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Статті в журналах з теми "KIT proto-oncogene"

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Автор: Grafiati

Опубліковано: 10 грудня 2022

Оновлено: 28 січня 2023

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1

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.

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Анотація:

Abstract The c-kit proto-oncogene encodes a receptor tyrosine kinase that is thought to play an important role in hematopoiesis. In a series of human acute myeloblastic leukemia (AML), the expression of the c-kit proto-oncogene and its product was studied by means of Northern blot and immunoblot analyses. The c-kit mRNA was expressed in 20 of 25 cases of AML, and in those cases the product of the c-kit proto-oncogene was detected by immunoblotting with anti-c-kit antibody. The expression of c-kit transcripts and protein was barely detectable in normal bone marrow cells as a control. The expression of c-kit transcript did not correlate with the French-American-British classification nor clinical manifestations. In 6 of 11 cases that expressed c-kit product, AML cells were found to proliferate in response to recombinant human stem cell factor (rhSCF), the ligand for c-kit, and the synergistic stimulation of AML cells was observed by rhSCF and granulocyte- macrophage colony-stimulating factor. Immunoblotting with anti- phosphotyrosine antibody showed that the c-kit receptor protein was detectably phosphorylated in 7 of 12 cases tested before the stimulation with rhSCF, while the rhSCF treatment resulted in an increased tyrosine phosphorylation of c-kit in AML cells. These results indicate that c-kit proto-oncogene is expressed in most cases of AML and is functional in terms of supporting proliferation.

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2

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.bloodjournal78112962.

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Анотація:

The c-kit proto-oncogene encodes a receptor tyrosine kinase that is thought to play an important role in hematopoiesis. In a series of human acute myeloblastic leukemia (AML), the expression of the c-kit proto-oncogene and its product was studied by means of Northern blot and immunoblot analyses. The c-kit mRNA was expressed in 20 of 25 cases of AML, and in those cases the product of the c-kit proto-oncogene was detected by immunoblotting with anti-c-kit antibody. The expression of c-kit transcripts and protein was barely detectable in normal bone marrow cells as a control. The expression of c-kit transcript did not correlate with the French-American-British classification nor clinical manifestations. In 6 of 11 cases that expressed c-kit product, AML cells were found to proliferate in response to recombinant human stem cell factor (rhSCF), the ligand for c-kit, and the synergistic stimulation of AML cells was observed by rhSCF and granulocyte- macrophage colony-stimulating factor. Immunoblotting with anti- phosphotyrosine antibody showed that the c-kit receptor protein was detectably phosphorylated in 7 of 12 cases tested before the stimulation with rhSCF, while the rhSCF treatment resulted in an increased tyrosine phosphorylation of c-kit in AML cells. These results indicate that c-kit proto-oncogene is expressed in most cases of AML and is functional in terms of supporting proliferation.

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3

Takayuki, 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.

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4

Vučićević, 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.

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Abstract Histopathological examination, grading, immunohistochemical staining and molecular genetic examinations are the proposed criteria that should be used for cutaneous mast cell tumors (CMCTs) classification. The presence of aberrant CD117 expression and mutations of the c-kit proto-oncogene could be an indicative parameter for final histological grading. Determination of the connection between the localization of KIT receptor expression and the histological grade of CMCTs without c-kit proto-oncogene mutations was the main goal of this study. The study included twenty four CMCTs and six control skin samples from 30 dogs of different ages, breed and sex. Formalinfixed and paraffin-embedded tissue samples were stained with hematoxylin-eosin and toluidine blue and immunohistochemically tested for CD117 expression. DNA was extracted from the same paraffin blocks and subsequent polymerase chain reaction amplification was performed using PE1 and PE2 primers. Degree of malignancy was determined based on the presence of mitotic figures, multinucleated cells, bizarre nuclei and karyomegaly in 10 high power fields. Based on histological features, fourteen of 24 CMCTs were of a high histological grade, while ten were classified as a lowgrade malignancy. CD117 cytoplasmic expression was observed in nine of fourteen high-grade malignancy CMCTs, which confirms the link between the aberrant CD117 expression and increased cell proliferation.

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5

Graphodatsky, 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.

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6

Yared, 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.

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7

Syrris, 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.

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8

Erika, 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.

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9

Williams, 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.

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10

Catlett, 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.

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Анотація:

The c-kit proto-oncogene encodes a receptor having tyrosine-specific kinase activity and has been mapped to chromosome 4 in the human and chromosome 5 in the mouse, at the dominant white spotting locus (W). Mutations at the W locus affect various aspects of murine hematopoiesis. The c-kit proto-oncogene has been shown to be expressed by leukemic myeloblasts, but not by normal unseparated human bone marrow cells. The role of this oncogene in differentiation and proliferation of human hematopoietic progenitors is presently undefined. To determine c-kit expression by normal hematopoietic progenitors, CD34+ cells were isolated from disease-free human bone marrow, and RNA-based polymerase chain reaction (PCR) techniques were used to assess expression. By this method, we have demonstrated c-kit expression by CD34+ bone marrow progenitors. To address the functional requirement for c-kit expression in normal human hematopoiesis, CD34+ cells were incubated in the presence of sense, antisense, or missense oligonucleotides to c-kit, and subsequently cultured in the presence of either recombinant human granulocyte-macrophage colony-stimulating factor (rhGM-CSF) or recombinant human interleukin-3 (rhIL-3). Exposure of CD34+ cells to c-kit antisense oligonucleotides significantly inhibited colony-forming ability of cells cultured in the presence of rhIL-3, but had no effect on colony formation of cells cultured in rhGM- CSF. Together, these data suggest a possible role for c-kit in hematopoietic proliferation and differentiation that may be linked to some, but not all, stimulatory factors.

