Letteratura scientifica selezionata sul tema "MET/HGF"
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Articoli di riviste sul tema "MET/HGF":
Toiyama, Y., K. Tanaka, H. Yasuda, S. Saigusa, H. Fujikawa, Y. Mohri, Y. Inoue, C. Miki, T. Tabata e M. Kusunoki. "Use of co-expression of HGF and c-Met to predict peritoneal dissemination established by autocrine HGF/c-Met signaling in gastric cancer." Journal of Clinical Oncology 29, n. 4_suppl (1 febbraio 2011): 40. http://dx.doi.org/10.1200/jco.2011.29.4_suppl.40.
Zhang, Hongli, Qingqing Feng, Wei-Dong Chen e Yan-Dong Wang. "HGF/c-MET: A Promising Therapeutic Target in the Digestive System Cancers". International Journal of Molecular Sciences 19, n. 11 (23 ottobre 2018): 3295. http://dx.doi.org/10.3390/ijms19113295.
Weimar, Iris S., Daphne de Jong, Egbert J. Muller, Toshikazu Nakamura, Joost M.H.H. van Gorp, Gijsbert C. de Gast e Winald R. Gerritsen. "Hepatocyte Growth Factor/Scatter Factor Promotes Adhesion of Lymphoma Cells to Extracellular Matrix Molecules Via α4β1 and α5β1 Integrins". Blood 89, n. 3 (1 febbraio 1997): 990–1000. http://dx.doi.org/10.1182/blood.v89.3.990.
Gallo, Simona, Valentina Sala, Stefano Gatti e Tiziana Crepaldi. "Cellular and molecular mechanisms of HGF/Met in the cardiovascular system". Clinical Science 129, n. 12 (11 novembre 2015): 1173–93. http://dx.doi.org/10.1042/cs20150502.
De Silva, Dinuka M., Arpita Roy, Takashi Kato, Fabiola Cecchi, Young H. Lee, Kunio Matsumoto e Donald P. Bottaro. "Targeting the hepatocyte growth factor/Met pathway in cancer". Biochemical Society Transactions 45, n. 4 (3 luglio 2017): 855–70. http://dx.doi.org/10.1042/bst20160132.
Kauma, Scott, Natalie Hayes e Shannon Weatherford. "The Differential Expression of Hepatocyte Growth Factor and Met in Human Placenta*". Journal of Clinical Endocrinology & Metabolism 82, n. 3 (1 marzo 1997): 949–54. http://dx.doi.org/10.1210/jcem.82.3.3806.
Yamasaki, Koji, Shoichiro Mukai, Takahiro Nagai, Kozue Nakahara, Masato Fujii, Naoki Terada, Akinobu Ohno et al. "Matriptase-Induced Phosphorylation of MET is Significantly Associated with Poor Prognosis in Invasive Bladder Cancer; an Immunohistochemical Analysis". International Journal of Molecular Sciences 19, n. 12 (22 novembre 2018): 3708. http://dx.doi.org/10.3390/ijms19123708.
Woolf, A. S., M. Kolatsi-Joannou, P. Hardman, E. Andermarcher, C. Moorby, L. G. Fine, P. S. Jat, M. D. Noble e E. Gherardi. "Roles of hepatocyte growth factor/scatter factor and the met receptor in the early development of the metanephros." Journal of Cell Biology 128, n. 1 (1 gennaio 1995): 171–84. http://dx.doi.org/10.1083/jcb.128.1.171.
Tanaka, Ryota, Mizue Terai, Eric Londin e Takami Sato. "The Role of HGF/MET Signaling in Metastatic Uveal Melanoma". Cancers 13, n. 21 (30 ottobre 2021): 5457. http://dx.doi.org/10.3390/cancers13215457.
Czyz, Malgorzata. "HGF/c-MET Signaling in Melanocytes and Melanoma". International Journal of Molecular Sciences 19, n. 12 (3 dicembre 2018): 3844. http://dx.doi.org/10.3390/ijms19123844.
Tesi sul tema "MET/HGF":
Ding, Shunli. "Rôle du couple HGF/C-MET dans l'angiogenèse". Paris 7, 2004. http://www.theses.fr/2004PA077188.
Moore, Amy Elizabeth. "The role of HGF/Met signalling in colorectal tumorigenesis". Thesis, University of Bristol, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.544331.
