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A experiment about BCAR3 breast cancer anti-estrogen resistance 3

Observe the relationship tamoxifen resistant breast cancer cells BCAR3 breast cancer anti-estrogen resistance expression and epithelial-mesenchymal transition (EMT) phenomena and migration of breast cancer invasion. Explore the correlation of tamoxifen resistance and breast cancer cell EMT phenomenon. Detection of breast cancer: real-time quantitative PCR and Westernblot epithelioid and mesenchymal-like cell lineBCAR3 breast cancer anti-estrogen resistance 3 expression; Westernblot detect breast cancer MCF27 MCF2BCAR3 and BT2549 mediate EMT transcription factor Twist epithelial marker genes E2 cadherin change of the hormone (E2cadherin) and interstitial marker genes N2 the cadherin (N2cadherin) expression. Transwell invasion assay detection of breast cancer MCF27, MCF2BCAR3 and BT2549 invasion and metastasis. Results: BCAR3 breast cancer anti-estrogen resistance 3 in breast epithelial-like expression in the cell lines was significantly lower than the mesenchymal-like cell line; the MCF27 cell, protein E2cadherin expressed as positive, negative Twist, and N2cadhern expression; tamoxifen Fen-resistant cells MCF2BCAR3 E2cadherin protein is missing, while the Twist and N2cadherin expression positive. BCAR3 breast cancer anti-estrogen resistance 3 overexpression led to the migration and invasion of breast cancer cells MCF27 enhanced. Conclusion: The overexpression BCAR3 enhance breast cancer cell migration and invasion, and tamoxifen treatment become resistant, may BCAR3 induced breast epithelial-mesenchymal transition-related.
9.9.12 10:50


DC vaccine treatment of glioma has broad prospects

Dendritic cells (Dendritic Cells, DCs) vaccine treatment of cancer has developed rapidly in recent years, made ​​a very important result. The the Center Chief tumor immunology expert from the University of Michigan Professor Li Jiao further pointed out that in 2010 dendritic cell vaccine Dendreon's Provenge was approved by the U.S. Food and Drug Administration (FDA) to market, the flower of the 2011 Nobel Prize in Medicine off DC's Father, Professor Steinman is very a landmark event. Recently, a number of application of DC vaccine therapy glioma study was published, announced. In March 2011, "Clinical Cancer Research" magazine published the results of an application of a dendritic cell vaccine for treatment of glioblastoma. The study shows that, after receiving immunosuppressive therapy achieved very good results, and median overall survival of 31.4 months was significantly higher than conventional radiotherapy and chemotherapy patients 18.6 months, and patients with primary GBM patients were followed up for more than 6 years. Than the above studies simply load glioma cells, glioma stem cell center DC vaccine load a glioma cells and glioma stem cell treatment in principle, from the source to prevent glioma recurrence of this glioma therapy bottlenecks and improve the overall efficacy of glioma treatment worth the wait.
6.9.12 05:42

Spinal cord tumors

Spinal tumors (intraspinaltumor) originated in a variety of tumor-like lesions of the spinal tissue such as spinal cord and nerve roots meninges or vertebrae. The incidence of tumors in pediatric spinal significantly reduced compared with intracranial tumors occur in the more common adult meningioma and neurofibroma embryonic remnant tumor (epidermoid cyst, dermoid cyst) in children is particularly rare childhood. The main clinical manifestations of spinal tumors can occur in the spine of any segment of the the tumor plane where the nerve root damage and below the level of long tract involvement signs and symptoms.

Spinal tumor is a growth in the spinal various organizations, such as the spinal cord, meninges, nerve roots, blood vessels and fatty tissue of the primary or secondary tumor.

1887 with Gower and Horsley First cut spinal cord tumors success. Elsberg (1925), brought together clinical experience in the diagnosis and treatment of spinal cord tumors in the tumor of the spinal cord in the monograph. With the rapid progress since 1921 Sicard and Forestier open up myelography, spinal cord tumors. In recent years, with ongoing selective spinal angiography and microsurgical techniques, the diagnosis and treatment of spinal cord tumors can be said that a landmark entered a new era.

Spinal tumor incidence 2.5 / 100,000 population, according to foreign statistics for domestic accounts for about 2.5% of the inpatients disease of the nervous system. 1:6 - 10.7) compared with intracranial tumors. Such as the spinal cord and brain volume ratio 1:8, the that both tumor is considerable. Spinal tumor is not rare, and the vast majority are benign tumors, early diagnosis and treatment, the efficacy is satisfied.
4.9.12 13:13

The drug vandetanib increases Deterioration of the disease-free survival of thyroid cancer patient