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11

Catlett, 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.v78.12.3186.3186.

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Анотація:

Abstract The c-kit proto-oncogene encodes a receptor having tyrosine-specific kinase activity and has been mapped to chromosome 4 in the human and chromosome 5 in the mouse, at the dominant white spotting locus (W). Mutations at the W locus affect various aspects of murine hematopoiesis. The c-kit proto-oncogene has been shown to be expressed by leukemic myeloblasts, but not by normal unseparated human bone marrow cells. The role of this oncogene in differentiation and proliferation of human hematopoietic progenitors is presently undefined. To determine c-kit expression by normal hematopoietic progenitors, CD34+ cells were isolated from disease-free human bone marrow, and RNA-based polymerase chain reaction (PCR) techniques were used to assess expression. By this method, we have demonstrated c-kit expression by CD34+ bone marrow progenitors. To address the functional requirement for c-kit expression in normal human hematopoiesis, CD34+ cells were incubated in the presence of sense, antisense, or missense oligonucleotides to c-kit, and subsequently cultured in the presence of either recombinant human granulocyte-macrophage colony-stimulating factor (rhGM-CSF) or recombinant human interleukin-3 (rhIL-3). Exposure of CD34+ cells to c-kit antisense oligonucleotides significantly inhibited colony-forming ability of cells cultured in the presence of rhIL-3, but had no effect on colony formation of cells cultured in rhGM- CSF. Together, these data suggest a possible role for c-kit in hematopoietic proliferation and differentiation that may be linked to some, but not all, stimulatory factors.

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12

Orr-Urtreger, A., A. Avivi, Y. Zimmer, D. Givol, Y. Yarden, and P. Lonai. "Developmental expression of c-kit, a proto-oncogene encoded by the W locus." Development 109, no. 4 (August 1, 1990): 911–23. http://dx.doi.org/10.1242/dev.109.4.911.

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Анотація:

Developmental expression of the c-kit proto-oncogene, a receptor tyrosine kinase encoded by the W locus, was investigated by in situ hybridization in normal mouse embryos. Early after implantation transcripts were detectable only in the maternal placenta (6 1/2-7 1/2 days p.c.). Subsequently (8 1/2 days p.c.) numerous ectodermal (neural tube, sensory placodes) and endodermal (embryonic gut) derivatives expressed c-kit. Later transcripts were detected also in the blood islands of the yolk sac and in the embryonic liver, the main sites of embryonic hemopoiesis. Around midgestation, transcripts accumulated in the branchial pouches and also in primordial germ cells of the genital ridges. This complex pattern of expression remained characteristic also later in gestation, when c-kit was expressed in highly differentiated structures of the craniofacial area, in presumptive melanoblasts and in the CNS. In the adult ovary, maternal c-kit transcripts were detected. They were present in the oocytes of both immature and mature ovarian follicles, but not in the male germ line, where c-kit expression may be down regulated. Thus, c-kit activity is complex and appears in multiple tissues including those that also display defects in mutations at the W locus where c-kit is encoded. Correlation between W phenotypes and c-kit expression, as well as the regulation of the complex and multiple expression of polypeptide growth factors and receptors, is discussed.

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13

Sillaber, C., H. Strobl, D. Bevec, L. K. Ashman, J. H. Butterfield, K. Lechner, D. Maurer, P. Bettelheim, and P. Valent. "IL-4 regulates c-kit proto-oncogene product expression in human mast and myeloid progenitor cells." Journal of Immunology 147, no. 12 (December 15, 1991): 4224–28. http://dx.doi.org/10.4049/jimmunol.147.12.4224.

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Abstract The c-kit proto-oncogene encodes the receptor for a novel hemopoietic cytokine, termed stem cell factor (SCF) or mast cell growth factor (MGF) according to its stimulating spectrum. The human receptor for SCF/MGF is expressed in a subset of normal bone marrow progenitor cells, in leukemic myeloid cells, and in mast cells. In the present study, the effects of recombinant human growth regulators (IL-1 through -9, granulocyte-macrophage/granulocyte/macrophage-CSF, IFN, and TNF) on c-kit proto-oncogene product expression were analyzed by indirect immunofluorescence, by using the anti-SCF/MGFR mAb YB5.B8, and Northern blot analyses, by using a c-kit oligonucleotide probe. Of all cytokines tested, IL-4 was found to down-regulate expression of YB5.B8 Ag in the human mast cell line HMC-1 (maximum inhibition, 51.05 +/- 16.36% mean fluorescence intensity of control; p less than 0.02), as well as in primary leukemic myeloid cells. IL-4 was also found to down-regulate expression of YB5.B8 Ag in normal enriched bone marrow progenitor cells. The effects of IL-4 on expression of YB8.B8 Ag in myeloid/mast cell progenitors was dose and time dependent (maximum effects observed on days 2 and/or 4, by using 50 U/ml of rIL-4) and could be neutralized by using anti-IL-4 mAb. Moreover, IL-4 was found to down-regulate expression of c-kit mRNA in leukemic myeloid cells as well as in HMC-1 cells. Together, these observations identify IL-4 as a regulator of c-kit proto-oncogene product expression in the human system. The effects of IL-4 on human hemopoietic progenitor cells and mast cells may be mediated in part through regulation of SCF/MGFR expression.