Besret, Soizic. "Ligations chimiques : synthèse d'inhibiteurs extracellulaires de la signalisation HGF/SF-MET". Phd thesis, Université du Droit et de la Santé - Lille II, 2011. http://tel.archives-ouvertes.fr/tel-00630962.
Murat, Cahue de Bernardis. "Estudo molecular dos componentes da via de sinalização HGF/MET em insulinomas". Universidade de São Paulo, 2013. http://www.teses.usp.br/teses/disponiveis/5/5135/tde-03102013-110107/.
In an attempt to better understand the molecular processes involved in the tumourigenesis of islet beta-cells, the present study evaluated the expression of genes belonging to the hepatocyte growth factor and its receptor (HGF/MET) system, namely, MET, HGF; HGFAC and ST14 (encode HGF activator and matriptase, respectively, two serine proteases that catalyze conversion of pro-HGF to active HGF); and SPINT1 and SPINT2 (encode serine peptidase inhibitors Kunitz type 1 and type 2, respectively, two potent inhibitors of HGF activator and of matriptase) in 27 sporadic insulinomas; 16 grade 1 (G1), six grade 2 (G2), two grade 3 (G3) and three hepatic metastases. Quantitative reverse-transcriptase polymerase chain reaction was employed to assess RNA expression of the target genes and immunohistochemical analysis was used to evaluate the expression of MET and SPINT1. Somatic mutations of MET gene were searched by direct sequencing of exons 2, 10, 14, 16, 17 and 19. Overexpression of MET was observed in grouped G3 insulinomas and metastases concomitantly with upregulation of the genes encoding HGF and matriptase and downregulation of SPINT1. Positive correlations were observed between MET RNA expression and Ki-67 proliferation index while a negative correlation was detected between SPINT1 expression and the mitotic index. No somatic mutations were found in MET gene. The final effect of the increased expression of HGF, its activator (matriptase) and its specific receptor (MET) together with a decreased expression of one potent inhibitor of matriptase (SPINT1) is probably a contribution to tumoural progression and malignancy in insulinomas
Mekki, Meriem Sarah. "Conséquences de l'hypoxie sur la régulation de la signalisation HGF/SF-MET". Thesis, Lille 2, 2015. http://www.theses.fr/2015LIL2S047/document.
The receptor tyrosine kinase MET and its ligand the Hepatocyte Growth Factor/Scattor Factor (HGF/SF) are essential for migration, morphogenesis and survival of epithelial cells. Beside its physiological involvement, deregulation of MET signaling has been shown to promote tumor progression and invasion in many cancers. Inside the tumors, hypoxia is also a crucial phenomenon promoting an adaptive response able to induce invasion, metastasis and resistance to treatment.We show that under hypoxia, MET phosphorylation induced by ligand-stimulation, activating mutation or overexpression, is drastically decreased both in cell culture and in experimental tumors. This decrease in MET phosphorylation occurs within minutes and is reversible when cells are returned to normoxia. While phosphorylation of the proximal signaling adaptor GAB1 is also decreased in hypoxia, activation of the downstream kinases ERK and AKT is not affected, but is still dependent on MET receptor activity. Consistently, several cellular responses induced by HGF/SF, including motility, morphogenesis or survival, are still efficiently induced. Interestingly, treatment with two tyrosine kinase inhibitors targeting MET (PHA-665752 and SU11274) are less efficient to inhibit the downstream kinases ERK and AKT and cellular responses induced by MET in hypoxia compared to normoxia. Similarly to MET phosphorylation, this resistance to TKI is a reversible phenomenon. Therefore, while hypoxia does not affect downstream signaling and cellular responses, it decreases MET sensitivity to TKIs targeting the receptor thus providing an immediate resistance. This may provide new insights in the use of MET targeted therapies in solid tumors
Tjin, Esther Pit Mien. "The HGF/MET and WNT signaling pathways in B cell differentiation and neoplasia". [S.l. : Amsterdam : s.n.] ; Universiteit van Amsterdam [Host}, 2005. http://dare.uva.nl/document/17835.
Stefan, Monica. "Identifizierung eines neuen Interaktionspartners des HGF-Rezeptors c-Met SHIP-1 spielt eine Schlüsselrolle bei der Vermittlung der HGF-induzierten Tubulogenese von Epithelzellen /". [S.l.] : [s.n.], 2001. http://deposit.ddb.de/cgi-bin/dokserv?idn=961707232.
