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Carcinoma pancreatic

Growth inhibition by TGF- 3, associated with inhibition of c-myc, cdks, reduction in cyclin D1 levels, and inhibition of cdk-4-associated Rb kinase activity, as well as induction of cdk inhibitors pi5 and p27, has been noted in intestinal epithelial cells. Loss of responsiveness to growth inhibition from TGF- 3 occurs in many cell types including breast, colorectal carcinoma, and pancreatic carcinoma cells. Mutational inactivation of T 3RH represents one mechanism of this process, which in many cases, leads to the development of gastrointestinal cancer. Thirteen percent of colorectal carcinomas are thought to be associated with a replication error (RER) or microsatellite instability phenotype. Subsequent inactivation of T 3RII and... [Pg.1231]

AP 12009 Antisense oligonucleotide TGF- 32 Glioma, pancreatic carcinoma, melanoma... [Pg.1232]

Data about curcunfin encapsulated in liposomes have been reported recently. The authors encapsulated curcumin into a liposomal delivery system in order to study the in vitro and in vivo effects of this compound on proliferation, apoptosis, signaling, and angiogenesis using human pancreatic carcinoma cells. Carotenoids of different polarities and in competition with cholesterol were specifically incorporated into liposomes in order to mimic the physiological uptake by cells and monitor their antioxidant capacities. ... [Pg.316]

Altomare, D.A., Tanno, S., De Rienzo, A. et al. 2003. Frequent activation of AKT2 kinase in human pancreatic carcinomas. J. Cell. Biochem. 88 470-476. [Pg.479]

As might be expected from a screen in which the target tumor was a soft tissue sarcoma, those tumors were among the most sensitive to the compound, along with ovarian tumors, mesotheliomas, melanomas, and lung carcinomas. Tumors least sensitive to this compound included pancreatic carcinomas, neuroblastomas, and especially, renal cell carcinomas. As a rule, for the seven classes of compounds identified in the screen, soft tissue sarcomas, ovarian carcinomas, and mesotheliomas were the most sensitive tumor types. [Pg.158]

VIP receptors Colonic carcinomas, gastrin carcinomas, pancreatic carcinomas, lymphomas... [Pg.267]

Moertel CG, Frytak S, Hahn RG, et at. Therapy of locally unresectable pancreatic carcinoma A randomized comparison of high dose (6000 rads) radiation alone, moderate dose radiation (4000 rads +... [Pg.40]

Many dietary and environmental factors have been implicated as possible etiologic factors in the development of pancreatic cancer, but no definite causal relationships have been established. The strongest evidence points to cigarette smoking as a risk factor associated with pancreatic cancer (20-24). Occupational exposure to certain chemicals has also been linked to pancreatic carcinoma (25). Others in the high-risk group include stone miners, cement workers, gardeners, textile workers, and leather tanners (17,26). [Pg.258]

Pancreatic carcinoma is one of the most rapidly fatal malignancies. The highest benefit will come from studies to detect early disease. Even in patients with localized pancreatic carcinoma, the curative resection rate is much less than desired and curatively resected tumors do not often result in prolonged survival of patients. A great deal of work is necessary. It would also be important to further understand molecular biology of this disease to facilitate early detection and potentially for developing more effective treatments. [Pg.262]

Nomoto S, et al. Chnical application of K-ras oncogene mutations in pancreatic carcinoma detection of micrometastases. Semin Surg Oncol 1998 15(l) 40-46. [Pg.267]

PassikSD, Breitbart WS. Depression in patients with pancreatic carcinoma. Diagnostic and treatment issues. Cancer 1996 78(3 Suppl) 615-626. [Pg.267]

Nakao A, et al. Clinical usefulness of CA-19-9 in pancreatic carcinoma. Semin Surg Oncol 1998 15(1) 15—22. [Pg.268]

GITSG, A multi-institutional comparative trial of radiation therapy alone and in combination with 5 -fluoro uracil for locally unresectable pancreatic carcinoma. The Gastrointestinal T umor Study Group. Ann Surg 1979 189(2) 205-208. [Pg.268]