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14

FUKUDA, Ryo, Naoharu HAMAMOTO, Yasushi UCHIDA, Kohichiro FURUTA, Tomoko KATSUBE, Hideaki KAZUMORI, Shunji ISHIHARA, et al. "Gastrointestinal Stromal Tumor with a Novel Mutation of KIT Proto-oncogene." Internal Medicine 40, no. 4 (2001): 301–3. http://dx.doi.org/10.2169/internalmedicine.40.301.

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15

Eroğlu, Aydan, and Aliye Sari. "Expression of c-kit proto-oncogene product in breast cancer tissues." Medical Oncology 24, no. 2 (June 2007): 169–74. http://dx.doi.org/10.1007/bf02698036.

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16

Di Lorenzo, G., R. Autorino, F. P. D'Armiento, C. Mignogna, M. De Laurentiis, M. De Sio, M. D'Armiento, R. Damiano, G. Vecchio, and S. De Placido. "Expression of proto-oncogene c-kit in high risk prostate cancer." European Journal of Surgical Oncology (EJSO) 30, no. 9 (November 2004): 987–92. http://dx.doi.org/10.1016/j.ejso.2004.07.017.

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17

DILORENZO, G., R. AUTORINO, F. DARMIENTO, C. MIGNOGNA, M. DELAURENTIIS, M. DESIO, M. DARMIENTO, R. DAMIANO, G. VECCHIO, and S. DEPLACIDO. "Expression of proto-oncogene c-kit in high risk prostate cancer." European Journal of Surgical Oncology 30, no. 9 (November 2004): 987–92. http://dx.doi.org/10.1016/s0748-7983(04)00205-7.

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18

Yorke, Rebecca, Minnie Chirala, and Mamoun Younes. "c-Kit Proto-Oncogene Product Is Rarely Detected in Colorectal Adenocarcinoma." Journal of Clinical Oncology 21, no. 20 (October 15, 2003): 3885–86. http://dx.doi.org/10.1200/jco.2003.99.213.

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19

Yilmaz, Ercan, Onder Celik, Yavuz Simsek, Ilgin Turkcuoglu, Ebru Celik, Mehmet Gül, Seyma Hascalik, and Engin Aydin. "c-Kit proto-oncogene expression in endometrial hyperplasia and endometrial cancer." Archives of Gynecology and Obstetrics 286, no. 1 (March 6, 2012): 197–200. http://dx.doi.org/10.1007/s00404-012-2276-8.

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20

Ratajczak, Wariusz Z., Selina M. Luger, and Alan M. Gewirtz. "The c-kit proto-oncogene in normal and malignant human hematopoiesis." International Journal of Cell Cloning 10, no. 4 (1992): 205–14. http://dx.doi.org/10.1002/stem.5530100403.

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21

Lev, S., Y. Yarden, and D. Givol. "Receptor functions and ligand-dependent transforming potential of a chimeric kit proto-oncogene." Molecular and Cellular Biology 10, no. 11 (November 1990): 6064–68. http://dx.doi.org/10.1128/mcb.10.11.6064-6068.1990.

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Анотація:

The c-kit proto-oncogene, the cellular homolog of the transforming gene of a feline retrovirus, encodes a transmembrane tyrosine kinase homologous to receptors for growth factors. To study the cellular function of c-kit, we constructed a chimeric molecule composed of the extracellular portion of the receptor for epidermal growth factor (EGF) and the transmembrane and cytoplasmic domains of p145kit. The hybrid molecule was properly expressed in murine fibroblasts and displayed specific binding of EGF (Kd, 3 x 10(-8) M). Activation of the chimeric receptor by EGF stimulated the tyrosine kinase activity of kit and led to the generation of a potent mitogenic signal. Moreover, cells expressing the chimeric receptor acquired a transformed phenotype once they were stimulated with the heterologous ligand.

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22

Lev, S., Y. Yarden, and D. Givol. "Receptor functions and ligand-dependent transforming potential of a chimeric kit proto-oncogene." Molecular and Cellular Biology 10, no. 11 (November 1990): 6064–68. http://dx.doi.org/10.1128/mcb.10.11.6064.

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Анотація:

The c-kit proto-oncogene, the cellular homolog of the transforming gene of a feline retrovirus, encodes a transmembrane tyrosine kinase homologous to receptors for growth factors. To study the cellular function of c-kit, we constructed a chimeric molecule composed of the extracellular portion of the receptor for epidermal growth factor (EGF) and the transmembrane and cytoplasmic domains of p145kit. The hybrid molecule was properly expressed in murine fibroblasts and displayed specific binding of EGF (Kd, 3 x 10(-8) M). Activation of the chimeric receptor by EGF stimulated the tyrosine kinase activity of kit and led to the generation of a potent mitogenic signal. Moreover, cells expressing the chimeric receptor acquired a transformed phenotype once they were stimulated with the heterologous ligand.

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23

Yee, K., TR Bishop, C. Mather, and LI Zon. "Isolation of a novel receptor tyrosine kinase cDNA expressed by developing erythroid progenitors." Blood 82, no. 4 (August 15, 1993): 1335–43. http://dx.doi.org/10.1182/blood.v82.4.1335.1335.

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Abstract Activation of distinct receptor tyrosine kinases (RTK), such as the products of the c-fms and c-kit proto-oncogenes, profoundly affects hematopoietic development. We have isolated a novel RTK cDNA, called met-related kinase (MRK), which is expressed on early erythroid progenitors. MRK is also expressed in many hematopoietic cell lines, and is not lineage restricted. Several regions within the catalytic domain of MRK have amino acid similarity to the c-met proto-oncogene and v-sea oncogene. Specific polyclonal anti-MRK antisera detects an 84- Kd polypeptide in COS cells transfected with an expression vector containing the MRK cDNA. Further studies of this novel RTK will provide potential insight into its role during hematopoiesis.