Arlt, Franziska. "Das neu identifizierte Gen MACC1 ist ein Regulator des HGF/Met-Signalweges und ist prognostisch für die Metastasierung des Kolonkarzinoms". Doctoral thesis, Humboldt-Universität zu Berlin, Mathematisch-Naturwissenschaftliche Fakultät I, 2009. http://dx.doi.org/10.18452/15974.
Colon cancer is one of the most frequent malignant diseases worldwide. About 50% of the patients develop distant metastasis. These patients have only few therapy options and very poor survival rates. Therefore cancer research focuses on the identification of novel molecular markers to provide a better prognosis of the metastatic risk. Identified high-risk patients would get access to an early, individualized therapy. MACC1 (metastasis associated in colon cancer 1) is a newly identified gene that is overexpressed in colon carcinomas and their distant metastases. The MACC1 domain structure is characteristic for proteins of the receptor tyrosine kinase signalling pathways. Aim of this study was the analysis of the cellular function of MACC1, its role in tumor progression and its evaluation as a molecular, prognostic marker for metastasis. MACC1 overexpressing tumor cells revealed higher migratory, invasive, and proliferative potential in in vitro assays. The impact of MACC1 on the metastatic potential of tumors was also shown in mouse models. The hepatocyte growth factor (HGF) induced epithelial-mesenchymal-transition in MACC1 positive cells and MACC1´s nuclear translocation. Expression of the HGF receptor Met was strongly elevated in these cells. Reporter gene experiments confirmed the transcriptional regulation of Met by MACC1. Analyses in human colon carcinomas showed a significantly higher MACC1 expression in tumors that developed distant metastases. MACC1 is a newly identified regulator of the HGF/Met signalling pathway. It contributes decisively to the metastatic capacity of tumor cells. MACC1 has great potential as new prognostic marker for colon cancer metastasis and is a promising candidate as target for effective, molecular intervention strategies for metastasis prevention.
Rocha, Angélica Gomes 1989. "Estudo da expressão proteica da via HGF/c-Met/STAT3 no carcinoma diferenciado da tiroide". [s.n.], 2014. http://repositorio.unicamp.br/jspui/handle/REPOSIP/310289.
Dissertação (mestrado) - Universidade Estadual de Campinas, Faculdade de Ciências Médicas
Made available in DSpace on 2018-08-26T01:02:11Z (GMT). No. of bitstreams: 1 Rocha_AngelicaGomes_M.pdf: 1644333 bytes, checksum: e3503fb6e2c8209f7a6696df111d6a78 (MD5) Previous issue date: 2014
Resumo: Marcadores de malignidade, especialmente capazes de distinguir lesões de padrão folicular, que sejam de fácil implantação na rotina do diagnóstico de nódulos tireoidianos, continuam sendo extremamente necessários, dado o crescente aumento de nódulos tireoidianos diagnosticados nos últimos anos. A via HGF/c-Met/STAT3 está relacionada com desenvolvimento e progressão tumoral, sendo que a expressão de c-Met, HGF e de STAT3 foram descritas em grande parte dos carcinomas papilíferos de tireoide (CPT), mas não em tecido tireoidiano normal, sugerindo sua relação com o desenvolvimento e progressão do CPT. Para avaliar a utilidade da expressão proteica de c-Met, HGF, STAT3, e de sua proteína fosforilada (pSTAT3) no diagnóstico e no prognóstico de pacientes com nódulos tireoidianos, analisamos 356 tecidos tireoidianos, sendo 153 carcinomas papilíferos (CPT), dos quais 95 eram clássicos (CPC), 47 carcinomas papilíferos variante folicular (CPVF), e 11 carcinomas papilíferos de células altas (CPCA); 34 carcinomas foliculares (CFT), 34 adenomas foliculares (AF), 124 bócios e 11 tecidos normais. Todos os pacientes foram tratados e acompanhados de acordo com um mesmo protocolo padrão por 1-10 anos (Mo=5 anos). Áreas representativas do tecido foram selecionadas para a construção de uma lâmina de tissue microarray (TMA) que foi submetida à técnica de imunoistoquímica e analisada pelo score de Allred. A expressão citoplasmática de c-Met foi capaz de diferenciar nódulos malignos de benignos (p<0,0001, sensibilidade 86%, especificidade 76%, VPP 77%, VPN 86%); CPT de CF (p=0,0003, sensibilidade 96%, especificidade 31%, VPP 87%, VPN 63%); variante folicular de CPT de CF (p=0,0232 sensibilidade 93%, especificidade 31%, VPP 66%, VPN 77%); assim como variante folicular de CPT de AF (p=0,0003, sensibilidade 93%, especificidade 50%, VPP 68%, VPN 87%). Além disso, a expressão de c-Met se correlacionou com tireoidite (p<0,0001) e multifocalidade (p=0,0028), mas não com presença de cápsula, invasão, tamanho do tumor, estadiamento