Academic literature on the topic 'KIT proto-oncogene'
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Journal articles on the topic "KIT proto-oncogene"
Ikeda, H., Y. Kanakura, T. Tamaki, A. Kuriu, H. Kitayama, J. Ishikawa, Y. Kanayama, T. Yonezawa, S. Tarui, and JD Griffin. "Expression and functional role of the proto-oncogene c-kit in acute myeloblastic leukemia cells." Blood 78, no. 11 (December 1, 1991): 2962–68. http://dx.doi.org/10.1182/blood.v78.11.2962.2962.
Full textIkeda, H., Y. Kanakura, T. Tamaki, A. Kuriu, H. Kitayama, J. Ishikawa, Y. Kanayama, T. Yonezawa, S. Tarui, and JD Griffin. "Expression and functional role of the proto-oncogene c-kit in acute myeloblastic leukemia cells." Blood 78, no. 11 (December 1, 1991): 2962–68. http://dx.doi.org/10.1182/blood.v78.11.2962.bloodjournal78112962.
Full textTakayuki, Kubota, Hikono Hirokazu, Sasaki Erika, and Sakurai Michiharu. "Sequence of a bovine c-kit proto-oncogene cDNA." Gene 141, no. 2 (April 1994): 305–6. http://dx.doi.org/10.1016/0378-1119(94)90592-4.
Full textVučićević, Ivana, Darko Marinković, Vladimir Kukolj, Miloš Vučićević, Milorad Mirilović, Slađan Nešić, and Sanja Aleksić-Kovačević. "Kit Receptor Expression in Canine Cutaneous Mast Cell Tumors (CMCTs) Without C-Kit Mutation." Acta Veterinaria 66, no. 2 (June 1, 2016): 222–33. http://dx.doi.org/10.1515/acve-2016-0019.
Full textGraphodatsky, Alexander S., Anna V. Kukekova, Dmitry V. Yudkin, Vladimir A. Trifonov, Nadezhda V. Vorobieva, Violetta R. Beklemisheva, Polina L. Perelman, et al. "The proto-oncogene C-KIT maps to canid B-chromosomes." Chromosome Research 13, no. 2 (February 2005): 113–22. http://dx.doi.org/10.1007/s10577-005-7474-9.
Full textYared, Marwan A., Lavinia P. Middleton, Funda Meric Bernstam, Massimo Cristofanilli, and Aysegul A. Sahin. "Expression of c-kit Proto-Oncogene Product in Breast Tissue." Breast Journal 10, no. 4 (July 2004): 323–27. http://dx.doi.org/10.1111/j.1075-122x.2004.21351.x.
Full textSyrris, Petros, Kirsten Heathcote, Romeo Carrozzo, Koen Devriendt, Nursel Elçioglu, Christine Garrett, Meriel McEntagart, and Nicholas D. Carter. "Human piebaldism: six novel mutations of the proto-oncogene KIT." Human Mutation 20, no. 3 (August 21, 2002): 234. http://dx.doi.org/10.1002/humu.9057.
Full textErika, Sasaki, Okamura Hiroshi, Chikamune Tateki, Kanai Yukio, Watanabe Miho, Naito Mitsuru, and Sakurai Michiharu. "Cloning and expression of the chicken c-kit proto-oncogene." Gene 128, no. 2 (June 1993): 257–61. http://dx.doi.org/10.1016/0378-1119(93)90571-j.
Full textWilliams, Douglas E., June Eisenman, Allison Baird, Charles Rauch, Kirk Van Ness, Carl J. March, Linda S. Park, et al. "Identification of a ligand for the c-kit proto-oncogene." Cell 63, no. 1 (October 1990): 167–74. http://dx.doi.org/10.1016/0092-8674(90)90297-r.
Full textCatlett, JP, JA Leftwich, EH Westin, S. Grant, and TF Huff. "c-kit expression by CD34+ bone marrow progenitors and inhibition of response to recombinant human interleukin-3 following exposure to c-kit antisense oligonucleotides." Blood 78, no. 12 (December 15, 1991): 3186–91. http://dx.doi.org/10.1182/blood.v78.12.3186.bloodjournal78123186.
Full textDissertations / Theses on the topic "KIT proto-oncogene"
Qiu, Fei-Hua. "Proto-oncogene c-kit : structure and relationship to the transmembrane receptor kinases /." Access full-text from WCMC, 1989. http://proquest.umi.com/pqdweb?did=744572251&sid=1&Fmt=2&clientId=8424&RQT=309&VName=PQD.
