Abstract: The present inventors used a model of intrasplenically induced liver metastasis to determine whether or not NF-?B activation in the liver is involved in the onset of metastatic tumors. When IKK? was deleted from both liver cells and hematopoietically-derived cells, the onset of tumors was reduced remarkably. Tumor cells activated neighboring bone marrow cells (Kupffer cells) and produced mitogens such as interleukin (IL)-6, and this promoted angiogenesis and growth of tumors. The mitogen production depended on NF-?B in hematopoietically-derived Kupffer cells. Furthermore, treatment with an anti-IL-6 receptor antibody decreased the degree of metastatic tumor development. That is, the present inventors showed that tumor metastasis depends on inflammation, and proinflammatory intervention that targets Kupffer cells is useful for chemical prevention of metastatic tumors.

Abstract: The present inventors used a model of intrasplenically induced liver metastasis to determine whether or not NF-?B activation in the liver is involved in the onset of metastatic tumors. When IKK? was deleted from both liver cells and hematopoietically-derived cells, the onset of tumors was reduced remarkably. Tumor cells activated neighboring bone marrow cells (Kupffer cells) and produced mitogens such as interleukin (IL)-6, and this promoted angiogenesis and growth of tumors. The mitogen production depended on NF-?B in hematopoietically-derived Kupffer cells. Furthermore, treatment with an anti-IL-6 receptor antibody decreased the degree of metastatic tumor development. That is, the present inventors showed that tumor metastasis depends on inflammation, and proinflammatory intervention that targets Kupffer cells is useful for chemical prevention of metastatic tumors.

Abstract: The present inventors used a model of intrasplenically induced liver metastasis to determine whether or not NF-?B activation in the liver is involved in the onset of metastatic tumors. When IKK? was deleted from both liver cells and hematopoietically-derived cells, the onset of tumors was reduced remarkably. Tumor cells activated neighboring bone marrow cells (Kupffer cells) and produced mitogens such as interleukin (IL)-6, and this promoted angiogenesis and growth of tumors. The mitogen production depended on NF-?B in hematopoietically-derived Kupffer cells. Furthermore, treatment with an anti-IL-6 receptor antibody decreased the degree of metastatic tumor development. That is, the present inventors showed that tumor metastasis depends on inflammation, and proinflammatory intervention that targets Kupffer cells is useful for chemical prevention of metastatic tumors.

Abstract: Provided are compositions, transgenic animals and methods for screening and analyzing agents useful for treating inflammatory bowel diseases. Also provided are methods to treat inflammatory bowel disease, Crohn's disease and Blau syndrome.

Abstract: Dibenzazecines of the general formula: ##SPC1##(wherein R.sup.1 and R.sup.2 are the same or different, each representing a hydrogen atom, a hydroxy group, a lower alkoxy group, an aralkoxy group, or a hydroxymethyl group; or when adjacent to and taken together with each other, they can be an alkylenedioxy group; R.sup.3, R.sup.4, and R.sup.5 are the same or different, each representing a hydrogen atom, a hydroxy group, or a lower alkoxy group, or two of them, when adjacent and bound to each other, they can be an alkylenedioxy group; and R.sup.6 represents a hydrogen atom, an alkyl group, and R.sup.6 represents a hydrogen atom, an alkyl group, an alkenyl group, an aralkyl group or a cycloalkyl group) or acid addition salts thereof, exhibiting CNS depressant actions such as analgesic action, sedative action, and so on; which can be produced from the dibenzoquinolizines.