TNM, e presença de metástase no diagnóstico e na evolução. A expressão nuclear de STAT3 diferenciou os nódulos benignos dos malignos (p<0,0001, sensibilidade 83%, especificidade 74%, VPP 75%, VPN 83%); CF de AF (p=0,0457, sensibilidade 80%, especificidade 52%, VPP 65%, VPN 71%); bócios de CPT variante folicular (p<0,001, sensibilidade 89%, especificidade 65%, VPP 91%, VPN 60%); bócio de CF (p<0,0001, sensibilidade 89%, especificidade 80%, VPP 95%, VPN 60%); bócio de AF (p=0,0005, sensibilidade 89%, especificidade 80%, VPP 95%, VPN 60%). Além disso, a expressão de STAT3 se correlacionou com tireoidite (p=0,0095) e multifocalidade (p<0,0001), mas não com presença de cápsula, invasão, tamanho do tumor, estadiamento TNM, e presença de metástase no diagnóstico e na evolução. A expressão de pSTAT3 e HGF não auxiliou no diagnóstico dos nódulos, e tampouco se correlacionou com características de agressividade dos tumores. Conclui-se que as proteínas c-Met e STAT3 podem ser consideradas marcadores clínicos úteis na rotina de laboratórios, uma vez que foram capazes de diferenciar os nódulos malignos dos benignos, alguns tipos histológicos dos nódulos, além de se correlacionarem com fatores de agressividade dos tumores
Abstract: Malignancy markers, especially the ones that are capable of distinguishing follicular lesions and with easy deployment in the routine diagnosis of thyroid nodules are much needed, given the increasing number of thyroid nodules in recent years. The HGF/c-Met/STAT3 pathway is related to the development and progression of many types of cancers, and c-Met, HGF and STAT3 expression were described in most papillary thyroid carcinomas (PTC), but not in normal thyroid tissue, suggesting it is related with the development and progression of PTC. To evaluate the usefulness of c-Met, HGF, STAT3, and its phosphorylated form (pSTAT3) protein expression in the diagnosis and prognosis of patients with thyroid nodules, we analyzed 356 thyroid tissues, including 153 papillary carcinomas (PTC), 95 classical type, 47 follicular variants of papillary carcinoma, and 11 tall cells carcinomas; 34 follicular carcinomas (FC), 34 follicular adenomas (FA), 124 goiters and 11 normal tissues. All patients were treated and monitored according to the same standard protocol for 1-10 years (Mo = 5 years). Representative tissue areas were selected for the construction of a tissue microarray (TMA) which was subjected to immunohistochemistry and analyzed by the Allred score. The cytoplasmic expression of c-Met was able to differentiate malignant from benign nodules (p <0.0001, sensitivity 86%, specificity 76%, PPV 77%, 86% NPV); PTC from FCT (p = 0.0003, sensitivity 96%, specificity 31%, PPV 87%, 63% NPV); follicular variant of PTC from FCT (p = 0.0232 sensitivity 93%, specificity 31%, PPV 66%, NPV 77%); as well as follicular variant of CPT from FA (p = 0.0003, sensitivity 93%, specificity 50%, PPV 68%, 87% NPV). Furthermore, c-Met expression was correlated to the presence of thyroiditis (p<0.0001) and multifocality (p=0.0028), but not with the presence of capsule, invasion, tumour size, TNM staging, and metastasis at diagnosis or evolution of the disease. The nuclear expression of STAT3 differentiated benign from malignant nodules (p <0.0001, sensitivity 83%, specificity 74%, PPV 75%, NPV 83%); FCT from FA (p = 0.0457, sensitivity 80%, specificity 52%, PPV 65%, NPV 71%); goiter follicular variant of PTC (p <0.001, sensitivity 89%, specificity 65%, PPV 91%, 60% NPV); goiter from FCT (p <0.0001, sensitivity 89%, specificity 80%, PPV 95%, NPV 60%); goiter from FA (p = 0.0005, sensitivity 89%, specificity 80%, PPV 95%, NPV 60%). In addition, STAT3 expression was associated with thyroiditis (p=0.0095) and multifocality (p<0.0001), but not with the presence of capsule, invasion, tumour size, TNM staging, and metastasis at diagnosis or evolution of the disease. The expression of pSTAT3 and HGF did not help the diagnostic of nodules and was not correlated with any tumour characteristic of aggressiveness. We concluded that c-Met and STAT3 could be useful as molecular markers in laboratory routine, helping to differentiate malignant from benign nodules, and some histological types of nodules, and was also associated with some tumour characteristics of aggressiveness
Mestrado
Ensino em Saúde
Mestra em Clínica Médica
Chmielowiec, Jolanta. "The role of the Met tyrosine kinase receptor in skin maintenance and regeneration". Doctoral thesis, Humboldt-Universität zu Berlin, Mathematisch-Naturwissenschaftliche Fakultät I, 2007. http://dx.doi.org/10.18452/15690.