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24

Yee, K., TR Bishop, C. Mather, and LI Zon. "Isolation of a novel receptor tyrosine kinase cDNA expressed by developing erythroid progenitors." Blood 82, no. 4 (August 15, 1993): 1335–43. http://dx.doi.org/10.1182/blood.v82.4.1335.bloodjournal8241335.

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Анотація:

Activation of distinct receptor tyrosine kinases (RTK), such as the products of the c-fms and c-kit proto-oncogenes, profoundly affects hematopoietic development. We have isolated a novel RTK cDNA, called met-related kinase (MRK), which is expressed on early erythroid progenitors. MRK is also expressed in many hematopoietic cell lines, and is not lineage restricted. Several regions within the catalytic domain of MRK have amino acid similarity to the c-met proto-oncogene and v-sea oncogene. Specific polyclonal anti-MRK antisera detects an 84- Kd polypeptide in COS cells transfected with an expression vector containing the MRK cDNA. Further studies of this novel RTK will provide potential insight into its role during hematopoiesis.

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25

Nagata, H., AS Worobec, T. Semere, and DD Metcalfe. "Elevated expression of the proto-oncogene c-kit in patients with mastocytosis." Leukemia 12, no. 2 (February 1998): 175–81. http://dx.doi.org/10.1038/sj.leu.2400906.

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26

Wang, Lina, Juan C. Felix, Joyce L. Lee, Peik Y. Tan, David E. Tourgeman, Anne T. O’Meara, and Charles A. Amezcua. "The proto-oncogene c-kit is expressed in leiomyosarcomas of the uterus." Gynecologic Oncology 90, no. 2 (August 2003): 402–6. http://dx.doi.org/10.1016/s0090-8258(03)00274-9.

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27

Izquierdo, Miguel A., Paul Van Der Valk, Jannette Van Ark-otte, Gonzalo Rubio, Jose R. Germa-Lluch, Ryuzo Ueda, Rik J. Scheper, Takashi Takahashi, and Giuseppe Giaccone. "Differential expression of the c-kit proto-oncogene in germ cell tumours." Journal of Pathology 177, no. 3 (November 1995): 253–58. http://dx.doi.org/10.1002/path.1711770307.

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28

Vigon, I., F. Dreyfus, J. Melle, F. Viguie, V. Ribrag, L. Cocault, M. Souyri, and S. Gisselbrecht. "Expression of the c-mpl proto-oncogene in human hematologic malignancies." Blood 82, no. 3 (August 1, 1993): 877–83. http://dx.doi.org/10.1182/blood.v82.3.877.877.

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Анотація:

Abstract Similar to two other hematopoietic growth factor receptors, the c-fms (macrophage colony-stimulating factor receptor) and the c-kit genes, c- mpl has been discovered through the study of oncogenic retroviruses. Unlike c-fms and c-kit, which both belong to a subgroup of tyrosine kinase receptors, the c-mpl proto-oncogene encodes a new member of the cytokine receptor superfamily. We have studied the expression of c-mpl in a series of 105 patients with hematologic malignancies using Northern blot analysis. The levels of c-mpl transcripts in lymphoid malignancies and in chronic myeloproliferative disorders were not significantly different from those found in normal bone marrow cells, in which c-mpl was barely detectable. In contrast, c-mpl expression was increased in 26 of 51 patients with acute myeloblastic leukemia (AML) and in 5 of 16 patients with myelodysplastic syndromes. Amplification of the c-mpl gene was detected in genomic DNA of one M4 AML patient. There was no significant correlation between c-mpl expression and the French-American-British classification of AML. Patients with high c-mpl expression appeared to belong to a subgroup of AML with a low rate of complete remission and a poor prognosis, including secondary leukemia and AML with unfavorable cytogenetic abnormalities.

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29

Vigon, I., F. Dreyfus, J. Melle, F. Viguie, V. Ribrag, L. Cocault, M. Souyri, and S. Gisselbrecht. "Expression of the c-mpl proto-oncogene in human hematologic malignancies." Blood 82, no. 3 (August 1, 1993): 877–83. http://dx.doi.org/10.1182/blood.v82.3.877.bloodjournal823877.

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Анотація:

Similar to two other hematopoietic growth factor receptors, the c-fms (macrophage colony-stimulating factor receptor) and the c-kit genes, c- mpl has been discovered through the study of oncogenic retroviruses. Unlike c-fms and c-kit, which both belong to a subgroup of tyrosine kinase receptors, the c-mpl proto-oncogene encodes a new member of the cytokine receptor superfamily. We have studied the expression of c-mpl in a series of 105 patients with hematologic malignancies using Northern blot analysis. The levels of c-mpl transcripts in lymphoid malignancies and in chronic myeloproliferative disorders were not significantly different from those found in normal bone marrow cells, in which c-mpl was barely detectable. In contrast, c-mpl expression was increased in 26 of 51 patients with acute myeloblastic leukemia (AML) and in 5 of 16 patients with myelodysplastic syndromes. Amplification of the c-mpl gene was detected in genomic DNA of one M4 AML patient. There was no significant correlation between c-mpl expression and the French-American-British classification of AML. Patients with high c-mpl expression appeared to belong to a subgroup of AML with a low rate of complete remission and a poor prognosis, including secondary leukemia and AML with unfavorable cytogenetic abnormalities.

