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Recent News and Articles on the Keywords: brain tumor + mit + 0.31  Related to the article below (Last Update: 8/5/2008)

Your cell phone has the power to kill you or save your life.
Chicago Tribune, United States - Jul 24, 2008
Gap in safety data: Researchers are fairly certain that the use of mobile phones for up to 10 years is not associated with brain tumor risk, ...
NCI to Roll Out Cancer Molecular Analysis Portal to Integrate ...
bio1nf0rm (subscription), NY - Jul 18, 2008
?The reason for lining this up right after TCGA is to enable comparisons and correlations between two brain tumor datasets and neuro-oncologists will ...
Risky Business
American Spectator - Jul 29, 2008
By Gregory Conko Senator Ted Kennedy returned to the Capitol recently following successful surgery to remove a tumor from his brain. ...
Imoukhuede tackling postdoctoral fellow at John Hopkins
Southtown Star, IL - Jul 27, 2008
MIT is where Imoukhuede earned her bachelor's of science degree while researching brain tumor medication among other pursuits. Imoukhuede said she was drawn ...
Megliola: The strength of family
Daily News Tribune, MA - Jul 26, 2008
Might be a brain tumor, the doctors thought. An MRI showed none. They took Billy to Children's Hospital. The doctors came up with three different diagnoses, ...
Three Pharma Giants Bankroll Newcomer To Develop PGx Tools for ...
Pharmacogenomics Reporter (subscription), NY - Jul 23, 2008
?An example would be a drug delivery technology that addresses a specific problem ? [for instance] delivery across the blood brain barrier ? that can be ...
Washington gets an ?Aha!? moment
Plant Services, IL - Jul 11, 2008
That was two weeks before we heard the news about his brain tumor. I cherish those moments even more now, and pray for him and his family after hearing ...
Source: Google News

Chemotherapy in experimental brain tumor, part 1: In vitro colorimetric MTT assay -
CM Hand, JR Vender, P Black - Journal of Neuro-Oncology, 1998 - Springer
... VP-16 0.31?80 ?M ... MIT 7.8?1000 nM ... this would expand the range of ex- perimental options
for the study of chemother- apeutic agents for human brain tumor. ...

Postoperative venous thromboembolism and brain tumors: part II. Hemostatic profile -
R Sawaya, P Glas-Greenwalt - Journal of Neuro-Oncology, 1992 - Springer
... Plasminogen activator inhibitor-1 14 0.31 0.26 ... associated with removal of a primary
brain tumor. ... zur Fibrinolyse bei Patienten mit metastasierended Malignomen ...

Uptake of 51 Cr-?-glycerophosphate by experimental brain tumor -
LJ Anghileri - Journal of Cancer Research and Clinical Oncology, 1969 - Springer
... yon 72 Std speicherte der Tumor, wenn mit Hirn verglichen ... 12 0.10? 2.461.23
1.75:J=0.31 2.852.97 ... Uptake of sCr-fl-Glycerophosphate by Experimental Brain Tumor ...
-

… (E. coli) injection on HSP70 levels in the liver and brain of adrenalectomized rats -
… , PEN Giviziez, JA Ferro, MIT Ferro, M Macari - Journal of Thermal Biology, 1999 - Elsevier
... Mol. Brain Res. 34, pp. ... Effect of heat stress on LPS-induced fever and tumor necrosis
factor. Am. ... Macari, M., Gabriel, JE, Ferro, JA and Ferro, MIT, 1997. ...

… and tamoxifen of the growth of an estrogen dependent transplantable pituitary tumor (MtT/F84) in … -
A Ito, K Kawashima, N Fujimoto, H Watanabe, M … - Cancer Res, 1985 - AACR
... A mixture of 0.06 ml tumor cell and brain homogenate was inoculated into 1 to 5
different sites per rat at subcutaneous fat ... tumor strain MIT/F84 through ...

Survival and Prognostic Factors in Patients with Brain Metastases from Malignant Melanoma -
S Meier, BG Baumert, T Maier, G Wellis, G Burg, B … - Onkologie, 2004 - content.karger.com
... wird in der Zukunft bei Patienten mit Hirnmetastasen vom ... 22], location of the primary
tumor [22], Clark ... histological type [23], number of brain metastases [6 ...

[PDF] Selectivity of 18 F-FLT and 18 F-FDG for differentiating tumor from inflammation in a rodent model -
A van Waarde, DC Cobben, AJ Suurmeijer, B Maas, W … - J Nucl Med, 2004 - mips.stanford.edu
... Rest of brain 0.06 0.01 0.04 0.02 1.45 0.33 NS 0.001 ... Submandibularis 0.31 0.11 0.34
0.17 1.18 0.30 NS 0.001 C6 tumor 0.55 0.06 1.14 0.62 2.34 0.72 NS 0.05 ...
-

Comparison of Tumor Uptake and Kinetics of Different Radiopharmaceuticals Under Experimental … -
D Emrich, A M?hlen, F Willgeroth, A Lammich - Acta Oncologica, 1972 - informaworld.com
... Page 4. TUMOR UPTAKE AND KINETICS OF DIFFERENT RADIOPHARMACEUTICALS 569 Table 2
(cont.) ... 0.36 0.22 10.02 *0.02 0.34 0.25 10.02 10.03 0.89 0.31 *0.06 f0.03 ...