Met and its ligand, HGF/SF are expressed in the hyperproliferative epithelium of the wound. This suggests that receptor and ligand may act in an autocrine manner to promote wound healing in the skin. Using Keratin 14 cre recombinase, Met receptor was specifically knockout in the epidermis. In this way, it was demonstrated that Met receptor is essential for wound healing process and that keratinocytes, which contributed to the wound closure were Met-postitive. In the Met mutant mice, wound closure was slightly attenuated, but occurred exclusively by a few keratinocytes that had escaped recombination. Met is therefore the fist gene, which is absolutely required for re-epithelialization of the wound. This finding is fundamental for understanding the regulation of wound healing process.
Libri sul tema "MET/HGF":
1948-, Goldberg I. D., e Rosen E. M, a cura di. Hepatocyte growth factor-scatter factor (HGF-SF) and the C-met receptor. Basel: Birkhäuser, 1992.
Somerset, David Alan. Hepatocyte growth factor (HGF) and its receptor c-met, in healthy and pathological human placentae. Birmingham: University of Birmingham, 2001.
Alami, Jennifer. The role of HGF and met in Wilms tumour. 2004.
Long, Isolde Marie Seiden. Functional relationships between hepatocyte growth factor receptor (HGF)/Met signaling and Ki-ras oncogenic mutation in colon carcinoma cells. 2005.
Capitoli di libri sul tema "MET/HGF":
Ray, Mandira, J. G. Garcia e Ravi Salgia. "HGF/c-MET Signaling in Advanced Cancers". In Cancer Genome and Tumor Microenvironment, 273–92. New York, NY: Springer New York, 2009. http://dx.doi.org/10.1007/978-1-4419-0711-0_12.
Vande Woude, G. F., M. Jeffers, J. Cortner, G. Alvord, I. Tsarfaty e J. Resau. "Met-HGF/SF: Tumorigenesis, Invasion and Metastasis". In Ciba Foundation Symposium 212 - Plasminogen-Related Growth Factors, 119–32. Chichester, UK: John Wiley & Sons, Ltd., 2007. http://dx.doi.org/10.1002/9780470515457.ch8.
Thewke, Douglas P., Jianqun Kou, Makenzie L. Fulmer e Qian Xie. "The HGF/MET Signaling and Therapeutics in Cancer". In Current Human Cell Research and Applications, 155–81. Singapore: Springer Singapore, 2017. http://dx.doi.org/10.1007/978-981-10-7296-3_8.
Zambelli, Alberto, Giuseppe Biamonti e Angela Amato. "HGF/c-Met Signalling in the Tumor Microenvironment". In Advances in Experimental Medicine and Biology, 31–44. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-47189-7_2.
Karsten, Ruud, e Joost Roeters. "Behandeling Van Een PatiëNt Met Erfelijke Of Idiopathische Gingivafibromatose (HGF)". In Tandheelkundige casuïstiek, 481–92. Houten: Bohn Stafleu van Loghum, 2008. http://dx.doi.org/10.1007/978-90-313-8811-0_92.
Abounader, Roger, e John Laterra. "HGF/c-Met Signaling and Targeted Therapeutics in Brain Tumors". In CNS Cancer, 933–52. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-553-8_39.