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30

Ashman, LK, AC Cambareri, LB To, RJ Levinsky, and CA Juttner. "Expression of the YB5.B8 antigen (c-kit proto-oncogene product) in normal human bone marrow." Blood 78, no. 1 (July 1, 1991): 30–37. http://dx.doi.org/10.1182/blood.v78.1.30.30.

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Анотація:

Abstract The c-kit proto-oncogene product is a member of the family of growth factor receptors with intrinsic tyrosine kinase activity. In the mouse c-kit maps to the W locus, which is known to be of central importance in hematopoiesis. Monoclonal antibody (MoAb) YB5.B8, which was raised against peripheral blood blast cells from a patient with acute myeloid leukemia (AML), was recently shown to bind to the extracellular domain of the c-kit product. This antibody does not bind detectably to normal peripheral blood cells and identifies a sub-group of AML patients with poor prognosis. We have used MoAb YB5.B8 to study the expression of c- kit by normal human bone marrow cells by immunofluorescence and flow cytometry, and to isolate multipotential and erythroid colony-forming cells. In a series of 11 normal adult bone marrow specimens, MoAb YB5.B8 bound to 4.0% +/- 1.8% of the cells in the low-density fraction. Dual-labeling experiments were performed with YB5.B8, and CD33, CD34, and CD10 MoAbs. Three populations of cells binding YB5.B8 could be identified based on their pattern of coexpression of the other markers; ie, YB5.B8+/CD34+/CD33-, YB5.B8+/CD34+/CD33+ and YB5.B8+/CD34+/CD33+. These populations had distinctive two-dimensional light scatter characteristics and are likely to correspond to precursor colony- forming cells, colony-forming cells, and maturing mast cells, respectively. No cells binding both YB5.B8 and an MoAb to the early lymphoid marker CD10 were found, implying that most early lymphoid cells do not express c-kit. MoAbs to the c-kit protein should prove valuable in multimarker studies of human hematopoietic stem and progenitor cells. Definition of a reference range of c-kit expression in normal human bone marrow will provide a sound basis for further studies of this marker in diagnosis and prognosis in AML.

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31

Ashman, LK, AC Cambareri, LB To, RJ Levinsky, and CA Juttner. "Expression of the YB5.B8 antigen (c-kit proto-oncogene product) in normal human bone marrow." Blood 78, no. 1 (July 1, 1991): 30–37. http://dx.doi.org/10.1182/blood.v78.1.30.bloodjournal78130.

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Анотація:

The c-kit proto-oncogene product is a member of the family of growth factor receptors with intrinsic tyrosine kinase activity. In the mouse c-kit maps to the W locus, which is known to be of central importance in hematopoiesis. Monoclonal antibody (MoAb) YB5.B8, which was raised against peripheral blood blast cells from a patient with acute myeloid leukemia (AML), was recently shown to bind to the extracellular domain of the c-kit product. This antibody does not bind detectably to normal peripheral blood cells and identifies a sub-group of AML patients with poor prognosis. We have used MoAb YB5.B8 to study the expression of c- kit by normal human bone marrow cells by immunofluorescence and flow cytometry, and to isolate multipotential and erythroid colony-forming cells. In a series of 11 normal adult bone marrow specimens, MoAb YB5.B8 bound to 4.0% +/- 1.8% of the cells in the low-density fraction. Dual-labeling experiments were performed with YB5.B8, and CD33, CD34, and CD10 MoAbs. Three populations of cells binding YB5.B8 could be identified based on their pattern of coexpression of the other markers; ie, YB5.B8+/CD34+/CD33-, YB5.B8+/CD34+/CD33+ and YB5.B8+/CD34+/CD33+. These populations had distinctive two-dimensional light scatter characteristics and are likely to correspond to precursor colony- forming cells, colony-forming cells, and maturing mast cells, respectively. No cells binding both YB5.B8 and an MoAb to the early lymphoid marker CD10 were found, implying that most early lymphoid cells do not express c-kit. MoAbs to the c-kit protein should prove valuable in multimarker studies of human hematopoietic stem and progenitor cells. Definition of a reference range of c-kit expression in normal human bone marrow will provide a sound basis for further studies of this marker in diagnosis and prognosis in AML.

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32

Asano, Y., M. A. Brach, A. Ahlers, S. de Vos, J. H. Butterfield, L. K. Ashman, P. Valent, H. J. Gruss, and F. Herrmann. "Phorbol ester 12-O-tetradecanoylphorbol-13-acetate down-regulates expression of the c-kit proto-oncogene product." Journal of Immunology 151, no. 5 (September 1, 1993): 2345–54. http://dx.doi.org/10.4049/jimmunol.151.5.2345.

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Abstract Modulation of expression of the c-kit proto-oncogene product, the receptor for the recently identified stem cell factor, was studied on 12-O-tetradecanoylphorbol-13-acetate (TPA)-stimulated cultures of CD34+ normal bone marrow progenitor cells, blast cells from patients with primary acute myelogenous leukemia, cells from the leukemia cell lines HEL and MO7E, as well as cultured HMC-1 mast cells. Expression of c-kit was assessed on both RNA and protein level employing standard Northern blotting, reverse transcription, and polymerase chain reaction-based Southern blotting, as well as cell surface labeling with anti-c-kit mAb YB5.B8. Treatment of virtually all cell types with nontoxic concentrations of TPA (10(-9) M) for at least 48 h was associated with down-regulation of synthesis of c-kit transcripts and stem cell factor-receptor surface expression. Studies on the mechanism of action of TPA utilizing the HEL erythroleukemia line showed that TPA was primarily acting by accelerating the turnover of c-kit RNA most likely through induction of a destabilizing protein. The effect of TPA on c-kit expression levels was independent of TPA-mediated induction of differentiation since other compounds including IFN-gamma, vitamin D3, retinoic acid, arabinofuranosylcytosine, butyric acid, and camptothecin, which also effectively induced differentiation of HEL cells, failed to alter levels of c-kit expression.

