Sentences with phrase «model of lung cancer»

«BMI1 plays a substantial role in many solid tumors, including one of the most aggressive models of lung cancer, and its expression is linked with tumor growth, invasion, metastasis, prognosis and recurrence,» Levantini said.

Chen, X, Su, Y, Fingleton, B, Acuff, H, Matrisian, LM, Zent, R, Pozzi, A. Orthotopic models of lung cancer to follow primary and metastatic NSCLC growth in integrin α1 - null mice.

Not exact matches

«Indeed, in a second tumor model of metastatic breast cancer, we demonstrated that mice treated with the EphA2 - targeting paclitaxel conjugate presented nearly no lung metastases, while a large numbers of lesions were observed in both untreated mice and in mice treated with just paclitaxel.»

In the Cell study, Dr. Massagué, with Fellow Manuel Valiente, PhD, and other team members, found that in mouse models of breast and lung cancer — two tumor types that often spread to the brain — many cancer cells that enter the brain are killed by astrocytes.

«We developed Drosophila lung cancer models by targeting Ras alone and in combination with PTEN knockdown in the tracheal system of the fruit fly,» says Cagan, PhD, Professor in the Department of Developmental & Regenerative Biology, Senior Associate Dean of the Graduate School of Biomedical Sciences, and Director of the Center for Personalized Cancer Therapeutics at Icahn School of Medicine at Mount cancer models by targeting Ras alone and in combination with PTEN knockdown in the tracheal system of the fruit fly,» says Cagan, PhD, Professor in the Department of Developmental & Regenerative Biology, Senior Associate Dean of the Graduate School of Biomedical Sciences, and Director of the Center for Personalized Cancer Therapeutics at Icahn School of Medicine at Mount Cancer Therapeutics at Icahn School of Medicine at Mount Sinai.

A team of researchers, led by Ross Cagan, PhD, developed a multi-gene lung cancer model in the fruit fly Drosophila to better understand the mechanisms that promote tumors in NSCLC.

To test this idea, the researchers utilized two mouse models of human breast cancer metastasis and found dormant disseminated tumor cells residing upon the membrane microvasculature of lung, bone marrow and brain tissue.

To determine whether endothelial cells — the cells that line the interior surface of blood vessels — directly influence breast cancer cell growth, they then created unique organotypic models of lung and bone marrow microvascular niches, in which endothelial cells formed blood vessel - like structures in culture as they would in the original organ.

«The result was an extensive inhibition of tumor growth and prevention of metastasis to the lung in HER2 - positive animal models of breast cancer,» notes Navasona Krishnan, Ph.D., a postdoctoral investigator in the Tonks lab who performed many of the experiments and is lead author on the paper reporting the results.

The study, called «Molecular Determinants of Drug - Specific Sensitivity for Epidermal Growth Factor Receptor (EGFR) Exon 19 and 20 Mutants in Non-Small Cell Lung Cancer,» and published online in the journal Oncotarget, demonstrates how computer modeling of EGFR mutations found in lung cancer can elucidate their molecular mechanism of action and consequently optimize the selection of therapeutic agents to treat patieLung Cancer,» and published online in the journal Oncotarget, demonstrates how computer modeling of EGFR mutations found in lung cancer can elucidate their molecular mechanism of action and consequently optimize the selection of therapeutic agents to treat patCancer,» and published online in the journal Oncotarget, demonstrates how computer modeling of EGFR mutations found in lung cancer can elucidate their molecular mechanism of action and consequently optimize the selection of therapeutic agents to treat patielung cancer can elucidate their molecular mechanism of action and consequently optimize the selection of therapeutic agents to treat patcancer can elucidate their molecular mechanism of action and consequently optimize the selection of therapeutic agents to treat patients.

Their initial experiments found increased bone activity in two mouse models of a common form of lung cancer and in 70 lung cancer patients, even in absence of bone metastasis.

