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The immune-deficient nude mouse with human tumor xenografts is an appropriate model system for performing detailed growth kinetic examinations. In the present study one estrogen and progesterone receptor-negative (T60) and three receptor-positive (Br-10, MCF-7, T61) human breast cancer xenografts in nude mice were investigated. The proliferative tumor characteristics were examined by growth curves, thymidine labelling technique, and flow cytometric DNA analysis performed on fine-needle aspirations. The results showed that the tumors had growth kinetics comparable to other human tumor types with cell generation times of 42 to 60 hours. The three receptor-positive tumors had slower growth rate, larger tumor volume doubling time, and smaller growth fraction and labelling index than the receptor-negative tumor. However, no single proliferation parameter was sufficient to characterize the growth kinetics of individual tumors or to describe proliferative differences between the tumors.
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Tumor growth was inhibited by the knockdown of TRIM28 in nude mice. (A) Representative western blot analysis of TRIM28 and β-actin proteins from PAa cells transfected with siRNAs and tumors excised from two groups. (B) The expression level of each band was measured by densitometry and normalized to the corresponding β-actin. The data represent mean SD (n=3); *P
Histology and immunohistochemistry of tumor tissues from xenografted nude mice. (A) Top, H&E staining. As indicated by the red arrow, the red-stained material in tumors from the control group is erythrocytes and the adjacent structures are blood vessels, which are rarely observed in tumors from PAa/TRIM28-siRNA treated mice (magnification, 400). Middle, immunostaining for Ki-67 (magnification, 400). Bottom, TUNEL staining (magnification, 200). (B) The percentages of Ki-67-positive nuclei was determined on four slides for each group and expressed as mean SD. (C) Analysis of the degree of apoptosis in tumors from mice. *P
Human tumor tissue from two patients with PMP was successfully implanted into the peritoneal cavity of nude mice to establish two novel, orthotopic animal models. Xenografts have retained fundamental properties of the implanted specimens through several passages, harboring strict peritoneal, noninvasive growth, absence of metastases, and almost identical morphologic appearance of tumor tissue and immunohistochemical staining patterns.
Yakushiji et al were able to grow tissue from an ovarian tumor both i.p. and s.c. in nude mice, and based on microscopic appearance it was classified as "ovarian pseudomyxoma peritonei" [15]. Although no detailed histopathological description was provided, published images certainly suggest the presence of mucinous tumor tissue, and the described growth patterns, dependable take rates and favored i.p. growth seem well in keeping with our findings. Similar to our findings, mucinous deposits were reported to be positive for alcian blue staining, and serum levels of CEA were elevated in tumor bearing mice compared to control mice, indicating relevance of CEA in this model as well. Interestingly, the authors also succeeded in utilizing the model to assess the effect of i.p. injections of cisplatin and adriamycin on tumor growth, thus confirming the usefulness of this strategy for in vivo studies of i.p. chemotherapeutic efficacy.
Histone deacetylase (HDAC) inhibition in cancer treatment is an emerging therapeutic concept. Currently, a dozen HDAC inhibitors are under investigation in clinical trials, and suberoylanilide hydroxamic acid (SAHA) has recently been approved for refractory cutaneous T-cell lymphoma. In addition to a direct antitumor activity, HDAC inhibitors have been shown to sensitize tumors to ionizing radiation in various experimental models. HDAC inhibitors cause hyperacetylation of histone proteins, which has been associated with the increased radiosensitivity, and based on in vitro studies, the presence of histone hyperacetylation at the time of radiation exposure has been suggested as a permissive requirement to achieve increased radiocytotoxicity. The aim of the present study was to experimentally evaluate the radiosensitizing properties of SAHA on in vitro clonogenicity and in vivo tumor growth and the possible requirement of histone hyperacetylation at the time of radiation exposure. When HCT116 colorectal carcinoma cells were incubated with SAHA, rapid hyperacetylation of histones H3 and H4 was observed, and removal of SAHA resulted in rapid recovery of baseline acetylation levels. The inhibitory effect of ionizing radiation on clonogenicity was improved by SAHA irrespective of the presence or absence of histone hyperacetylation. Following intraperitoneal injection of SAHA in nude mice bearing HCT116 xenografts, hyperacetylation of core histones was detected in tumors after 0.5-6 hours, while baseline levels were attained after 12 hours. Xenografts were treated for five days with daily SAHA and/or radiation (2 Gy) applied 3 or 12 hours after drug injection, and tumor growth was significantly delayed in both groups, whereas SAHA alone did not influence tumor growth. In conclusion, the HDAC inhibitor SAHA sensitized HCT116 colorectal carcinoma cells and xenografts to the therapeutic effect of ionizing radiation. Interestingly, in the current model system, this effect was independent of tumor histone acetylation status at the time of radiation exposure, suggesting that mechanisms not directly related to histone hyperacetylation are involved in tumor radiosensitization by HDAC inhibition.
Athymic nude mice (Silaike Laboratory Animal Co., Ltd, Shanghai, China) were used to assess the effect of VEGFR-1 shRNA on tumor growth and metastasis in vivo. The protocol was approved by the Animal Care and Use Committee of Xi'an Jiaotong University. Mice were divided into two groups, with six per group. Approximately 2106 cells (MDA-MB-231/shNC, MDA-MB-231/VEGFR-1 shRNA), which were suspended in 0.2 ml serum-free medium, were inoculated into the fat pad of mice. Tumor formation was measured every day. The volume of tumors was calculated using the following formula: length x width20.5. The experiments were terminated after 30 days because more than half of the mice became cachectic. Tumor-bearing athymic nude mice were observed by IVIS imaging system (IVIS spectrum, Xenogen, CA, USA) before sacrifice. The tumor tissues were removed for immunohistochemical staining.
Finally, we investigated the effect of down-regulation of VEGFR-1 expression on tumor growth and metastasis in female athymic nude mice. As shown in Figure 6A, tumors expressing shRNA against VEGFR-1 grew significantly slower than those in the control group (P
Not only is VEGFR-1 involved in angiogenesis, it also directly contributes to tumor cell survival, and thus may attribute to the development of human breast cancer [24]. Consistent with this previous report, our data showed that all six of the breast cancer cell lines tested expressed VEGFR-1. In agreement with a prior study in which VEGF had no effect of breast cancer cell motility [3], we found that exogenous VEGF did not alter the invasion capacity of MDA-MB-231 and MCF-7 cells in the transwell assay (data not shown). Since PlGF, a ligand for VEGFR-1, acts as an autocrine factor to activate the VEGFR-1 signaling pathway [42], we detected PlGF expression in conditioned media derived from breast cancer cell lines. We found that MDA-MB-231 cells expressed a high level of PlGF, while MCF-7 cells expressed less, and this correlated with their metastatic capacity. Furthermore, we found that PlGF-mediated VEGFR-1 activation promoted the migration and invasion in breast cancer cell lines, which is consistent with the report using a pancreatic cancer model [29]. However, it remains to be elucidated how PlGF activates cytoplasmic VEGFR-1 and why VEGF does not cause activation. Consistent with these results, MDA-MB-231 breast xenografts treated with VEGFR-1/shRNA showed significant suppression of tumor growth and metastasis capacity in athymic nude mice.
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