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33

Yoshida, Hisahiro, Shin-Ichi Nishikawa, Hitoshi Okamura, Teruyo Sakakura, and Moriaki Kusakabe. "The Role of c-kit Proto-oncogene during Melanocyte Development in Mouse. In vivo Approach by the In utero Microinjection of Anti-c-kit Antibody. (c-kit proto-oncogene/melanogenesis/monoclonal anti-c-kit antibody/microinjection/white spotting)." Development, Growth and Differentiation 35, no. 2 (April 1993): 209–20. http://dx.doi.org/10.1111/j.1440-169x.1993.00209.x.

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34

Peterková, Kateřina, Ivo Durník, Radek Marek, Janez Plavec, and Peter Podbevšek. "c-kit2 G-quadruplex stabilized via a covalent probe: exploring G-quartet asymmetry." Nucleic Acids Research 49, no. 15 (August 7, 2021): 8947–60. http://dx.doi.org/10.1093/nar/gkab659.

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Abstract Several sequences forming G-quadruplex are highly conserved in regulatory regions of genomes of different organisms and affect various biological processes like gene expression. Diverse G-quadruplex properties can be modulated via their interaction with small polyaromatic molecules such as pyrene. To investigate how pyrene interacts with G-rich DNAs, we incorporated deoxyuridine nucleotide(s) with a covalently attached pyrene moiety (Upy) into a model system that forms parallel G-quadruplex structures. We individually substituted terminal positions and positions in the pentaloop of the c-kit2 sequence originating from the KIT proto-oncogene with Upy and performed a detailed NMR structural study accompanied with molecular dynamic simulations. Our results showed that incorporation into the pentaloop leads to structural polymorphism and in some cases also thermal destabilization. In contrast, terminal positions were found to cause a substantial thermodynamic stabilization while preserving topology of the parent c-kit2 G-quadruplex. Thermodynamic stabilization results from π–π stacking between the polyaromatic core of the pyrene moiety and guanine nucleotides of outer G-quartets. Thanks to the prevalent overall conformation, our structures mimic the G-quadruplex found in human KIT proto-oncogene and could potentially have antiproliferative effects on cancer cells.

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35

Feng, Huailiang, Jay I. Sandlow, and Alexander Sandra. "Expression and Function of the c-kit Proto-Oncogene Protein in Mouse Sperm1." Biology of Reproduction 57, no. 1 (July 1, 1997): 194–203. http://dx.doi.org/10.1095/biolreprod57.1.194.

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36

Feng, H., J. I. Sandlow, and A. Sandra. "Expression and Function of the c-kit Proto-Oncogene Protein in Mouse Sperm." Journal of Urology 160, no. 2 (August 1998): 622. http://dx.doi.org/10.1016/s0022-5347(01)62978-1.

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37

KUBO, Kihei, Satoshi MATSUYAMA, Kumiko KATAYAMA, Chizu TSUTSUMI, Kumiko YONEZAWA, Terumasa SHIMADA, Takeo KOTANI, Sadashige SAKUMA, Fumihito OHASHI, and Yasuhiko TAKAMORI. "Frequent Expression of the c-kit Proto-Oncogene in Canine Malignant Mammary Tumor." Journal of Veterinary Medical Science 60, no. 12 (1998): 1335–40. http://dx.doi.org/10.1292/jvms.60.1335.

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38

Yilmaz, Ercan, Onder Celik, Yavuz Simsek, Ilgin Turkcuoglu, Ebru Celik, Mehmet Gül, Seyma Hascalik, and Nasuhi Engin Aydin. "Erratum to: c-Kit proto-oncogene expression in endometrial hyperplasia and endometrial cancer." Archives of Gynecology and Obstetrics 286, no. 1 (March 25, 2012): 201. http://dx.doi.org/10.1007/s00404-012-2297-3.

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39

Medina, Benjamin D., Mengyuan Liu, Gerardo A. Vitiello, Adrian M. Seifert, Shan Zeng, Timothy Bowler, Jennifer Q. Zhang, et al. "Oncogenic kinase inhibition limits Batf3-dependent dendritic cell development and antitumor immunity." Journal of Experimental Medicine 216, no. 6 (April 18, 2019): 1359–76. http://dx.doi.org/10.1084/jem.20180660.

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Gastrointestinal stromal tumor (GIST) is driven by an activating mutation in the KIT proto-oncogene. Using a mouse model of GIST and human specimens, we show that intratumoral murine CD103+CD11b− dendritic cells (DCs) and human CD141+ DCs are associated with CD8+ T cell infiltration and differentiation. In mice, the antitumor effect of the Kit inhibitor imatinib is partially mediated by CD103+CD11b− DCs, and effector CD8+ T cells initially proliferate. However, in both mice and humans, chronic imatinib therapy decreases intratumoral DCs and effector CD8+ T cells. The mechanism in our mouse model depends on Kit inhibition, which reduces intratumoral GM-CSF, leading to the accumulation of Batf3-lineage DC progenitors. GM-CSF is produced by γδ T cells via macrophage IL-1β. Stimulants that expand and mature DCs during imatinib treatment improve antitumor immunity. Our findings identify the importance of tumor cell oncogene activity in modulating the Batf3-dependent DC lineage and reveal therapeutic limitations for combined checkpoint blockade and tyrosine kinase inhibition.