Full textGari, Mamdooh Abdullah Mahmoud. "Pathogenesis of c-kit proto-oncogene mutations in acute and chronic myeloproliferative disorders." Thesis, University of Sheffield, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.341830.
Full textWang, Hong. "The proto-oncogene c-Kit inhibits tumor growth by behaving as a dependence receptor." Thesis, Lyon, 2018. http://www.theses.fr/2018LYSE1172/document.
Full textC-Kit has been generally considered as a receptor tyrosine kinase and a proto-oncogene, whose upregulation and mutation lead to tumor progression through its kinase activity. Clinically, drugs targeting the kinase activity of c-Kit, such as Imatinib (Gleevec), have been wildly used to treat patients with c-Kit related diseases. While the role of c-Kit as a proto-oncogene is of no doubt, some research reports and database analysis do not fit well the tumor promoting role of c-Kit, indicating a possible different role of c-Kit in cancer. Here, we show that c-Kit belongs to the dependence receptor family, similarly to other receptor tyrosine kinases such as MET, RET and TrkC. In the absent of its ligand SCF (stem cell factor), instead of staying inactive, c-Kit triggers apoptosis, which can be enhanced by silencing its kinase activity. Besides, we have shown that c-Kit is able to bind and activate caspase-9. Moreover, similarly to other dependence receptors, c-Kit is also cleaved by caspases-like protease at aspartic acid residue D816, which is crucial for its pro-apoptotic activity. The mutation of D816 site inhibits the c-Kit/caspase-9 binding and silences the pro-apoptotic activity of c-Kit. Of interest, c-Kit D816 mutation is one of the most common mutation of this receptor in many c-Kit related cancers and it promotes resistance against Gleevec treatment. We also show that overexpression of kinase mutated c-Kit is able to inhibit tumor growth in animal models, while the mutation of D816 site impairs the tumor suppressing activity. Furthermore, we develop a tool to block the SCF/c-Kit interaction, which unleashes the pro-apoptotic activity of c-Kit in cancers expressing this receptor. By using the pro-apoptotic activity of c-Kit, in combination with kinase inhibitors like Gleevec, we propose a novel therapeutic strategy. In conclusion, we demonstrate that c-Kit is a member of dependence receptor family, harboring intrinsic pro-apoptotic activity, which can be used as an alternative tool in cancer treatment
Chui, Chung-hin, and 徐宗憲. "Molecular characterization of C-KIT proto-oncogene in Hong Kong leukemia patients: 'culprit or bystander'." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1998. http://hub.hku.hk/bib/B31236790.
Full textChui, Chung-hin. "Molecular characterization of C-KIT proto-oncogene in Hong Kong leukemia patients : 'culprit or bystander' /." Hong Kong : University of Hong Kong, 1998. http://sunzi.lib.hku.hk/hkuto/record.jsp?B1947037X.
Full textEstrozi, Bruna. "Avaliação anatomoclínica e molecular do melanoma cutâneo em pacientes jovens (idade 18-30 anos)." Universidade de São Paulo, 2015. http://www.teses.usp.br/teses/disponiveis/5/5144/tde-01042015-144721/.
