Relevant bibliographies by topics / Met oncogenicity

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  1. Journal articles
  2. Dissertations / Theses

Academic literature on the topic 'Met oncogenicity'

Author: Grafiati
Published: 4 June 2021
Last updated: 17 February 2022

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Journal articles on the topic "Met oncogenicity"

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Tervonen, T. A., D. Belitškin, S. M. Pant, et al. "Deregulated hepsin protease activity confers oncogenicity by concomitantly augmenting HGF/MET signalling and disrupting epithelial cohesion." Oncogene 35, no. 14 (2015): 1832–46. http://dx.doi.org/10.1038/onc.2015.248.

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Cañadas, I., M. Arumi, L. Lema, et al. "MET in small cell lung carcinoma (SCLC): Effects of a MET inhibitor in SCLC cell lines and prognostic role of MET status in patients." Journal of Clinical Oncology 27, no. 15_suppl (2009): e14617-e14617. http://dx.doi.org/10.1200/jco.2009.27.15_suppl.e14617.

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e14617 Purpose: HGF/MET pathway is aberrantly activated by receptor overexpression and mutations in SCLC preclinical models, enhancing their oncogenicity. The significance of MET expression in SCLC remains unclear. Our aim was to analyze the effects of MET inhibition in chemosensitive/refractory SCLC models and to study the expression pattern and prognostic impact of total and phosphorylated (p) MET in SCLC patients. Methods: Total and p-MET expression (Western Blot), gene copy number (FISH), and exon 14 activating mutations (sequencing) were evaluated in H69 and H69AR SCLC cell lines. PHA-665
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Li, Xinran, Amy Y. T. Lau, Angel S. N. Ng та ін. "Cancer-associated mutations in the p85α N-terminal SH2 domain activate a spectrum of receptor tyrosine kinases". Proceedings of the National Academy of Sciences 118, № 37 (2021): e2101751118. http://dx.doi.org/10.1073/pnas.2101751118.

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The phosphoinositide 3-kinase regulatory subunit p85α is a key regulator of kinase signaling and is frequently mutated in cancers. In the present study, we showed that in addition to weakening the inhibitory interaction between p85α and p110α, a group of driver mutations in the p85α N-terminal SH2 domain activated EGFR, HER2, HER3, c-Met, and IGF-1R in a p110α-independent manner. Cancer cells expressing these mutations exhibited the activation of p110α and the AKT pathway. Interestingly, the activation of EGFR, HER2, and c-Met was attributed to the ability of driver mutations to inhibit HER3 u
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Kuge, Tomoo, Takashi Shibata, Michael S. Willett, Patricia Turck, and Karl A. Traul. "Lack of Oncogenicity of Wood Creosote, the Principal Active Ingredient of Seirogan, an Herbal Antidiarrheal Medication, in Sprague-Dawley Rats." International Journal of Toxicology 20, no. 5 (2001): 297–305. http://dx.doi.org/10.1080/109158101753253036.

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Seirogan, an herbal medicine containing wood creosote (tablets, 10.0% w/w), has been developed and marketed for almost a century in various countries for the control of acute diarrhea and treatment of associated symptoms, such as abdominal cramping. Wood creosote (CAS no. 8021–39–4) is a mixture of simple phenolic compounds, including guaiacol and creosol and related compounds, and is chemically distinct from, and should not be confused with, coal tar creosote, a known carcinogen. In the current study, the oncogenic potential of wood creosote was assessed in a 96/103-week oral gavage study in
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Chesters, Peter M., Lorraine P. Smith, and Venugopal Nair. "E (XSR) element contributes to the oncogenicity of Avian leukosis virus (subgroup J)." Journal of General Virology 87, no. 9 (2006): 2685–92. http://dx.doi.org/10.1099/vir.0.81884-0.