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40

Marinković, Darko, Natalija Milčić-Matić, Milan Jovanović, Ivana Vučićević, Slađan Nešić, Milan Aničić, and Sanja Aleksić-Kovačević. "Morphological Features and KIT Receptor Expression in Canine Cutaneous Mast Cell Tumor and Systemic Mastocytosis / Morfološke Karakteristike I Ekspresija KIT Receptora Kod Kutanih Mastocitoma I Sistemske Mastocitoze Pasa." Acta Veterinaria 65, no. 2 (June 1, 2015): 226–37. http://dx.doi.org/10.1515/acve-2015-0019.

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Abstract Mast cell neoplasia in dogs can occur in two different forms: common as cutaneous tumor, or less common as a systemic form of neoplastic mast cell proliferation - systemic mastocytosis. The aim of this study was to compare the histological and cytological features, KIT receptor expression and presence of c-KIT proto-oncogene mutations in neoplastic cells of dogs with canine cutaneous mast cell tumor (CMCT) and systemic mastocytosis. Microscopical examination of the cytological smears obtained from all selected dogs revealed that cellular specimens were constituted mostly of round cells with a central nuclei and fine to coarse purple cytoplasmic granules. Histopathological examination of skin samples of dogs with CMCT and a dog with systemic mastocytosis showed proliferation of the neoplastic mast cells in the superficial and/or deep dermis. Similar findings were observed in tissue samples derived from lymph nodes, spleen, liver, myocardium and kidneys of a dog with systemic mastocytosis. Three dogs with high grade CMCT as well as one dog with systemic mastocytosis showed cytoplasmic CD117 expression, while 3 dogs with low grade CMCT, had membranous expression of CD117. Based on our study, histological features and cytoplasmic CD117 expression in neoplastic cells of dogs with systemic mastocytosis are similar to those in dogs with high grade CMCTs. Nevertheless, mutations of c-KIT proto-oncogene were not found in tumor samples either from dogs with CMCT or dog with systemic mastocytosis.

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41

Gözükara, Ilay, T. U. Kutlu Dilek, Hüseyin Durukan, Duygu Düsmez Apa, Suna Kabil Kucur, and Saffet Dilek. "Extragastrointestinal Stromal Tumor during Pregnacy." Case Reports in Obstetrics and Gynecology 2012 (2012): 1–3. http://dx.doi.org/10.1155/2012/846747.

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Extragastrointestinal stromal tumors (EGISTs) are mesenchymal neoplasms without connection to the gastrointestinal tract. Gastrointestinal stromal tumors (GISTs) and EGIST are similar according to their clinicopathologic and histomorphologic features. Both of them most often express immunoreactivity for CD-117, a c-kit proto-oncogene protein. The coexistence of GIST and pregnancy is very rare, with only two cases reported in the literature. In this paper, we presented the first EGIST case during pregnancy in the literature.

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42

Chao, Wan-Ru, Chi-Kuan Chen, Lih-Min Han, and Chih-Ping Han. "Mutation-free expression of c-Kit proto-oncogene in primary adenocarcinoma of uterine cervix." Taiwanese Journal of Obstetrics and Gynecology 55, no. 5 (October 2016): 741–42. http://dx.doi.org/10.1016/j.tjog.2015.05.007.

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43

Wang, Hong, Amina Boussouar, Laetitia Mazelin, Servane Tauszig-Delamasure, Yan Sun, David Goldschneider, Andrea Paradisi, and Patrick Mehlen. "The Proto-oncogene c-Kit Inhibits Tumor Growth by Behaving as a Dependence Receptor." Molecular Cell 72, no. 3 (November 2018): 413–25. http://dx.doi.org/10.1016/j.molcel.2018.08.040.

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44

London, Cheryl A., Stephen J. Galli, Toshifumi Yuuki, Zhi-Qing Hu, Stuart C. Helfand, and Edwin N. Geissler. "Spontaneous canine mast cell tumors express tandem duplications in the proto-oncogene c-kit." Experimental Hematology 27, no. 4 (April 1999): 689–97. http://dx.doi.org/10.1016/s0301-472x(98)00075-7.

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45

Yamaguchi, Yasuo, Kazutoshi Okabe, Fujio Matsumura, Eiji Akizuki, Teishi Matsuda, Hajime Ohshiro, Jian Liang, Kojiroh Ishihara, Katsutaka Mori, and Michio Ogawa. "Expression of the c-kit proto-oncogene in rat hepatic allografts during acute rejection." Hepatology 29, no. 1 (January 1999): 133–39. http://dx.doi.org/10.1002/hep.510290105.

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46

Szatkowski, Damian, and Andrzej Hellmann. "The Overexpression of KIT Proto-Oncogene in Acute Leukemic Cells Is Not Necessarily Caused by the Gene Mutation." Acta Haematologica 133, no. 1 (September 20, 2014): 116–23. http://dx.doi.org/10.1159/000360214.