Advanced differentiated thyroid cancer (advanced differentiated thyroid cancer, DTC) patient Phase II randomized clinical trial results showed that the receiving oral targeted drug vandetanib (vandetanib) treatment of patients without disease progression survival than placebo-treated those patient long nearly doubled (11.2 months, 5.9 months). The findings, published online in the journal Lancet Oncology, is the first to provide clear evidence that the use of targeted drug vandetanib in patients with advanced differentiated thyroid cancer can extend a patient's disease-free progression-free survival (on progression free survival, PFS) . For now, it does not exist yet effective treatment from the treatment of this cancer. In the past 10 years, the incidence of thyroid cancer in the world more than doubled. Recently, multi-target kinase inhibitor (multi-targeted kinase inhibitor) is becoming a promising treatment of advanced differentiated thyroid cancer drug candidate, but until then, scientists have never carried out, placebo-controlled clinical trial research. Martin Schlumberger and colleagues from France, Gustave - Roussy (Institut Gustave Roussy) In this study, aimed at determining the vandetanib --- The drug targeting known in the growth of thyroid cancer and play a role in the proliferation of protein: endothelial growth factor receptor (endothelial growth factor receptor, EGFR) and the vascular endothelial growth factor (vascular endothelial growth factor, VEGF) and infection during the rearrangement of the original oncogene RET (rearranged during transfection protooncogene ) --- whether the impact of the deterioration of the disease-free survival and overall survival (overall survival, OS). In this study, researchers randomized to 145 from seven European countries with advanced differentiated thyroid cancer assigned to two groups: 72 patients received 300 mg daily vandetanib treatment; 73 patients placebo treatment. Compared with the placebo-treated group of patients, taking vandetanib patients without disease progression-free survival was significantly improved (increased from 5.9 months to 11.1 months) is associated. 6 months after treatment, compared to placebo-treated group of patients receiving vandetanib therapy patients also have more good disease control rate (as disease control rate, DCR). Patients, however, does not exist in the overall survival significantly different from Interestingly, vandetanib treatment, people with the more common papillary thyroid carcinoma (papillary thyroid cancer, PTC) patients have than follicular thyroid carcinoma (follicular thyroid cancer, FTC) patients and differentiated thyroid cancer (the first two median disease-free progression-free survival was 7.7 months) and long disease progression-free survival (median disease-free progression-free survival of 16.2 months). Accept the to vandetanib treatment of patients also experienced more side effects, especially the QT interval (QTc) to extend the time to increase, diarrhea, weakness and fatigue. The group of patients receiving vandetanib treatment, there are two patients with treatment-related death. These results indicate that the van der his Nicole can be a potentially effective treatment options to maintain a stable condition advanced differentiated thyroid cancer, particularly papillary thyroid cancer. However, more research is needed to better illustrate kinase inhibitors may be the most effective of which advanced differentiated thyroid cancer, in order to develop a personalized therapy to treat advanced differentiated thyroid cancer.
3.9.12 08:21

microRNA-7 reduces expression of FAK to suppress breast cancer metastasis

August 13, 2012 News / Bio Valley BIOON / - focal adhesion kinase (FAK) is an extracellular matrix integrin signaling and cell motility, cell proliferation and cell survival regulatory factors. FAK expression in a variety of solid tumors are proved to be significantly increased, increased in tumor metastasis and poor prognosis of FAK expression is closely related. PLoS ONE recently published a study found that miR-7 can directly regulate FAK expression. Compared to normal breast tissue, miR-7 expression in malignant tissue is reduced, and miR-7 expression in patients with breast cancer metastasis is inversely proportional. miR-7 expression rates will increase the expression of E-cadherin in breast cancer cells, lower expression of fibronectin and vimentin. The expression levels of miR-7 and E-cadherin expression was positively correlated with vimentin expression levels in breast cancer samples were negative correlation. MiR-7 expression increased invasive breast cancer cell lines, and inhibition of tumor cell proliferation, anchorage independent growth capacity as well as migration and invasion. In contrast, inhibition of mammary epithelial cell line HBL-100, miR-7 expression promotes cell proliferation and anchorage independent growth capacity. Recovery of FAK expression of miR-7 can reverse the inhibition of breast cancer cell migration and invasion. miR-7 can also inhibit the development of breast cancer xenografts in nude mice with primary breast tumors, local invasion and metastasis. Therefore, metastatic breast cancer miR-7 expression decreased tumor epithelial cell differentiation level, can inhibit metastatic tumor progression.
1.9.12 08:19

Cancer cells can activate the molecular mechanisms of oncogene expression by "hijacking" activities