Chandel, Vaishali, Sibi Raj, Ramesh Choudhari e Dhruv Kumar. "Role of c-Met/HGF Axis in Altered Cancer Metabolism". In Cancer Cell Metabolism: A Potential Target for Cancer Therapy, 89–102. Singapore: Springer Singapore, 2020. http://dx.doi.org/10.1007/978-981-15-1991-8_7.
Corso, Simona, e Silvia Giordano. "Mechanisms of Resistance to Molecular Therapies Targeting the HGF/MET Axis". In Resistance to Targeted Anti-Cancer Therapeutics, 67–87. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67932-7_4.
Cortner, J., G. F. Vande Woude e S. Rong. "The Met-HGF/SF autocrine signaling mechanism is involved in sarcomagenesis". In Experientia Supplementum, 89–121. Basel: Birkhäuser Basel, 1995. http://dx.doi.org/10.1007/978-3-0348-9070-0_6.
Joffre, Carine, Rachel Barrow, Ludovic Ménard e Stéphanie Kermorgant. "RTKs as Models for Trafficking Regulation: c-Met/HGF Receptor-c-Met Signalling in Cancer—Location Counts". In Vesicle Trafficking in Cancer, 261–77. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-6528-7_13.
Atti di convegni sul tema "MET/HGF":
Chen, Dawei, Ziyong Sun, Likun Zhang, Jie Cai, Davy X. Ouyang, Jean-Pierre Wery e Henry Li. "Abstract 747: Paracrine c-MET/HGF HCC PDX: evaluation of a biologics targeting c-MET". 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.am2016-747.
Wortinger, Mark A., Wei Zeng, Wei Jennifer Yang, Victoria Peek, Lei Yan, Jirong Lu, Chi-Kin Chow et al. "Abstract 695: LA480, a c-Met antibody with neutralization and internalization properties, inhibits HGF-dependent and HGF-independent c-Met pathway activation and tumor growth". In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-695.
Gordon, Marcia, Alexandra Croft, Chi-Ming Li, Sean Taylor, Sean R. Caenepeel e Kim Quon. "Abstract LB-241: HGF promotes resistance to MET inhibitor AMG337 in MET-amplified gastric cancer cells". 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-lb-241.
Owusu, Benjamin Y., Phanindra K. Venukadasula, Robert A. Galemmo e Lidija Klampfer. "Abstract 1583: SRI31215, a novel inhibitor of oncogenic HGF/MET signaling". 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.am2016-1583.
Yu, Yanlin, Liping Huang e Glenn Merlino. "Abstract 4114: Blocking Ezrin can inhibit HGF/Met signaling-induced metastasis". 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.am2016-4114.
Hughes, Veronica S., e Dietmar W. Siemann. "Abstract 4102: Effect of HGF concentrations on c-Met inhibition investigation". 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.am2016-4102.
Vierkant, Robert A., Kimberly R. Kalli, Kristin L. White, Melissa C. Larson, Brooke L. Fridley, Gary L. Keeney, Trynda N. Oberg et al. "Abstract 893: Associations between HGF, MET, and phospho-MET expression, overall survival, andHGFgenotypes in epithelial ovarian cancer". In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-893.
Chen, Dawei, Xiaoming Song, Jie Cai, Taiping Chen, Yiyou Chen e Henry Q. X. Li. "Abstract 1322: Autocrine c-met/HGF HCC patient derived xenograft (PDX) models for evaluating c-met inhibitors". In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-1322.
Taniguchi, Hirokazu, Shinji Takeuchi, Koji Fukuda, Tadaaki Yamada, Shuichi Sakamoto, Manabu Kawada e Seiji Yano. "Abstract 4763: Targeted therapy by MET inhibitors against small-cell lung cancer with aberrant activation of HGF/MET pathway". 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.am2016-4763.
Hultberg, Anna, Cristina Basilico, Cristophe Blanchetot, Natalie D. Jonge, Valérie Hanssens, Gitte D. Boeck, Alessia Mira et al. "Abstract LB-330: Four individually druggable Met hotspots mediate HGF-driven tumor progression". In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-lb-330.
Rapporti di organizzazioni sul tema "MET/HGF":
Bordeaux, Jennifer. Met (HGF Receptor) in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, settembre 2010. http://dx.doi.org/10.21236/ada535659.
Bordeaux, Jennifer. Met (HGF Receptor) in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, settembre 2009. http://dx.doi.org/10.21236/ada515399.