Full textThe incidence of cutaneous melanoma in young adults has dramatically increased in recent years. However, there is scarce data about the clinicopathological and molecular characteristics on the melanomas occurring at this age group. The present study aimed to evaluate 132 patients aged between 18 and 30 years with primary cutaneous melanoma with emphasis on the study of clinical, histopathological characteristics and molecular evaluation of mutations in BRAF, NRAS and KIT genes. Regarding the clinical and histopathological findings, the following results were found: female predominance (61.4%), trunk was the most commonly anatomical site involved (44.3%) and superficial spreading melanoma, was the most common histological type (79.5 %). The V600E mutation in BRAF (BRAFV600E) gene was analyzed in 93 cases, using RT-PCR. It was present in 38.7% (36/93) and statistically related to the vertical growth phase (p = 0.01), mild inflammatory infiltration (p = 0.02) and the presence of intradermal mitosis (p = 0.004). There was, also, strongly evidence of an association with the presence of ulceration (p = 0.05). Worse prognosis was associated with these variables. There was a predominance of BRAFV600E mutation in anatomical regions related to intermittent sun exposure. No cases of melanoma with BRAFV600E mutation showed regression phenomenon (p < 0.05). There was no significant association between BRAFV600E and gender, histological type, Clark level, Breslow thickness, solar elastosis, angiolymphatic and perineural invasion, sattelitosis, coexisting melanocytic nevus and survival. The presence of a mutation in NRAS, by RT-PCR was seen in 3.95% (3/76) of the cases. All these three mutations were of type 61K, occurred in male patients and the head and neck region. BRAFV600E and NRAS mutations, when present, were mutually exclusive. The frequency of KIT mutations, analyzed by sequencing, was 11.1% (3/27). The three mutations identified in this gene were located in exon 9 (G510, G498S and 489I). Concomitant mutations were found between KIT and NRAS and BRAFV600E. Due to the small number of KIT and NRAS mutated cases, it was not possible to establish clinical and histopathological correlations and mutation status in these genes. This study was the first to describe the G510D and G498S mutations in KIT gene in cutaneous melanomas. In the present study, BRAFV600E mutation in cutaneous melanoma of young adults correlated with anatomic and clinical features of worse prognosis compared to wild type
Hagger, Robert William. "Chronic idiopathic constipation : role of colonic motor activity interstital cells of cajal and the c-kit proto-oncogene." Thesis, St George's, University of London, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.404569.
Full textMendonça, Ullyanov Bezerra Toscano de. "Análise de mutações do gene KIT em pacientes com melanoma de mucosa de cabeça e pescoço e relação clínica retrospectiva." Universidade de São Paulo, 2015. http://www.teses.usp.br/teses/disponiveis/5/5132/tde-14122015-114016/.
Full textUnlike their cutaneous counterparts, head and neck mucosal malignant melanomas (HNMM) behave much more aggressively and their prognostic markers have not been fully elucidated. In recent studies, some molecular pathways have been found to be involved in the pathogenesis of melanomas. Among these, there is a proliferative MAPK pathway (\"Mitogen Activated Protein Kinase\"). This signaling pathway is involved in controlling cell growth, proliferation and migration, with a role in the development and progression of melanoma. In addition, KIT gene mutation has been identified in melanomas, indicating that there may be potential therapeutic benefits of tyrosine kinase inhibitors. Objectives: Evaluation of KIT mutation prevalence in a subset of 28 patients with HNMM treated at a single institution, establishing the relationship between different mutations and outcome (DFS and OS). The primary end-point of the study was to define the incidence of KIT mutations in HNMM, including the relationship between KIT mutations with disease-free survival (DFS) and overall survival (OS) in HNMM. Secondary end-points were correlation among therapeutic options, histopathological findings, demographic data and clinical response. Methods: This retrospective study comprised data of 28 patients with HNMM treated at Brazilian National Cancer Institute (INCA) between 2000 and 2011. Clinical analysis included patients characteristics, staging, primary and palliative treatments, disease free survival and overall survival. Progression-free survival and overall survival were analyzed using the Kaplan-Meier method, with SPS 11.0 software. KIT analysis: paraffin blocks were selected following analyses of histologic preparations, enabling DNA extraction. Different DNA concentrations were employed in PCR amplifications, based on DNA integrity. PCR amplification of exon, 9, 11, 13 and 17 was performed. . Results: Patients were predominantly females (57%). The age of presentation ranged from 27 to 85 years. The sinonasal region was the most frequent primary site (75%). All patients underwent surgical resection. Seventeen patients received adjuvant radiotherapy (37%). Recurrences occurred in 82% patients. Oncologic mutations in KIT were found in 7 (25%) of seven tumors, 3 in exon 9, 3 in exon 11 and 1 in exon 13. Predictive factors for recurrence were mitotic rate (p=0.05), vascular invasion (p=0.043), and perineural spread (p=0.034). There were no significant differences in DFS and OS according to KIT mutation. Conclusion: HNMM remains a rare disease. The present single-institution series includes 28 cases treated in single institution. Seven cases (25%) had activating KIT mutations, which is an increased prevalence of activating KIT mutations in this specific subset of mucosal melanomas. This finding suggests that there is a group of patients who might benefit with appropriate targeted therapy with kinase inhibitors
Zhang, Qiangnu [Verfasser], and Stephanie [Akademischer Betreuer] Rössler. "FUNCTIONAL ANALYSIS OF PROTO-ONCOGENE c-KIT IN THE DEVELOPMENT AND PROGRESSION OF HEPATOCELLULAR CARCINOMA / Qiangnu Zhang ; Betreuer: Stephanie Rössler." Heidelberg : Universitätsbibliothek Heidelberg, 2019. http://d-nb.info/1193347270/34.
