April 15, 2007, 8:53 PM CT

MicroRNAs as tumor suppressors

In the May 1st issue of G&D, Drs. Yong Sun Lee and Anindya Dutta (UVA) reveal that microRNAs can function as tumor suppressors in vitro.

"Overexpression of HMGA2 is an important feature of a number of medically important tumors like uterine fibroids, explains Dr. Dutta. It is very exciting to realize that microRNAs have an important role in suppressing the overexpression of HMGA2, and so may have a role in the causation and perhaps the cure of a disease that is responsible for the vast majority of hysterectomies in the Western world".

Studying chromosomal HMGA2 translocations that are linked to human tumors, the scientists observed that in normal cells, a microRNA called let-7 binds to the 3 end of the HMGA2 mRNA transcript and suppresses its expression in the cell cytosol. However, chromosomal breaks that shorten the 3 end of the HMGA2 transcript, and prevent let-7 binding, result in aberrantly high levels of HMGA2 expression and tumorigenesis. This paper establishes that HMGA2 is a target of let-7, and that the let-7 microRNA functions as a tumor suppressor to prevent cancer formation in healthy cells......... Posted by: Jesmi24      Read more         Source

April 11, 2007, 11:02 PM CT

Deadly Secrets Of Ovarian Cancer

A new University of Michigan Medical School study sheds light on cell defects that lead to one common type of ovary cancer and puts forth a promising new mouse model that already is being used for preclinical drug testing.

The study, reported in the recent issue of Cancer Cell, focuses on ovarian endometrioid adenocarcinoma, the second most common form of a baffling, deadly disease for which early detection methods and effective therapys have been elusive so far. The American Cancer Society estimates there will be 22,430 new cases of ovary cancer and 15,280 deaths from the disease in the United States this year.

The new mouse model developed in the U-M lab is based on molecular defects shown to be present in human ovarian tumor cells, says senior author Kathleen R. Cho, who treats patients as a member of the U-M Comprehensive Cancer Center. Chos and others existing mouse models, if designed to mimic the four major types of ovary cancer, should provide key tools for learning how gene mutations and cell changes lead to disease, and for finding therapys during ovary cancers early stages, when therapys are most likely to be effective.

"We need models to do preclinical testing of new drugs that target the specific molecular defects in a patients tumor cells," says Cho, a professor of pathology and internal medicine at the U-M Medical School. Using the genetically engineered mice her lab developed, one preclinical study is already under way, testing an existing drug called Rapamycin. The labs mouse model can also be used to test new drug candidates that inhibit the cell-messaging systems defective in ovarian endometrioid adenocarcinoma......... Posted by: Jesmi24      Read more         Source

April 1, 2007, 9:19 PM CT

Genetic Risk Factors For Prostate Cancer

A study led by researchers at the Keck School of Medicine of the University of Southern California (USC) and Harvard Medical School has identified seven genetic risk factorsDNA sequences carried by some people but not othersthat predict risk for prostate cancer. According to the study's findings, these risk factors are clustered in a single region of the human genome on chromosome 8 and powerfully predict a man's probability of developing prostate cancer. The paper would be published in the online edition of Nature Genetics on April 1.

"The study has identified combinations of genetic variants that predict more than a fivefold range of risk for prostate cancer," says senior author David Reich, assistant professor of genetics at Harvard Medical School and associate member of the Broad Institute of Harvard and MIT. "Both high- and low-risk combinations of variants are common in human populations".

"The identification of these genetic variants is an important step in helping us understand the higher risk for prostate cancer in African Americans compared with other U.S. populations and, more importantly, why some men develop prostate cancer and others do not," says lead author Christopher Haiman, assistant professor of preventive medicine at the Keck School of Medicine of USC......... Posted by: Jesmi24      Read more         Source

March 29, 2007, 10:40 PM CT

Protein Averts Cell Suicide

Scientists have discovered how an unusual protein helps a cell bypass damage when making new DNA, thereby averting the cell's self-destruction.

But they also discovered that this protein, an enzyme called Dpo4, often makes errors when copying the genomic DNA sequence that later might cause the cell to become cancerous.

The findings by researchers with Ohio State University 's Comprehensive Cancer Center are described in two back-to-back papers in The Journal of Biological Chemistry.

