Pancreatic cancer xenograft mouse model

cancerul pulmonar simptome

Received Mar 9; Accepted Apr 8. Copyright © Chi-Ming Lee et al. This is an open access article distributed under the Creative Commons Attribution Pancreatic cancer xenograft mouse model, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

This article has been cited by other articles in PMC. Associated Data Supplementary Materials S1. The error bars indicate standard error of the average.

Significance was determined by the Student t-test. All animals were humanely sacrificed after 4 weeks of monitoring due to the excessive tumor burden.

However, radiation-induced tumor cell death is limited by a number of factors, including the adverse response of the tumor microenvironment to the treatment and either intrinsic or acquired mechanisms of evasive resistance, and the existence of cancer stem cells CSCs.

Introduction Hepatocelluar carcinoma HCC represents one of the most common cancer types in the world.

pancreatic cancer xenograft mouse model

The standard treatment options for HCC often involve radiation- and chemo-therapy. Despite advances in the detection and treatment of the disease, mortality rate remains high because current therapies are limited by the emergence of radiation- and chemo-therapy-resistant cancer cells.

Existing radiation-therapies against HCC are usually developed against the bulk of the tumor mass, where although they are able to initially shrink the size of the tumor, they fail to eradicate the lesion in full, thus resulting in disease relapse.

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Recently, HCC progression has been thought to be driven by cancer stem cells CSC through their capacity for self-renewal, production of heterogeneous progeny, and resistance to radiation-therapy and to limitlessly divide.

Therefore, clarification of the radioresistance mechanism is essential for developing novel therapeutic modalities to sensitize hepatoma cells to radiation and improve patient survival.

CSCs are a subpopulation of tumors that are responsible for tumor maintenance and spreading.

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These cells are characterized to possess unlimited proliferation potential, self-renewal ability, and differentiation capability to generate progenies that constitute the major tumor population [ 2 ].

The existence of CSCs has been described in a variety of hematologic and solid tumors including those pancreatic cancer xenograft mouse model the breast, brain, colon, pancreas, lung, liver, and esophagus.

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CSCs are resistant to many current cancer treatments, including chemo- and radiation therapy [ 3 ]. In addition to driving tumorigenesis, CSCs might contribute to distant metastasis and disease relapse [ 4 ].

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This suggests that the standard interventions, while killing the bulk of tumor cells, may ultimately fail because they do not eliminate CSCs but represent a selection pressure for CSCs.

Since CSCs share similarities with stem cells, stem cell-associated surface markers have been used to identify and isolate CSCs in vitro. In addition, CSCs can form spherical colonies in suspension cultures characterized and termed tumorspheres.

Importantly, isolated CSCs exhibit increased resistance to chemotherapeutic agent and ionizing radiation [ 2 ]. Therefore, CSCs have become an important target for drug development.

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Pterostilbene has attracted much attention because it has been demonstrated to have both chemopreventive activity and tumor-killing effects similar to those of resveratrol. For instance, pterostilbene was indicated to induce cell cycle arrest and apoptosis in a variety of cancer cell lines including lung, liver, breast, and pancreas [ 7 ].

Pancreatic Cancer Overview

Recently, it has been reported that pterostilbene prevents azoxymethane- AOM- induced colon tumorigenesis in mice via suppressing cancer cell proliferation and the induction of apoptotic pathways [ 8 ]. In addition, several pharmacological properties of pterostilbene make it an ideal anticancer agent for development.

Structurally, pterostilbene contains two methoxy groups and one hydroxyl group as compared to those of resveratrol which has three hydroxyl groups.

The two methoxy groups substantially increase the lipophilicity and oral absorption of pterostilbene leading to a higher potential for cellular uptake. Furthermore, pterostilbene's half-life is also seven times longer than resveratrol, min versus 14 min [ 10 ].

Collectively, pterostilbene possesses many desired pancreatic cancer xenograft mouse model properties for the development as potential clinical agent.

Pancreatic cancer xenograft mouse model and Methods 2.

  1. Because of the central role of transcription factor nuclear factor-κB NF-κB in pancreatic cancer, we investigated the roles of NF-κB in apigenin-induced growth inhibition in pancreatic cancer cells.
  2. Глаза его отсутствующе смотрели в пространство.

  3. Cancer de prostata patologia

Materials Pterostilbene 3,5-dimethoxyhydroxystilbene, Pterostilbene was dissolved in DMSO and further diluted in sterile culture medium immediately prior to use. Cell culture and subsequent experiments were used and carried out according to the guidelines established by Environmental and Experimental Safety Committee, Taipei Medical University, Taiwan.

pancreatic cancer xenograft mouse model

The cells were placed on a 1 cm bolus and treated with a posterior-anterior direction portal to allow a 1 cm radiation buildup.