Abstract | BACKGROUND: Some exocrine pancreatic carcinomas are responsive to hormonal manipulations, but the mechanism is not fully understood. MATERIALS AND METHODS: Human pancreatic cancer xenografts (PZX-15/F4) grown in immunosuppressed mice were treated with Sandostatin (2 x 100 micrograms/b.w. s.c.) for 4 weeks. Mitotic and apoptotic activities were assessed and supplemented with immunohistochemical detection of phosphotyrosine and bcl-2 protein. RESULTS: In the treated group 5/16 tumors exhibited a 20-68% volume reduction, and the number of apoptotic cells was significantly increased (18.1 +/- 3.1/mm2 vs. 6.2 +/- 1.1/mm2 in controls, P < 0.0012). At the same time, a highly significant reduction in the number of the phosphotyrosine-positive tumor cells was observed (40.9% from 64.9%; P < 0.0001). The mitotic activity did not change significantly. Both the untreated and the treated tumors proved to be bcl-2 negative. CONCLUSIONS: The results indicated that the octreotide triggered an apoptosis-induction in a human pancreatic cancer xenograft, coupled with the increased dephosphorylation state in the tumors, but the mitotic activity was not affected and bcl-2 expression has not been induced.
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Authors | A Zalatnai, V Pogány |
Journal | Anticancer research
(Anticancer Res)
2001 Jan-Feb
Vol. 21
Issue 1A
Pg. 477-80
ISSN: 0250-7005 [Print] Greece |
PMID | 11299782
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Antineoplastic Agents, Hormonal
- Phosphotyrosine
- Octreotide
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Topics |
- Animals
- Antineoplastic Agents, Hormonal
(pharmacology, therapeutic use)
- Apoptosis
(drug effects)
- Carcinoma
(drug therapy, metabolism, pathology)
- Humans
- Mice
- Mitotic Index
- Octreotide
(pharmacology, therapeutic use)
- Pancreatic Neoplasms
(drug therapy, metabolism, pathology)
- Phosphorylation
(drug effects)
- Phosphotyrosine
(metabolism)
- Xenograft Model Antitumor Assays
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