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  • About
  • The Global ETD Search service is a free service for researchers to find electronic theses and dissertations. This service is provided by the Networked Digital Library of Theses and Dissertations.
    Our metadata is collected from universities around the world. If you manage a university/consortium/country archive and want to be added, details can be found on the NDLTD website.
61

Ultrastructural and stereological investigation of the effects of hexamethylene bisacetamide on human colon carcinoma LoVo cells in vitro /

Lau, Yue-huen, Thomas. January 2000 (has links)
Thesis (M. Phil.)--University of Hong Kong, 2000. / Includes bibliographical references (leaves 152-169).
62

On the muscular activity of the colon in the dog ...

Lawson, Hampden Clisby. January 1932 (has links)
Thesis (Ph. D.)--University of Chicago, 1932. / Lithographed. "Private edition, distributed by the University of Chicago libraries, Chicago, Illinois." Bibliography: p. 13-15.
63

Novel chemotherapeutics against lung and colon cancer

Keller, Elizabeth Greer. January 2010 (has links)
Thesis (M.S.)--Villanova University, 2010. / Chemistry Dept. Includes bibliographical references.
64

Physiology of the colon

Larson, Lawrence Myrlin, Bargen, J. Arnold January 1900 (has links)
Thesis (Ph. D.)--University of Minnesota, 1932. / Caption title. Thesis note on p. [1] of each part. Vita on p. [1] on cover. Parts 2-3 have title: Action of cathartics on isolated dog's colon. Reprinted from the Archives of surgery, v. 27, 1933. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references. Bibliography on cover.
65

Studies on the motility of the colon ...

Borkon, Eli Leroy, January 1936 (has links)
Thesis (Ph. D.)--University of Chicago, 1936. / Lithoprinted. "Private edition, distributed by the University of Chicago Libraries, Chicago, Illinois." "List of references": p. 12.
66

Copper-64-labelled antibodies for the radioimmunotherapy of colon cancer in a mouse model /

Bryan, Jeffrey N. January 2005 (has links)
Thesis (M.S.)--University of Missouri--Columbia, 2004. / "December 2004." Typescript. Includes bibliographical references (leaves 76-82). Also issued on the Internet.
67

Copper-64-labelled antibodies for the radioimmunotherapy of colon cancer in a mouse model

Bryan, Jeffrey N. January 2005 (has links)
Thesis (M.S.)--University of Missouri--Columbia, 2004. / "December 2004" Typescript. Includes bibliographical references (l. 76-82). Also issued on the Internet.
68

Single nucleotide polymorphisms of CYP2C19 gene and AHR gene and their associations to colorectal cancer and breast cancer risk in Han Chinese population /

Lai, Man Po. January 2007 (has links)
Thesis (M.Phil.)--Hong Kong University of Science and Technology, 2007. / Includes bibliographical references (leaves 75-94). Also available in electronic version.
69

Identification of recruited myeloid cells important for the development of hepatic metastasis

Gordon-Weeks, Alex January 2015 (has links)
Hepatic metastases are a frequent cause of mortality in colon cancer patients. Many patients with hepatic metastasis have large tumour burden, signaling the need for therapies capable of down-staging metastatic disease. Research evidence indicates that immune cells promote the metastasis of various primary cancers. We wish to determine whether immune cells play a role in the promotion of hepatic colon cancer metastasis. Using the well-characterised method of intrasplenic tumour cell injection, we developed hepatic metastases in both immunocompetent and immunoincompetent mice using a range of murine and human cancer cell lines. We analysed the immune cell infiltrates associated with hepatic metastases using flow cytometry and identified chemokines responsible for their recruitment using targeted protein arrays. The effect of immune cell depletion or inhibition of immune cell recruitment was determined using various in-vivo imaging techniques. Hepatic metastases developed using the murine colon cancer cell line MC38 were associated with CD11b<sup>+</sup>/Gr1<sup>mid</sup>/CCR2<sup>+</sup> monocytes, the recruitment of which was delayed by inhibition of tumour-derived CCL2. In contrast, human HT29, HCT-116 and LoVo hepatic metastases in SCID mice were associated with infiltrates of CD45<sup>+</sup>/CXCR2<sup>+</sup> neutrophils recruited in response to tumour-derived Macrophage Inhibitory Factor (MIF). Depletion of Gr1<sup>mid</sup> cells in CD11b-DTR transgenic mice delayed MC38 metastasis development, whilst neutrophil depletion using anti-Ly6G antibodies significantly inhibited the growth of HT29, HCT-116 and LoVo hepatic metastases. The neutrophils recruited to HT29, HCT-116 and LoVo hepatic metastases promoted angiogenesis, potentially through the expression of fibtroblast growth factor-2. This work demonstrates a role for myeloid cells in the development of hepatic metastasis from colon cancer and in doing so identifies various potential therapeutic targets.
70