Laterality of Brain Tumors -
PD Inskip, RE Tarone, EE Hatch, TC Wilcosky, RG … - Logo, 2003 - content.karger.com
... Glioblastoma and gliosarcoma 99 114 17 11 241 0.87 0.31 Anaplastic astrocytoma
28 32 64 70 0.88 0.6 1 ... Page 4. Brain Tumor Laterality ...

Movement-associated cortical potentials in unilateral cerebral lesions -
H Shibasaki - Journal of Neurology, 1975 - Springer
... oder Faust- machen, wurden bei 20 Patienten mit unilateralen cerebralen ... These 2 patients
had brain tumor. ... and the frequency of MP abnormalities (P ---- 0.31). ...

Source: Google Scholar

MIT IDs Link Between Brain Tumor Proteins Work Could Guide Drugs For Especially Aggressive Cancer
MIT researchers have identified a critical link between two proteins found in brain tumors, a discovery that could eventually help treat a form of brain cancer that kills 99 percent of patients.

Glioblastoma multiforme (GBM), the most aggressive brain tumor in adults, strikes about 15,000 people in the United States each year. GBM is currently treated with a combination of surgery, radiation and chemotherapy, but those treatments have proven ineffective. Most patients die within a year.

Now, MIT scientists have uncovered a connection between two proteins found in the tumor cells, and they have demonstrated that attacking both of those proteins kills tumor cells much more effectively than targeting either one alone.
The researchers, led by Forest White, MIT associate professor of biological engineering, report their findings in the early online edition of the Proceedings of the National Academy of Sciences for the week of July 16-20.

Their work could guide drug developers seeking treatments for GBM, which has proven resistant to all drugs that have been tried against it.

The team focused on a protein called EGFRvIII, a mutated form of the cell receptor for epidermal growth factor (EGF). The mutated receptor, which is found in approximately a quarter of GBM tumors, is continuously active and relentlessly pushes cells to keep growing and dividing.

Doctors have tried treating GBM patients with drugs that inhibit EGFRvIII, but they have had little effect. This could be because the continuous stimulation of the receptor is so intense and because the receptor interacts with numerous other proteins that also promote tumor growth, said White, who is also affiliated with MIT's Center for Cancer Research and its Computational and Systems Biology Initiative.
The researchers believe it is the cumulative action of EGFRvIII and those other proteins that leads to tumor growth.

"It seems that it is not the activation of one receptor that results in cancer. It's the action of multiple receptors that leads to the tumors we see," said Paul Huang, a graduate student in biological engineering and lead author of the paper. "A potential way to overcome this is to attack multiple targets instead of just one."

To find out what other proteins are involved in tumor growth, the researchers used a tool known as mass spectrometry to analyze the network of proteins activated by EGFRvIII in GBM tumor cells.

They found that when EGFRvIII is activated, so is another receptor called c-Met. C-Met is normally active during human development, but it's turned off in most adult cells.

Until now, there had been no evidence of any "cross-talk" between c-Met and EGFRvIII in GBM. This discovery could offer an explanation for why GBM tumors are so invasive, because over-activated c-Met has already been implicated in very invasive types of lung and breast cancers.
The researchers don't know yet how EGFRvIII is activating c-Met, and whether other proteins are involved in the activation.

"The mechanism underlying this control has yet to be fully characterized," said White. "Our data shows that as EGFRvIII is activated, c-Met is activated as well. Whether it's direct, or indirect, is something that we are currently deciphering."

The new knowledge of c-Met's involvement could give researchers a potent tool to attack GBM tumors. When the MIT group treated tumor cells with drugs that inhibit EGFRvIII and c-Met, respectively, much lower doses were required to kill the cells than when either drug was given alone.

There are several EGFRvIII inhibitors in clinical trials now, and some have already been approved to treat other cancers. Drug companies are also working on c-Met inhibitors, and Huang estimated that some might be available in five to 10 years.

Other MIT authors on the paper are Ryan Flynn, a sophomore biology major, and Zachary Brewer, a senior chemical engineering major. This work was performed in collaboration with researchers at the Ludwig Institute of Cancer Research (San Diego Branch) led by Webster Cavenee and Frank Furnari. The research was funded by the National Cancer Institute, the National Institutes of Health and the Goldhirsh Foundation.

By Anne Trafton

Massachusetts Institute of Technology
 
 
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