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Among the six subgroups of Avian leukosis virus (ALV) that infect chickens, subgroup J (ALV-J) was isolated from meat-type chickens where it predominantly induces myeloid leukosis (ML) and erythroblastosis (EB). The sequence of HPRS-103, the ALV-J prototype virus, shows several distinct features, one of which is the presence of a distinct hairpin stem–loop structure called the E (also called XSR) element in the 3′ untranslated region. In order to determine the role of the E element in ALV-induced pathogenicity, a comparison was made of the oncogenicity of viruses derived from the provirus clon
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Shu, Lihua, Dongsheng Wang, Nabil F. Saba, and Zhuo G. Chen. "A Historic Perspective and Overview of H-Ras Structure, Oncogenicity, and Targeting." Molecular Cancer Therapeutics 19, no. 4 (2020): 999–1007. http://dx.doi.org/10.1158/1535-7163.mct-19-0660.

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PANDIRI, ARUN R., WILLIE M. REED, JODY K. MAYS, and ALY M. FADLY. "INFLUENCE OF STRAIN, DOSE OF VIRUS, AND AGE AT INOCULATION ON SUBGROUP J AVIAN LEUKOSIS VIRUS PERSISTENCE, ANTIBODY RESPONSE, AND ONCOGENICITY IN COMMERCIAL MEAT-TYPE CHICKENS." Avian Diseases Digest 2, no. 3 (2007): e10-e10. http://dx.doi.org/10.1637/1933-5334(2007)2[e10:iosdov]2.0.co;2.

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Pandiri, Arun R., Willie M. Reed, Jody K. Mays, and Aly M. Fadly. "Influence of Strain, Dose of Virus, and Age at Inoculation on Subgroup J Avian Leukosis Virus Persistence, Antibody Response, and Oncogenicity in Commercial Meat-Type Chickens." Avian Diseases 51, no. 3 (2007): 725–32. http://dx.doi.org/10.1637/0005-2086(2007)51[725:iosdov]2.0.co;2.

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Cui, Ning, Xuezhi Cui, Qinghua Huang, et al. "Isolation and Identification of Subgroup J Avian Leukosis Virus Inducing Multiple Systemic Tumors in Parental Meat-Type Chickens." Frontiers in Veterinary Science 7 (January 27, 2021). http://dx.doi.org/10.3389/fvets.2020.614854.

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Avian leukosis virus (ALV) continues evolving to obtain new genomic characters to enhance its pathogenicity. In the present study, an ALV-J strain LH20180301 was isolated from broiler breeder chickens that reached the speak of paralyzation before 20-week-old. The necropsy chickens showed subcutaneous and muscular hemorrhage, and developed tumors in multiple organs including bone, liver, spleen, and kidney. The complete provirus was then cloned and sequenced to investigate the molecular characteristics and oncogenicity etiology of this virus associated with the outbreak of disease. The genomic
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Lawson, James S., and Wendy K. Glenn. "Catching viral breast cancer." Infectious Agents and Cancer 16, no. 1 (2021). http://dx.doi.org/10.1186/s13027-021-00366-3.

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Abstract We have considered viruses and their contribution to breast cancer. Mouse mammary tumour virus The prevalence of mouse mammary tumour virus (MMTV) is 15-fold higher in human breast cancer than in normal and benign human breast tissue controls. Saliva is the most plausible means of transmission. MMTV has been identified in dogs, cats, monkeys, mice and rats. The causal mechanisms include insertional oncogenesis and mutations in the protective enzyme ABOBEC3B. Human papilloma virus The prevalence of high risk human papilloma viruses (HPV) is frequently six fold higher in breast cancer t
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Dissertations / Theses on the topic "Met oncogenicity"

1

Hervieu, Vilches Alexia. "Understanding and targeting PI3K downstream of oncogenic Met mutant." Thesis, Queen Mary, University of London, 2015. http://qmro.qmul.ac.uk/xmlui/handle/123456789/33935.

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The Receptor Tyrosine Kinase (RTK) Met, overexpressed or mutated in cancer, plays a major role in cancer progression and represents an attractive target for cancer therapy. This study aimed to investigate whether PI3K plays a role in Met oncogenicity. Three cell models were used: (i) NIH3T3 cells expressing WT Met or the constitutively active mutant M1268T Met; (ii) U87MG glioblastoma cells, with endogenous WT Met constitutively activated due to an autocrine loop; (iii) A549 lung cancer cells expressing endogenous WT Met, activated upon binding exogenous HGF. Met dependent Rac1 translocation t
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