Sentences with phrase «mouse lung cancer»
The result was a highly selective drug they named SBI - 0206965, which successfully killed a number of cancer cell types, including human and mouse lung cancer cells and human brain cancer cells, some of which were previously shown to be particularly reliant on cellular recycling.
https://www.salk.edu/ 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.»
To their surprise, they found that these Th17 - deficient mice experienced far more aggressive cancer growth than normal mice — with the cancer completely smothering the lungs within 16 days.
The researchers confirmed this hypothesis by showing that if they blocked YAP1 they could inhibit stem cells from undergoing self - renewal, forming blood vessel - like structures, and reduce lung cancer cell growth in mice.
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.
Now, in a provocative study that raises unsettling questions about the widespread use of vitamin supplements, Swedish researchers have showed that relatively low doses of antioxidants spur the growth of early lung tumors in cancer - prone mice, perhaps by hindering a well - known tumor suppressor gene.
Compared to a control (left), epalrestat treatment (right) reduces the number of metastatic tumors (arrowheads) in the lungs of mice injected with human basal - like breast cancer cells.
Loss of either GSTO1 or RYR1, the researchers report, decreased the number of cancer stem cells in the primary tumor, blocked metastasis of cancer cells from the primary tumor to the lungs, decreased the duration of chemotherapy required to induce remission and increased the duration of time after chemotherapy was stopped that the mice remained tumor - free.
Dr. Shay's study closely monitored lung cancer development in mice after irradiation.
In the first series of tests, researchers found that luteolin inhibited the metastasis of triple - negative cancer in the lungs of affected mice.
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.
By using molecular genetic tools to reduce the amount of PC in human lung cancer cells, the team observed decreased cell growth, a compromised ability to form colonies in soft agar (a gelatinous material specifically used to grow bacteria and other cells), and a reduced rate of tumor growth in mice.
Over several weeks, the researchers fed mice prone to lung cancer either capsaicin or 6 - gingerol alone, or a combination of both.
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.
Both the number and activity of osteoblasts — cells that produce and reshape bone tissue — were increased within the bone marrow of mice with lung tumors compared with cancer - free animals; and reducing the number of osteoblasts in mice not only limited neutrophil infiltration of tumors but also interrupted tumor progression.
The cells exhibited many functions associated with tumor progression; their presence within mouse tumors substantially accelerated cancer growth, and in human lung tumors, a SiglecFhigh neutrophil signature was associated with poor patient survival.
The findings, now published in PLOS Genetics, reveal how mice can actually mimic human breast cancer tissue and its genes, even more so than previously thought, as well as other cancers including lung, oral and esophagus.
«For example, mouse mammary tumors shared a signaling pathway that is found in human lung cancer and controls how cells reproduce and move from one location to another.»
The Manchester researchers tested a new drug that targets one of these molecules, MCT1, in lung cancer cells and in mouse models.
Mice injected with breast cancer cells making lots of a long strand of RNA called HOTAIR developed 10 times as many lung tumors as controls (left) did.
«Molecule designed to treat lung cancer shows promising results in mice.»
In a study appearing in Science Translational Medicine, the researchers report they have effectively and safely employed this stem cell - targeting system in mice to treat metastatic breast cancer that had spread to the lung.
Using lung cancer cells and mice the scientists showed that the combination of two drugs, called TRAIL and a CDK9 inhibitor, altered the molecular switches in the cell suicide process — forcing the cancer cells to self - destruct.
They showed that it slowed the growth of human lung cancer cells but not kidney cancer cells in these mice.
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).
The first experiment is to measure metastatic lung cancer in MMTV - PyMT transgenic mice crossed with the POSTN Knock out mice, and controls, with focus on the role of periostin in metastatic progression.
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).
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.
As a result, the mice had twice as many cancer cells zipping through their bloodstream and in their lungs compared with mice not treated with paclitaxel.
The 19 NIH institutes, centers and offices contributing to the Knockout Mouse Project are: the NIH Office of Strategic Coordination / Common Fund; NCRR; the National Eye Institute; NHGRI; the National Institute of Allergy and Infectious Diseases; the National Heart, Lung and Blood Institute; the National Institute on Aging; the National Institute of Alcohol Abuse and Alcoholism; the National Institute of Arthritis and Musculoskeletal and Skin Diseases; the Eunice Kennedy Shriver National Institute of Child Health and Human Development; NIDCD; the National Institute of Dental and Craniofacial Research; the National Institute of Environmental Health Sciences; the National Institute of General Medical Sciences; the National Institute of Mental Health; the National Institute of Neurological Disorders and Stroke; the National Institute of Diabetes and Digestive and Kidney Diseases; the National Cancer Institute; and the Office of AIDS Research.
Now, in a new study in the journal Cancer Cell, Shaw and a team of scientists at the Salk Institute for Biological Studies found that phenformin, a derivative of the widely - used diabetes drug metformin, decreased the size of lung tumors in mice and increased the animals» survival.
Salk scientists found that the diabetes drug phenformin was effective at reducing tumor size in mice with lung cancer.
The dual - drug therapy — with analogs already in use for other diseases — doubled the survival rate of mice with lung cancer and halted cancer in pancreatic cells.
These images show the development of cancer (dark purple) in the mouse lung, initiated by lentiviral vector.
When they blocked IKK2 activity in the mice with lung cancer, the mice had smaller tumors and lived longer, suggesting that the enzyme is necessary for NF - KB to stimulate tumor growth.
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.
To better understand how these normally helpful components of the immune system are put to nefarious tasks in cancer cells, Verma and his colleagues developed a new method of inducing non-small-cell lung cancer in mice.
Verma has successfully developed lentiviral vector - mediated mouse models for glioblastoma, lung adenocarcinoma and small cell lung cancer (SCLC).
The experimental metastasis assay we detail here includes tail - vein injection of cancer cells into the mouse and determination of the resulting secondary organ colonization, primarily in the lung, 10 d post dosing.
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 this study, human lung cancer cells with additional copies of the opioid receptor grew more than twice as fast as tumor cells that lacked extra receptors when transplanted into mice.
Furthermore, by combining this information with the characterization of mice genetically engineered to develop lung tumours, we attempt to elucidate the key genes driving lung cancer initiation, progression and response to therapy.
Bench and mouse studies have shown that the Notch1 gene is a crucial contributor to tumorigenesis in non — small - cell lung cancer (NSCLC).
One study presented in the journal — from a group led by Patrick Singleton, PhD, assistant professor of medicine at the University of Chicago Medicine — shows how opioids already present in the body can enhance the malignant tendencies of human lung cancer cells transplanted into mice, even without the addition of morphine.
Finally, to determine whether LARP7 KD also results in an increase in breast cancer metastasis in vivo, the T47D control or shLARP7 - 2 cells were injected intravenously into the nude mice, and lung metastasis was examined 12 weeks later.
National Cancer Institute research has shown that phytochemicals known as indoles found in kale «inhibit the development of cancer in several organs in rats and mice, including the bladder, breast, colon, liver, lung, and stomach.&Cancer Institute research has shown that phytochemicals known as indoles found in kale «inhibit the development of cancer in several organs in rats and mice, including the bladder, breast, colon, liver, lung, and stomach.&cancer in several organs in rats and mice, including the bladder, breast, colon, liver, lung, and stomach.»
The media has given an astounding amount of attention to a recent study that found vitamin E may increase tumor progression, and accelerate lung cancer, in mice.1
«Lung tumors in strain A mice: application for studies in cancer chemoprevention.»
In Wisconsin, a group of researchers conducted a study using mice to see if adding pomegranate juice to their diet made a significant impact on lung cancer cells.