Mouse Tumors (mouse + tumor)

Distribution by Scientific Domains


Selected Abstracts


Inhibition of heme oxygenase-1 by zinc protoporphyrin IX reduces tumor growth of LL/2 lung cancer in C57BL mice

INTERNATIONAL JOURNAL OF CANCER, Issue 3 2007
Kaeko Hirai
Abstract Heme oxygenase (HO)-1 is a key player reducing cytotoxicity and enhancing protumoral effects of nitric oxide (NO). We examined zinc protoporphyrin (ZnPP) IX, an HO-1 inhibitor, to affect tumor growth of LL/2 mouse lung cancer cells. ZnPPIX reduced HO-1 expression and HO activity in LL/2 cells, whereas cobalt PPIX (CoPPIX), an HO-1 activator, increased both. LL/2 cells treated with sodium nitropurusside, an NO donor, showed growth inhibition dose-dependently, which was enhanced by ZnPPIX cotreatment, but was reduced by CoPPIX. In mice tumors, ZnPPIX decreased HO-1 expression. LL/2-tumors were found in 88% (7/8) vehicle-treated mice, whereas tumors were found in 38% (3/8) and 25% (2/8) mice treated with 5 and 20 ,g/mouse ZnPPIX, respectively (p = 0.0302). Tumor growth was inhibited dose-dependently by ZnPPIX. Vascular endothealial growth factor concentration in tumors was reduced by ZnPPIX (p = 0.0341). Microvessel density (MVD) in ZnPPIX-treated tumors was lower than that in vehicle-treated tumors (p = 0.0362). Apoptotic cell count in ZnPPIX-treated tumors was higher than that in vehicle-treated tumors (p = 0.0003). In contrast, CoPPIX treatment increased HO-1 expression, enhanced tumorigenicity and MVD and reduced apoptosis. From these findings, inhibition of HO-1 by ZnPPIX provides relevant antitumoral effects. © 2006 Wiley-Liss, Inc. [source]


Small cell neuroendocrine carcinoma of the maxillary sinus,A case report and nude mouse transplantable model,

HEAD & NECK: JOURNAL FOR THE SCIENCES & SPECIALTIES OF THE HEAD AND NECK, Issue 5 2002
Kazuma Noguchi DDS
Abstract Background A rare case of small cell neuroendocrine carcinoma (SNEC) arising in the maxillary sinus is presented, and a SNEC tumor line serially transplantable in nude mice was established. Tumor marker for SNEC is also discussed. Methods The tumor tissues obtained from operated material were heterotransplanted subcutaneously into nude mice. Histopathologic studies and immunoradiometric assays for NSE and pro-GRP in serum were performed. Results The primary lesion was composed of tumor nests of small cells with hyperchromatic nuclei and was positive for NSE and chromogranin A immunohistochemically. Serum levels of NSE and pro-GRP changed dynamically, reflecting the clinical status. Nude mouse tumor showed similar histologic features to those of original tumor and expressed NSE. Neuroendocrine granules were detected in tumor cells in electron microscopy. Serum NSE level in nude mice was elevated in proportion to the relative tumor weight. Conclusions Serum NSE and pro-GRP were useful tumor markers for extrapulmonary SNEC. A SNEC tumor transplantable in nude mice would provide a valuable model for characterization of this lesion. © 2002 Wiley Periodicals, Inc. [source]


Tumoricidal activity of high-dose tumor necrosis factor-, is mediated by macrophage-derived nitric oxide burst and permanent blood flow shutdown

INTERNATIONAL JOURNAL OF CANCER, Issue 2 2008
Chandrakala Menon
Abstract This study investigates the role of tumor nitric oxide (NO) and vascular regulation in tumor ulceration following high-dose tumor necrosis factor-, (TNF) treatment. Using TNF-responsive (MethA) and nonresponsive (LL2) mouse tumors, tumor NO concentration was measured with an electrochemical sensor and tumor blood flow by Doppler ultrasound. Mice were also pretreated with a selective inducible nitric oxide synthase (iNOS) inhibitor, 1400 W. Tumors harvested from TNF-treated mice were cryosectioned and immunostained for murine macrophages, or/and iNOS. MethA tumor-bearing mice were depleted of macrophages. Pre- and post-TNF tumor NO levels were measured continuously, and mice were followed for gross tumor response. In MethA tumors, TNF caused a 96% response rate, and tumor NO concentration doubled. Tumor blood flow decreased to 3% of baseline by 4 hr and was sustained at 24 hr and 10 days post-TNF. Selective NO inhibition with 1400 W blocked NO rise and decreased response rate to 38%. MethA tumors showed tumor infiltration by macrophages post-TNF and the pattern of macrophage immunostaining overlapped with iNOS immunostaining. Depletion of macrophages inhibited tumor NO increase and response to TNF. LL2 tumors had a 0% response rate to TNF and exhibited no change in NO concentration. Blood flow decreased to 2% of baseline by 4 hr, recovered to 56% by 24 hr and increased to 232% by 10 days. LL2 tumors showed no infiltration by macrophages post-TNF. We conclude that TNF causes tumor infiltrating, macrophage-derived iNOS-mediated tumor NO rise and sustained tumor blood flow shutdown, resulting in tumor ulceration in the responsive tumor. © 2008 Wiley-Liss, Inc. [source]


Captan: Transition from ,B2' to ,not likely'.

JOURNAL OF APPLIED TOXICOLOGY, Issue 5 2007
How pesticide registrants affected the EPA Cancer Classification Update
Abstract On 24 November 2004 EPA changed the cancer classification of captan from a ,probable human carcinogen' (Category B2) to ,not likely' when used according to label directions. The new cancer classification considers captan to be a potential carcinogen at prolonged high doses that cause cytotoxicity and regenerative cell hyperplasia. These high doses of captan are many orders of magnitude above those likely to be consumed in the diet, or encountered by individuals in occupational or residential settings. This revised cancer classification reflects EPA's implementation of their new cancer guidelines. The procedures involved in the reclassification effort were agreed upon with EPA and involved an Independent Transparent Review as it related to four components that formed the basis of the original 1986 B2 classification: mouse tumors; rat tumors; mutagenicity; and structural similarity to other carcinogens. A Peer Review Panel organized and administered by Toxicology Excellence for Risk Assessment (TERA) met on 2,3 September 2003. The Panel concluded that captan acted through a non-mutagenic threshold mode of action that required prolonged irritation of the duodenal villi as the initial key event. EPA's Cancer Assessment Review Committee (CARC) met on 9 June 2004 and endorsed the Peer Review findings. EPA intended to have the FIFRA Scientific Advisory Panel (SAP) consider the basis for this reclassification but found the science was robust and judged that a SAP review was not warranted. Using the revised classification, the margin of exposure is approximately 1,200,000, supporting the ,not likely' characterization. Copyright © 2007 John Wiley & Sons, Ltd. [source]