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KIT is detected in a variety of cells, also in acute leukemia. Inhibition of wild-type KIT is not always satisfactory. The aim of this work was to evaluate the frequency of the most common KIT mutations in acute myeloid leukemia (AML) and determine the correlation between mutation and expression level. Samples were obtained from 75 patients with AL. CD117 presence was shown in 45 of 51 patients with AML and in 1 of 16 patients with acute lymphocytic leukemia (ALL). Asp816Val mutation was found in 3.5% of cases of AML and Val560Gly mutation in 1 sample with acute biclonal leukemia. Other genetic changes were found in 15 of 57 samples with AML: polymorphisms Met541Leu in 14% of cases, Lys546Lys in 7% and 1 case of acute biclonal leukemia, Ile798Ile in 5.3% of cases, Met541Leu in 1 acute biphenotypic leukemia and in 6.3% of ALL. Polymorphism Lys546Lys was also shown in 1 case of acute biclonal leukemia. Nonsilent genetic changes were detected in a total of 23% cases with core binding factor leukemia. There was no statistical significance between KIT expression and genetic changes. There was no correlation between the incidence and types of KIT mutations and its expression on cells in AML.

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47

Kuriu, A., H. Ikeda, Y. Kanakura, JD Griffin, B. Druker, H. Yagura, H. Kitayama, J. Ishikawa, T. Nishiura, and Y. Kanayama. "Proliferation of human myeloid leukemia cell line associated with the tyrosine-phosphorylation and activation of the proto-oncogene c-kit product." Blood 78, no. 11 (December 1, 1991): 2834–40. http://dx.doi.org/10.1182/blood.v78.11.2834.2834.

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Анотація:

Abstract We investigated the expression, degree of phosphorylation, and activation of the proto-oncogene c-kit product before and after stimulation with the c-kit ligand in a human factor-dependent myeloid leukemia cell line, MO7E. The culture supernatant of the BALB/3T3 fibroblast cell line, which contains the ligand for the murine c-kit product, was found to stimulate proliferation of the MO7E cell line in a dose-dependent manner. The proliferation was significantly inhibited by a tyrosine kinase inhibitor, genistein. An immunoblot technique with a monoclonal antibody specific for phosphotyrosine, showed that there was rapid, dose-dependent tyrosine-phosphorylation of the c-kit product in response to murine c-kit ligand. Furthermore, the murine c-kit ligand increased autokinase activity of the c-kit product in vitro. Similar results were obtained with human stem cell factor (SCF), a recombinant human ligand for the c-kit product. These results suggest that the phosphorylation and activation of the c-kit product are involved in proliferative signals of some human leukemia cells, as well as of normal hematopoietic cells.

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48

Kuriu, A., H. Ikeda, Y. Kanakura, JD Griffin, B. Druker, H. Yagura, H. Kitayama, J. Ishikawa, T. Nishiura, and Y. Kanayama. "Proliferation of human myeloid leukemia cell line associated with the tyrosine-phosphorylation and activation of the proto-oncogene c-kit product." Blood 78, no. 11 (December 1, 1991): 2834–40. http://dx.doi.org/10.1182/blood.v78.11.2834.bloodjournal78112834.

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Анотація:

We investigated the expression, degree of phosphorylation, and activation of the proto-oncogene c-kit product before and after stimulation with the c-kit ligand in a human factor-dependent myeloid leukemia cell line, MO7E. The culture supernatant of the BALB/3T3 fibroblast cell line, which contains the ligand for the murine c-kit product, was found to stimulate proliferation of the MO7E cell line in a dose-dependent manner. The proliferation was significantly inhibited by a tyrosine kinase inhibitor, genistein. An immunoblot technique with a monoclonal antibody specific for phosphotyrosine, showed that there was rapid, dose-dependent tyrosine-phosphorylation of the c-kit product in response to murine c-kit ligand. Furthermore, the murine c-kit ligand increased autokinase activity of the c-kit product in vitro. Similar results were obtained with human stem cell factor (SCF), a recombinant human ligand for the c-kit product. These results suggest that the phosphorylation and activation of the c-kit product are involved in proliferative signals of some human leukemia cells, as well as of normal hematopoietic cells.

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49

Buglione, Enrico, Domenico Salerno, Claudia Adriana Marrano, Valeria Cassina, Guglielmo Vesco, Luca Nardo, Mauro Dacasto, Riccardo Rigo, Claudia Sissi, and Francesco Mantegazza. "Nanomechanics of G-quadruplexes within the promoter of the KIT oncogene." Nucleic Acids Research 49, no. 8 (April 13, 2021): 4564–73. http://dx.doi.org/10.1093/nar/gkab079.

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Abstract G-quadruplexes (G4s) are tetrahelical DNA structures stabilized by four guanines paired via Hoogsteen hydrogen bonds into quartets. While their presence within eukaryotic DNA is known to play a key role in regulatory processes, their functional mechanisms are still under investigation. In the present work, we analysed the nanomechanical properties of three G4s present within the promoter of the KIT proto-oncogene from a single-molecule point of view through the use of magnetic tweezers (MTs). The study of DNA extension fluctuations under negative supercoiling allowed us to identify a characteristic fingerprint of G4 folding. We further analysed the energetic contribution of G4 to the double-strand denaturation process in the presence of negative supercoiling, and we observed a reduction in the energy required for strands separation.

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50

Chao, Wan-Ru, Wea-Lung Lin, Chi-Kuan Chen, Lih-Min Han, Jau-Chen Lin, and Chih-Ping Han. "Unusual c-KIT (+) squamous cell carcinoma of the uterine cervix showing paradoxical hypermethylation of the c-KIT proto-oncogene." European Journal of Obstetrics & Gynecology and Reproductive Biology 184 (January 2015): 130–31. http://dx.doi.org/10.1016/j.ejogrb.2014.11.034.

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