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Tumor stromal

Aghi M, Cohen KS, Klein RJ, Scadden DT, Chiocca EA (2006) Tumor stromal-derived factor-1 recruits vascular progenitors to mitotic neovasculature, where microenvironment influences their differentiated phenotypes. Cancer Res 66 9054-9064... [Pg.266]

Kawada, M, H Inoue, T Masuda, and D Ikeda. 2006. Insulin-like growth factor 1 secreted from prostate stromal cells mediates tumor-stromal cell interactions of prostate cancer. Cancer Res 66(8) 4419 I425. [Pg.461]

In this chapter, an account is given of well established and new methods that allow insight into the capacity of cells (tumor, stromal or immune) to degrade components of the extracellular matrix (ECM) and then overcome the anatomical barriers they face during invasion. [Pg.97]

Gleave, M., Hsieh, J. T., von Eschenbach, A. C. and Chung, L. W. (1992). Prostate and bone fibroblasts induce human prostate cancer growth in vivo implications for bidirectional tumor-stromal cell interaction in prostate carcinoma growth and metastasis. J. Urol. 147, 1151-1159. [Pg.294]

Provenzano PP, Eliceiri KW, Campbell JM, Inman DR, White JG, Keely PJ (2006) Collagen reorganization at the tumor-stromal interface facilitates local invasion. BMC Med 4 30... [Pg.91]

Tumor-Stromal Interaction in Colon Cancer Invasion ... [Pg.65]

Confident distinction between primary and metastatic ovarian cancers is not possible because of overlapping findings in imaging. Bilateral, sharply delineated, purely solid or predominantly solid tumors with necrosis strongly favor the diagnosis of a metastatic ovarian tumor, most likely Krukenberg tumors [68]. Contrast uptake aids in the differentiation of solid ovarian metastases from stromal tumors. Stromal tumors typically display a mild and delayed contrast uptake [69]. If metastases are cystic... [Pg.260]

When the chemosensitive human pancreatic carcinoma cell lines T3M4 and PT45-P1 were kept in coculture with fibroblasts, both cell lines became much less sensitive toward treatment with etoposide. The chemoresistant future of T3M4 and PT45-P1 cells was increased by the NO production from neighboring fibroblasts which exhibited significant iNOS expression and NO secretion. This suggests that there were tumor-stromal fibroblast interactions in the chemoresistance of pancreatic carcinoma due to NO production (Muerkoster et al. 2004). [Pg.122]

S unitinib (Sutent ) Pfizer TKI VEGFR, PDGFR, KIT, FLT-3, RET 1 matinib-resistant KIT overexpressing unresectable or metastatic gastro-intestinal stromal tumor... [Pg.1193]

E. (1978). The lymphatic spread of ovarian germinal and stromal tumors, Lymphology, 11, 22-26. [Pg.329]

Chemokines serve as the messengers in a reciprocal relationship that exists between brain tumors and their environment (Fig. 11.1). Brain tumors are dependent upon stromal sources of chemokines for their growth and spread. They also use chemokines... [Pg.265]

Barbero S, Bajetto A, Bonavia R, Porcile C, Piccioli P, Pirani P, Ravetti JL, Zona G, Spaziante R, Florio T, Schettini G (2002) Expression of the chemokine receptor CXCR4 and its ligand stromal cell-derived factor 1 in human brain tumors and their involvement in glial proliferation in vitro. Ann NY Acad Sci 973 60-69... [Pg.266]

The three major pathologic categories of ovarian tumors include sex-cord stromal, germ cell, and epithelial. About 85% to 90% of ovarian cancers are of epithelial origin. [Pg.1388]

Tumor necrosis factor a (TNF-a) is a multifunctional cytokine produced by activated monocytes-macrophages. TNF-a is one of the most potent osteoclastogenic cytokines produced in inflammation, and, in addition, TNF-a induces IL-1 synthesis. Like the other known stimulators of bone resorption, it acts through osteoblastic cells however, it has been demonstrated that TNF-a is able to induce osteoclast formation from stromal-depleted macrophages, with potency similar to that of RANKL (Kobayashi et al. 2000). TNF-a is able to induce bone resorption in vitro (Thomson et al. 1987) as well as in vivo (Koning et al. 1988). Osteoclasts induced by TNF-a have the capacity to form resorption pits on dentine slices only in the presence of IL-la. TNF-a, together with IL-1, plays an important role in bone resorption in inflammatory diseases (Kobayashi et al. 2000). Inhibition of TNF by TNF binding protein (TNFbp) completely prevents bone loss and osteoclast formation (Kimble et al. 1997). [Pg.176]

Kimble RB, Srivastava S, Ross FP, Matayoshi A, Pacifici R (1996) Estrogen deficiency increases the ability of stromal cells to support murine osteoclastogenesis via an interleukin-land tumor necrosis factor-mediated stimulation of macrophage colony-stimulating factor production. J Biol Chem 271 28890-28897... [Pg.192]


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See also in sourсe #XX -- [ Pg.97 ]




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