«Our preliminary data in cancers such as prostate, colon, liver and lung suggest a punctuated model of copy number evolution is also likely to be operative in other solid cancers,» said Navin.

The Manchester researchers tested a new drug that targets one of these molecules, MCT1, in lung cancer cells and in mouse models.

The article, titled «Entinostat Neutralizes Myeloid Derived Suppressor Cells and Enhances the Antitumor Effect of PD - 1 Inhibition in Murine Models of Lung and Renal Cell Carcinoma,» was published in Clinical Cancer Research and is available online.

2) The two repeated experiments analyze the source of POSTN expression in the lung and whether it affects the number / size of primary and secondary tumor formation in a spontaneous mouse model of breast cancer (MMTV - PyMT).

Shah and his team are currently developing similar animal models of brain metastasis from lung cancers and from melanoma.

Two of the genes modeled in this study, Pten and Nkx2.1, have been extensively studied in lung cancer.

Using the MMTV - PyMT mouse breast cancer model, which spontaneously metastasizes to the lungs, Malanchi and colleagues reported that only the CSC population, identified as CD24 + CD90 +, were capable of initiating lung metastases and secondary metastases (Guy et al., 1992; Lin et al., 2003; Malanchi et al., 2012).

We have developed pre-clinical models to identify genes, both in the tumour cells and in the microenvironment that regulate the spread of cancer to specific organs such as the liver, lungs and brain.

Navitoclax Enhances the Efficacy of Taxanes in Non — Small Cell Lung Cancer Models.

In the orthotopic breast cancer model around 12 % of tail injected iPSC - EPCs homed to the mammary pad region, while in the breast cancer lung metastasis model iPSC - EPCs were distributed predominantly to the lung region.

A 2012 paper co-authored by Ingber, for example, reported results from a study of a lung - on - a-chip model of pulmonary edema, which can affect cancer patients taking the drug interleukin - 2.

There, she used her modeling prowess to solve problems plaguing cancer treatment, focusing on a type of lung cancer, among others.

In 2012 she joined the laboratory of Dr. D.L. Konotyiannis at BSRC AL.Fleming, Greece as postdoctoral scientist, where she worked on the study of the RNA Binding Protein HuR during intestinal and lung inflammation and cancer, using inducible, KO and Tg mouse models and xenografts.

«We developed a new method of initiating lung cancer in mice, which has properties associated with human lung cancer, and used this model to identify the role of this enzyme in cancer proliferation.

Patient - derived xenograft models of non-small cell lung cancer and their potential utility in personalized medicine.

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In project on BRAF - mutant melanoma and EGFR - mutant non-small cell lung cancer, we conceived a novel drug sensitivity metric, the DIP rate, that makes it possible to incorporate drug - induced proliferation rates in predictive models of response.

In small cell lung cancer, starting from bioinformatics analyses of large gene expression datasets, we clustered subsets of co-expressed gene modules, derived networks of transcription factors and simulated their dynamics using logic - based mathematical modeling.

Life table modelling on the basis of these data estimated 33 % five year survival in 65 year old patients with early stage non-small cell lung cancer who continued to smoke compared with 70 % in those who quit smoking.

22) Taguchi A, Politi K, Pitteri SJ, Lockwood WW, Faça VM, Kelly - Spratt K, Wong CH, Zhang Q, Chin A, Park KS, Goodman G, Gazdar AF, Sage J, Dinulescu DM, Kucherlapati R, DePinho RA, Kemp CJ, Varmus HE, Hanash SM (2011) Lung cancer signatures in plasma based on proteome profiling of mouse tumor models.

In support of these findings, the APOBEC3A / B deletion was associated with young age at diagnosis among the cancer cases for both cancer forms (lung cancer: p = 0.02; dominant model and prostate cancer: p = 0.03; recessive model).

If the best oncologist in the world uses the world's best cancer model to plot the probability distribution function of my survival from the lung cancer he has just diagnosed, and I get hit my a bus on the way home from the appointment, is the model wrong?