., Szyluk, B., Lavrnic, D., Basta, I., Peric, S., Tallaksen, C., Maniaol, A., Gilhus, N. E., Casasnovas Pons, C., Pitha, J., Jakubíkova, M., Hanisch, F., Bogomolovas, J., Labeit, D., Labeit, S., Tzartos, S. J., and Evoli, Amelia (ORCID:0000-0003-0282-8787)

Abstract

Myasthenia gravis (MG) is an autoimmune disease caused by antibodies targeting the neuromuscular junction of skeletal muscles. Triple-seronegative MG (tSN-MG, without detectable AChR, MuSK and LRP4 antibodies), which accounts for ~ 10% of MG patients, presents a serious gap in MG diagnosis and complicates differential diagnosis of similar disorders. Several AChR antibody positive patients (AChR-MG) also have antibodies against titin, usually detected by ELISA. We have developed a very sensitive radioimmunoprecipitation assay (RIPA) for titin antibodies, by which many previously negative samples were found positive, including several from tSN-MG patients. The validity of the RIPA results was confirmed by western blots. Using this RIPA we screened 667 MG sera from 13 countries; as expected, AChR-MG patients had the highest frequency of titin antibodies (40.9%), while MuSK-MG and LRP4-MG patients were positive in 14.6% and 16.4% respectively. Most importantly, 13.4% (50/372) of the tSN-MG patients were also titin antibody positive. None of the 121 healthy controls or the 90 myopathy patients, and only 3.6% (7/193) of other neurological disease patients were positive. We thus propose that the present titin antibody RIPA is a useful tool for serological MG diagnosis of tSN patients.

Published
2016

3. Longitudinal epitope mapping in MuSK myasthenia gravis: Implications for disease severity

Author

Huijbers, Maartje G., Vink, Anna Fleur D., Niks, Erik H., Westhuis, Ruben H., van Zwet, Erik W., de Meel, Robert H., Rojas García, Ricardo, Díaz Manera, Jordi, Kuks, Jan B., Klooster, Rinse, Straasheijm, Kirsten, Evoli Stampanoni-B, Amelia, Illa, Isabel, van der Maarel, Silvère M., Verschuuren, Jan J., Evoli, Amelia (ORCID:0000-0003-0282-8787), Huijbers, Maartje G., Vink, Anna Fleur D., Niks, Erik H., Westhuis, Ruben H., van Zwet, Erik W., de Meel, Robert H., Rojas García, Ricardo, Díaz Manera, Jordi, Kuks, Jan B., Klooster, Rinse, Straasheijm, Kirsten, Evoli Stampanoni-B, Amelia, Illa, Isabel, van der Maarel, Silvère M., Verschuuren, Jan J., and Evoli, Amelia (ORCID:0000-0003-0282-8787)

Abstract

Muscle weakness in MuSK myasthenia gravis (MG) is caused predominantly by IgG4 antibodies which block MuSK signalling and destabilize neuromuscular junctions. We determined whether the binding pattern of MuSK IgG4 antibodies change throughout the disease course ("epitope spreading"), and affect disease severity or treatment responsiveness.We mapped the MuSK epitopes of 255 longitudinal serum samples of 53 unique MuSK MG patients from three independent cohorts with ELISA.Antibodies against the MuSK Iglike-1 domain determine disease severity. Epitope spreading outside this domain did not contribute to disease severity nor to pyridostigmine responsiveness. This provides a rationale for epitope specific treatment strategies.

Published
2016

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