August 16 2012 News / Bio valley BIOON / - Recently, researchers from the University of South Florida and Moffitt Cancer Center found a molecular mechanisms of cancer cells, can reveal how certain types of cancer cells "hijack" the body's biological response process to activate the growth of cancer cells as well as the expression of oncogenes. Related to study results published in a recent issue of the international magazine Nature Structural & Molecular Biology. This newly discovered mechanism involving histone class, histone cells in a class of strongly basic protein, can wrap DNA and its sort. Histone H2B in chromatin structure, one of five main histone. Chromatin in eukaryotic cells by DNA and proteins, and which constitutes the nucleus of the eukaryotic cell contents. The eukaryotic cells can be a variety of mechanisms to maintain the richness of histone at an appropriate level, wherein a mechanism is that the cells, once completed the synthesis of DNA, then histone transcription or synthetic stops, however the cell how to terminate histone the synthesis of the researchers do not know. The research team found that an histone modification can regulate its own synthesis, this modification is H2B 37 tyrosine phosphorylation, which is very important for the core histone mRNA synthesis inhibition. In additional experiments in mammals and yeast cells, the researchers confirmed their discovery mechanism is widespread and in evolutionary conserved. When the researchers found that the tyrosine kinase WEE1, cancer occurrence is beginning to emerge. The tyrosine kinases are a group transfer of a phosphate group, and enzymes play switch roles in cell function, which can adjust the critical cellular processes, including cell growth, proliferation and differentiation. Researchers Mahajan explained, we found WEE1 tyrosine kinase phosphorylation in mammalian cells and yeast cells H2B. WEE1 protein levels in the cell is tightly adjusted, and its role in the cell cycle in a very sturdy. The researchers found that WEE1 is a novel histone H2B regulon can be suppressed H2B, destroy its function, and ultimately lead to the lack of phosphorylation of H2B Tyr, and ultimately increase the transcription of multiple core histone gene. The data reveal a previously unknown mechanism that is Tyr (tyrosine) phosphorylated histone H2B and functional assessment. The study also reveals WEE1 previously unknown function, can be used as a cell regulator, plays a dual role in maintaining histone transcriptional level. WEE1 expression increased in glioblastoma and triple negative breast cancer, can reveal the molecular mechanisms of cancer cells by "hijacking" to reduce the levels of histone ultimately activate cancer cell growth and proliferation.
28.8.12 08:57

The target inflammation precipitating factor prevention and treatment of cancer

August 24, 2012 - / biological Valley BIOON / - Georgia Health Sciences University Cancer Center researchers found a gene that can destroy the liver cancer-related inflammation. Laboratory mice that lack this gene missing promote inflammatory protein TREM-1 makes its own exposure to carcinogens freedom from suffering from liver cancer. The study, published in the Journal of Cancer Research of the American Association for Cancer Research The GHSU Cancer Centre immunologist Dr. Anatolij Horuzsko, said: The study may be beneficial to develop cancer drugs targeting TREM-1. Horuzsko said: We have always thought that chronic inflammation in the initial stage of the cancer is a very powerful tool to promote tumor development or metastatic cancer. We focus on molecules that control the inflammatory response, in order to better understand how this process is to play a catalytic role in the tumor. We found that one important inflammatory trigger TREM-1 receptor. TREM-1 primarily in viral or bacterial infection, such as against the trigger inflammation, and play an important role in the maintenance of normal tissue function. However, Horuzsko research team found that liver function damage caused under normal circumstances, such as abuse of alcohol or other irritants, TREM-1 generation is out of control. TREM-1 leads to the generation of other inflammatory factors resulting in a chronic, low phase of the inflammatory response, which will result in more damage to the cells, causing the cells to mutate. Then these mutant cells will lead to the occurrence of cancer proliferation and growth. Of TREM-1 role in the last 14 months of the study period, Horuzsko and his team used a mouse model of liver cells in mice life is about three years, the length of study time set to imitate the human hepatoma 20 30-year stage. Experimental design the two groups of mice, a group of the TREM-1 knockout, a group of normal, two groups of mice were exposed to a carcinogenic agent diethylnitrosamine, diethyl nitrosamine is present in tobacco smoke chemical substances. Injection of diethylnitrosamine just 48 hours, the control group of mice liver cells damage and death in the Kupffer cells TREM-1 expression at a high level. These particular liver cells destroy bacteria and damaged red blood cells. 8 months later, these mice also appeared in a large area of ​​the liver tumors. However, excluding the TREM-1 gene in mice remain healthy, the symptoms appear very little, if any and subject to eight months time slowly tumor. The only difference between the two groups of Kupffer cells in the existence of TREM-1. Horuzko team hope for TREM-1 results as well as a potential cancer therapeutic strategy can also be applied to other cancers. TREM-1 may be a treatment of inflammation-related cancer target. Horuzsko said: In the future, we can use the targeting TREM-1 drug in the body to treat cancer. Currently we have been working in this direction. The state-of-the-art cancer treatment drugs is a growing field of research, immunotherapy is an important part of cancer treatments. In addition, the Horuzsko the research team also found that another potential drug therapeutic targets that liver cell damage and death of the product of HMGB1. HMGB1 is a previously unknown stimulus Kupffer cells produce the activating ligand of the TREM-1 protein and start the process of inflammation.

24.8.12 10:21

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