Full textShahidian, Lara Zorro. "Characterization of in vitro models for the study of candidate G-quadruplex ligands targeting the human c-KIT proto-oncogene promoter." Master's thesis, Universidade de Lisboa. Faculdade de Medicina Veterinária, 2013. http://hdl.handle.net/10400.5/6216.
Full textProto-oncogene c-KIT has been implicated in the development and growth of several tumors, e.g. mast cell tumors (MCT) in dogs and gastrointestinal stromal tumors (GIST) in humans. Several therapeutic approaches directed to the blocking of receptor tyrosine kinases (RTK), such as c-KIT, have been created. However, after a short period of recovery, these drugs lose efficiency and the tumor relapses. A new approach, aiming to control c-KIT’s transcription, is being tested. This approach relies on the use of small molecule inhibitors (SMI) that specifically block DNA secondary structures, G-quadruplexes, located on the promoter regions of many proto-oncogenes, including c-KIT. The main goal of this work is the development of in vitro models through which the study of candidate SMIs for human c-KIT is possible. An in vitro model, composed by cytotoxicity tests aimed for the determination of the SMI’s inhibitory concentration 50 (IC50) on two human cell lines and by real time quantitative PCR (qPCR) for the study of gene expression alterations, has been developed and validated. The cytotoxicity tests were also used to identify the IC50 of three candidate ligands for c-KIT.
RESUMO - Caracterização de modelos in vitro para o estudo de possíveis ligandos de G-quadruplex dirigidos à região promotora do proto-oncogene c-KIT no Homem - O proto-oncogene c-KIT tem sido relacionado com o desenvolvimento e crescimento de vários tumores, incluindo mastocitomas em cães e tumores do estroma gastrointestinal no Homem. Várias abordagens terapêuticas têm vindo a ser desenvolvidas tendo como objetivo bloquear os recetores de tirosina quinase, tais como c-KIT. No entanto, após um curto período de recuperação, estes fármacos perdem eficácia e o tumor reaparece. Está a ser testada uma nova abordagem, que visa controlar a transcrição de c-KIT. Esta abordagem recorre ao uso de pequenas moléculas inibidoras que bloqueiam, de forma específica, estruturas secundárias de ADN, G-quadruplex, localizadas na região promotora de vários proto-oncogenes, incluindo c- KIT. O principal objetivo deste trabalho é o desenvolvimento de modelos in vitro que possam ser utilizados para estudar possíveis moléculas inibidoras para o c-KIT humano. Assim foi desenvolvido e validado um modelo in vitro, composto por testes de citotoxicidade, que visam determinar a concentração inibitória 50 dos ligandos, em duas linhas celulares humanas, e por métodos de PCR quantitativo em tempo real, para o estudo das alterações na expressão génica. Os testes de citotoxicidade foram também utilizados para identificar a concentração inibitória 50 de três possíveis ligandos para c-KIT.
Book chapters on the topic "KIT proto-oncogene"
McCulloch, E. A., and M. D. Minden. "The cell surface receptor encoded by the proto-oncogene KIT and its ligand." In Leukemia: Advances in Research and Treatment, 45–77. Boston, MA: Springer US, 1993. http://dx.doi.org/10.1007/978-1-4615-3086-2_4.
Full textConference papers on the topic "KIT proto-oncogene"
Sanchez Calle, Anna, Kenta Hoshikawa, Neha Nair, Marta Prieto-Vila, Arun Vaidyanath, Tomonari Kasai, and Masaharu Seno. "Abstract 1725: The significance of c-Kit proto-oncogene in iCSC-derived PDAC model." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-1725.
Full textSissi, Claudia, Silvia Da Ros, Eleonora Zorzan, Caterina Musetti, Lara Zorro Shahidian, Manlio Palumbo, Mery Giantin, and Mauro Dacasto. "Abstract 4551: Impairment of c-kit expression in human cancer cell lines by a novel pharmacophoric unit selected for the recognition of the proto-oncogene KIT promotorial region." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-4551.
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