Ativação de autofagia com oxaliplatina em células de câncer colorretal

Bordin, Diana Lilian January 2013 (has links)
As céluals tumorais estão constantemente expostas a flutuações nas concentrações de nutrientes e oxigênio no microambiente tumoral. Através da ativação de diferentes vias de sinalização, as células tumorais sofrem uma reprogramação metabólica a fim de suportar as condições hostis impostas pelo microambiente tumoral. Uma das vias de sinalização ativada nessas condições é a autofagia, a qual tem sido considerada um dos principais mecanismos de sobrevivência celular em condições de estresse. Além disso, muitos medicamentos anti-câncer, como os agentes alquilantes, tem sido implicados na indução de autofagia. Apesar da autofagia contribuir com a sobrevivência da célula, uma superativação da via autofágica por períodos prolongados pode contribuir com a morte celular, o que faz com que o papel da autofagia no câncer seja ainda bastante debatido. Neste trabalho, buscou-se avaliar o papel da autofagia induzida em células de câncer colorretal da linhagem HCT116 continuamente cultivadas em baixa concentração de glicose e submetidas ao tratamento com o agente alquilante oxaliplatina. Os resultados demonstraram que a autofagia induzida em células HCT116 nessas condições exerce um papel citoprotetor, contribuindo para a resistência ao tratamento com oxaliplatina. A ativação da autofagia pelo tratamento com oxaliplatina em baixa concentração de glicose foi capaz de manter os níveis intracelualres de ATP e de reduzir a morte celular por apoptose. A utilização de inibidores ou de um ativador farmacológico da via autofágica, em combinação com a oxaliplatina, foi capaz de sensibilizar células HCT116 tratadas em baixa concentração de glicose, aumentando a morte celular por apoptose. Além disso, a indução de autofagia pela oxaliplatina foi mediada pela ativação de AMPK e inibição de mTOR. Estes dados demonstram que a ativação da autofagia em células de câncer colorretal HCT116 expostas a baixa concentração de glicose contribui para resistência ao tratamento com oxaliplatina. Estes dados também sugerem que a manipulação da via autofágica, pela sua inibição ou superativação, pode fornecer um maneira eficiente de limitar a progressão do tumor e aumentar a eficiência dos regimes quimioterápicos. / Tumor cells are constantly exposed to nutrients and oxygen concentration fluctuations at tumor microenvironment. Through activation of different signaling pathways, tumor cells undergo metabolic reprogramming to tolerate hostile conditions imposed by tumor microenvironment. One of the activated signaling pathways in such conditions is autophagy, which has been considered one of the central mechanisms of cell survival in stress conditions. Furthermore, many anticancer drugs, like alkylanting agents, have been implicated in autophagy induction. Despite autophagy contribution to cell survival, the autophagic pathway activation for prolonged periods may contribute to cell death, which creates extensively debates about the role of autophagy in cancer. In the present work we intended to evaluate the role of autophagy induced in colorectal cancer cells HCT116 grown continuously in low glucose concentration and treated with the alkylating agent oxaliplatin. Our results showed that autophagy induced in HCT116 cells in these conditions plays a cytoprotective role, contributing to oxaliplatin resistance. The activation of autophagy by oxaliplatin in low glucose concentration was able to maintain the intracellular levels of ATP and to reduce apoptotic cell death. The combined use of pharmacologic inhibitors or an activator of autohophagy with oxaliplatin was capable to sensitize HCT116 cells treated in low glucose concentration, increasing apoptotic cell death. Moreover, autophagy induction by oxaliplatin was mediated by the activation of AMPK and inhibition of mTOR. Our data demonstrate that autophagy activation in colorectal cancer cells HCT116 exposed to low glucose concentration contributes to the tolerance of oxaliplatin. These data also suggest that the manipulation of autophagic pathway, through its inhibition or hyperstimulation, may provide an effective manner of limiting tumor progression and increase chemotherapy effectiveness.

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