"Unrepaired DNA damage presents a big roadblock for the DNA replication machinery, which cannot go around it," says Zucai Suo, assistant professor of biochemistry. "This damage will trigger cell death because the DNA is not replicated.

"This protein bypasses the damage and saves cells from self-destructing, but it is very error prone, which suggests that it may also play a role in cancer".

Dpo4 is one of a family of enzymes called Y-family DNA polymerases that were first discovered about 10 years ago and are only now becoming understood.

"These enzymes provide a survival mechanism for cells," says first author Kevin Fiala, a graduate student in Suo's laboratory. "They allow DNA replication to continue, so the cell doesn't die. But they don't repair the DNA damage that exists"......... Posted by: Jesmi24      Read more         Source

March 29, 2007, 4:56 AM CT

Lack Of A Protein In Lung Tumors

A study of human lung tumors indicates that lung cancer patients who lack a particular protein may do more poorly than those with normal levels of that same protein.

If the findings are verified in a clinical trial, the absence of the protein might be used to identify lung cancer patients who need more aggressive therapy after surgery.

The protein is the product of a gene called Olig1, which previously has not been linked with lung cancer, and it is located in a chromosome region that is often lost in the tumor cells of many lung-cancer patients.

The research examined tumors from people with non-small cell lung cancer (NSCLC), the most common form of lung cancer. It sought to identify genes that are turned off, or silenced, by a process called aberrant DNA methylation.

The study wanted to learn if the pattern of silenced genes could distinguish between two subtypes of NSCLC, adenocarcinoma and squamous cell carcinoma.

The research identified 47 genes that together can differentiate between the two lung cancer subtypes. It also found that the silencing of the Olig1 gene - which results in the absence or low levels of its protein product - was linked to poor survival in NSCLC patients.

The study, led by researchers at the Ohio State University Comprehensive Cancer Center, is published in the March 27 issue of PLoS Medicine......... Posted by: Jesmi24      Read more         Source

March 19, 2007, 10:04 PM CT

Cancer Gene Work By Destroying Messenger

A new study suggests how a notorious cancer gene may contribute to tumor growth.

The insight emerged from a long-running study of a protein called PMR1, the key player in an unusual mechanism that cells use to quickly stop production of certain important proteins.

Researchers discovered that PMR1 is activated - or "turned on - by another molecule, an energy-packing protein called Src (pronounced "sark").

Discovered in 1977, Src became the first "oncogene" - mutated genes that help make cells cancerous. Oncogenes are altered forms of genes that control cell growth and cell division.

These findings provide insight into how Src might contribute to cancer development.

The study by researchers with the Ohio State University Comprehensive Cancer Center is published in the March 9 issue of the journal Molecular Cell.

"The link between Src and cancer was discovered 30 years ago, but to this day, we still don't know its exact role in tumor development," says principal investigator Daniel R. Schoenberg, professor of molecular and cellular biochemistry.

"Our data suggest that Src may promote cancer by causing PMR1 to halt production of proteins that normally put the brakes on cell growth - tumor-suppressor proteins, for example, or other growth-regulating proteins"......... Posted by: Jesmi24      Read more         Source

March 15, 2007, 9:27 PM CT

Surveillance In Colorectal Cancer Patients Improves Survival

Colorectal cancer patients who undergo colonoscopic surveillance during follow-up after surgery experience improved survival, according to a study would be published in the recent issue of Clinical Gastroenterology and Hepatology but currently available on-line. Results of the study suggest that colorectal cancer patients should undergo routine colonoscopic surveillance at one year after their surgery and that more intensive surveillance may be needed in patients found to have advanced neoplasia as well as those with a prior history of adenomatous colon polyps.

"The results of our study provide additional evidence that colorectal cancer survivors benefit from surveillance with colonoscopy, and it appears that the initial surveillance colonoscopy should be performed at one year after colon resection because of the significant risk of additional cancers and polyps in these patients," according to Stephen J. Rulyak, MD, MPH, lead author of the study and Acting Assistant Professor in the Division of Gastroenterology at the University of Washington in Seattle.