Griffin JF, et al. Patterns of failure after curative resection of pancreatic carcinoma. Cancer 1990 66(1) 56-61. [Pg.268]

Robertson JM, Shewach DS, Lawrence TS. Preclinical studies of chemotherapy and radiation therapy for pancreatic carcinoma. Cancer 1996 78(3 Suppl) 674—679. [Pg.268]

Molina MA, Sitja-Amau M, Lemoine MG, et al. Increased cyclooxygenase-2 expression in human pancreatic carcinomas and cell bnes growth inhibition by nonsteroidal anti-inflammatory drugs. Cancer Res 1999 59 4356 1362. [Pg.405]

Stimulates granulocyte and macrophage production after chemotherapy Islet cell pancreatic carcinoma, malignant carcinoid tumor Breast cancer... [Pg.654]

Uniabeied Uses Treatment of mastalgia, gynecomastia, pancreatic carcinoma, ovulation induction... [Pg.1171]

Pancreatic carcinoma Lymphoma, bronchogenic carcinoma Infectious diseases AIDS... [Pg.295]

AsPC-l cell <1> (<1> pancreatic carcinoma cell line, low amount of enzyme compared to HT-1080 cells [61]) [61]... [Pg.301]

Benzyl acetate was tested for carcinogenicity by gavage in one experiment in mice and in one experiment in rats, and by administration in the diet in two studies in rats and in one study in mice. In the gavage study in mice, increased incidences of liver adenomas and of combined liver adenomas and carcinomas were oberved in animals of each sex. An increased incidence of forestomach tumours was observed in mice of each sex. An increased incidence of acinar-cell adenomas of the pancreas was observed in male rats administered benzyl acetate by gavage. Benzyl acetate did not increase the incidence of tumours in either mice or rats when administered in the diet. A low incidence of pancreatic carcinomas in situ was reported in one study. [Pg.1262]

Kamohara H, Takahashi M, Ishiko T, Ogawa M, Baba H. 2007. Induction of interleukin-8 (CXCL-8) by tumor necrosis factor-alpha and leukemia inhibitory factor in pancreatic carcinoma cells Impact of CXCL-8 as an autocrine growth factor. Int J Oncol 31 627-632. [Pg.391]

Starr AN, Vexler A, Marmor S, Konik D, Ashkenasi-Voghera M, Lev-Ari S, Greif Y, Ben-Yosef R. 2005. Establishment and characterization of a pancreatic carcinoma cell line derived from malignant pleural effusion. Oncology 69 239-245. [Pg.396]

Tsuchida, T., Kijima, H., Hori, S., Oshika, Y., Tokunaga, T., Kawai, K. et al. (2000) Adenovirus-mediated anti-K-ras ribozyme induces apoptosis and growth suppression of human pancreatic carcinoma. Cancer Gene Ther., 7, 373-383. [Pg.65]

Vishwanatha, J.K., Chiang, Y., Kumble, K.D., Hollingsworth, M.A., and P.M. Pour, 1993, Enhanced expression of annexin II in human pancreatic carcinoma cells and primary pancreatic cancers. Carcinogenesis. 14(12) 2575—9. [Pg.27]

Streptozocin Zanosar Pancreatic carcinoma Nephrotoxicity Gl distress [nausea, vomiting] blood disorders [anemia, leukopenia, thrombocytopenia] local irritation at injection site... [Pg.571]


See other pages where Carcinoma pancreatic is mentioned: [Pg.199]    [Pg.337]    [Pg.265]    [Pg.353]    [Pg.117]    [Pg.152]    [Pg.50]    [Pg.481]    [Pg.105]    [Pg.122]    [Pg.629]    [Pg.216]    [Pg.535]    [Pg.472]    [Pg.1639]    [Pg.348]    [Pg.366]    [Pg.377]    [Pg.206]    [Pg.208]    [Pg.420]   
See also in sourсe #XX -- [ Pg.203 , Pg.204 ]

See also in sourсe #XX -- [ Pg.203 , Pg.204 ]




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