The study included a total of 1,002 patients identified from the Group Health Cooperative, a large health system in Washington State, and consisted of equal proportions of men and women, the majority of whom were aged 60 years or older. More than 700 (70 percent) were alive at the end of the study period and the cumulative survival for the study group was 96 percent at one year and 68 percent at five years......... Posted by: Jesmi24      Read more         Source

March 11, 2007, 8:32 PM CT

Target For Treatment For Leukemia

Ali Shilatifard, Ph.D., Investigator, has identified a cellular factor that can reverse histone trimethylation caused by the trithorax gene, the Drosophila homologue of the human mixed lineage leukemia gene, MLL. MLL, which is found in translocations in a variety of hematological malignancies, is a histone H3K4 methyltransferase.

The paper, "The trithorax-group gene little imaginal discs in Drosophila encodes a histone H3 trimethyl-Lys4 demethylase," was posted today in the Advanced Online Publication section of Nature Structural & Molecular Biology. The publication identified a cellular factor that can reverse histone trimethylation associated with mixed lineage leukemia. This, in turn, may allow for the identification of new targets for the treatment of leukemia caused by MLL translocations.

"This work demonstrates that a Drosophila gene product, little imaginal discs (Lid), removes methyl groups from histone H3K4," explains Dr. Shilatifard. "A reduction of Lid results in a specific genome-wide increase in H3K4 trimethylation levels with no effect on other patterns of histone trimethylations. Animals with reduced Lid levels have higher levels of H3K4 trimethylation, resulting in altered distribution of the chromo-helicase protein, the CHD1".

"Dr. Shilatifards first publication since joining the Institute earlier this year is a fascinating one," said Robb Krumlauf, Ph.D., Scientific Director. "The role of MLL in a variety of blood-related cancers has been well-established. These findings give us a promising option for developing targeted treatments to combat these types of leukemia"......... Posted by: Jesmi24      Read more         Source

Sat, 03 Mar 2007 01:56:38 GMT

Pink Motivation For Cool Girls

I'm a huge fan of kits. The cutest, the better.

This one is for the girl who loves cute, pink, useful kits: Pink Gym Kit

In my opinion, the Pink Gym Kit is an extra help to keep you from missing your exercise appointments.

You'll feel like going to the gym, just to use these pretty, cool things!

Pink Gym Kit includes:

- Pedometer with integrated FM radio and headphones.
- Micro-fiber towel.
- 500 ml water bottle with detachable jogger's belt and carry pack.
- Handy grab and go compact carry case with compartments for:
- Membership card
- Mobile phone
- Locker coins
- Key holder
- Kit bag with phone, money, key and card pockets.

Find more cool Pink Kits at GadgetPages.

Found Via: TechieDiva

Posted by: Michael      Read more     Source

March 1, 2007, 4:33 AM CT

Researchers Wake Up Viruses Inside Tumors

Researchers have found a way to activate Epstein-Barr viruses inside tumors as a way to identify patients whose infection can then be manipulated to destroy their tumors. They say this strategy could offer a novel way of treating many cancers associated with Epstein-Barr, including at least four different types of lymphoma and nasopharyngeal and gastric cancers.

In the March 1 issue of Clinical Cancer Research, a team of radiologists and oncologists from Johns Hopkins Medical Institutions describe how they used two agents already on the market − one of which is the multiple myeloma drug Velcade − to light up tumor viruses on a gamma camera. The technique is the first in the new field of in vivo molecular-genetic imaging that doesn't require transfecting tumors with a "reporter" gene, the scientists say.

"The beauty of this is that you don't have to introduce any reporter genes into the tumor because they are already there," says radiologist Martin G. Pomper, M.D., Ph.D. "This is the only example we know of where it is possible to image activated endogenous gene expression without having to transfect cells".

A variety of blood and solid cancers are more likely to occur in people who have been infected with the Epstein-Barr virus (EBV), but not everyone with these cancers has such infections. For those who do, researchers, such as Hopkins oncologist and co-author Richard F. Ambinder, M.D., Ph.D., have been working on ways to activate the reproductive, or "lytic" cycle, within the virus to make it replicate within the tumor cell. When enough viral particles are produced, the tumor will burst, releasing the virus. In animal experiments, this experimental therapy, called lytic induction therapy, results in tumor death......... Posted by: Jesmi24      Read more         Source