March 19, 2007, 10:03 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.

Scientists 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 malignant. 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 scientists with the Ohio State University Comprehensive Cancer Center is reported 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: Andria      Read more         Source

March 19, 2007, 10:01 PM CT

Stem Cell Signaling Pathway

A newly discovered small molecule called IQ-1 plays a key role in preventing embryonic stem cells from differentiating into one or more specific cell types, allowing them to instead continue growing and dividing indefinitely, according to research performed by a team of scientists who have recently joined the stem-cell research efforts at the Keck School of Medicine of the University of Southern California. Their findings are being published recently in an early online edition of the Proceedings of the National Academy of Sciences.

This discovery takes scientists another step closer to being able to grow embryonic stem cells without the feeder layer of mouse fibroblast cells that is essential for maintaining the pluripotency of embryonic stem cells, says the studys primary investigator, Michael Kahn, Ph.D., who was recently named the first Provosts Professor of Medicine and Pharmacy at USC. Such a layer is needed because it is currently the only proven method to provide the stem cells with the necessary chemical signals that prompt them to stay undifferentiated and to continue dividing over and over.

Still, growing human embryonic stem cells on a layer of mouse fibroblasts has never made much sense to the scientists forced to do just that. Stem cells that grow on feeders are contaminated with mouse glycoproteins markers, Kahn says. If you use them into humans, youd potentially have a horrible immune response......... Posted by: Andria      Read more         Source

March 19, 2007, 5:14 AM CT

Inflammation And Metastasis Of Prostate Cancer

Many would assume that "mounting an immune response" or "having your body fight the cancer" is a good thing. Now, research at the University of California, San Diego (UCSD) School of Medicine strongly suggests that inflammation associated with the progression of tumors actually plays a key role in the metastasis of prostate cancer.

The research, appearing online March 19 in advance of publication in the journal Nature, identifies a mechanism which triggers metastasis, which is the spread of cancer in late stages of prostate cancer development. The findings by Michael Karin, Ph.D., professor of pharmacology in UCSD's Laboratory of Gene Regulation and Signal Transduction, and colleagues may help solve the puzzle of why it takes so long for cancer to metastasize, as well as what causes it to do so. Furthermore, this new work may lead to development of anti-metastatic therapies.

A major hypothesis in cancer research has been that whether the cancer metastisizes or not is determined by genetic changes within the cancer cell itself. But this hypothesis didn't explain why metastases appear many years after the initial tumor.

"Our findings suggest that promoting inflammation of the cancerous tissue, for instance, by performing prostate biopsies, may, ironically, hasten progression of metastasis," said Karin. "We have shown that proteins produced by inflammatory cells are the 'smoking gun' behind prostate cancer metastasis. The next step is to completely indict one of them"......... Posted by: Andria      Read more         Source

March 15, 2007, 9:26 PM CT

Surveillance In Colorectal Cancer Patients Improves Survival

Colorectal cancer patients who undergo colonoscopic surveillance during follow-up after surgery experience improved survival, as per a research studywould be reported 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 previous 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," as per 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: Andria      Read more         Source

March 15, 2007, 9:13 PM CT

One WWOX Isn't Enough

A new study shows that the loss of even one of the two copies of a particular tumor-suppressor gene greatly increases the risk that lung cancer will develop in experimental animals.

The study examined the Wwox gene, a suspected tumor-suppressor gene, and showed that even when mice have one working copy of the gene, they nonetheless develop five times more lung tumors than do mice with both copies of the gene. Tumor-suppressor genes normally keep damaged cells from becoming malignant.

The findings were reported in the Proceedings of the National Academy of Sciences by researchers at the Ohio State University Comprehensive Cancer Center.

"Classic tumor-suppressor genes don't increase cancer risk until cells lose both copies of the gene or when both copies are mutated," says first author Rami I. Aqeilan, research assistant professor of molecular virology, immunology and medical genetics at Ohio State.

"These findings suggest that losing one copy of Wwox can predispose normal cells to become malignant. This emphasizes the importance that Wwox may have in initiating the disease."

Surprisingly, the research also links loss of the gene and a form of bone cancer called chondroid osteosarcoma. The research may offer the first animal model for the study of this human disease......... Posted by: Andria      Read more         Source

March 13, 2007, 9:56 PM CT

Radiation After Surgery In Women Over Age 65

Eventhough women over 65 make up more than half of women diagnosed with breast cancer, the effects of therapy on this group have not been widely studied.

Studies show older women are less likely than younger women to receive common adjuvant (post-surgical) therapies like hormonal therapys or radiation treatment following surgery.

Some scientists have argued that radiation treatment is not necessary in women over 65 who have surgery and take tamoxifen, particularly because these women may face other life-threatening conditions. Others have argued that these women have less aggressive cancers and may not benefit from radiation because of the burden of travel, costs or other medical conditions.

Women under age 65 often receive more aggressive therapy when diagnosed with breast cancer. Upon diagnosis of early breast cancer, a woman may have breast conserving treatment (also called lumpectomy), a surgery in which the tumor is removed as well as a small portion of the tissue surrounding the tumor. Others receive mastectomy, the removal of the entire breast. In most cases, breast conserving surgery is followed by radiation, or the use of high-energy from x-rays, gamma rays, neutrons, and other sources to kill breast cancer cells and shrink tumors.

Women with estrogen receptor positive (ER+) breast cancers, or cancers that may grow faster in the presence of the hormone estrogen, often conclude their therapy by taking five years of hormonal treatment. At the time of this study, the standard therapy was tamoxifen (brand name: Nolvadex), a medicine that blocks the growth of hormone sensitive breast cancers by binding to estrogen receptors on the outside of cancer cells......... Posted by: Andria      Read more         Source

March 12, 2007, 9:02 PM CT

Compound With An Improbable Trigger

Even miniscule amounts of chromium 6 can cause cancer. Blame that do-gooder nutrient, vitamin C.

Brown University researchers have discovered that naturally occurring vitamin C reacts inside human lung cells with chromium 6, or hexavalent chromium, and causes massive DNA damage. Low doses of chromium 6, combined with vitamin C, produce up to 15 times as many chromosomal breaks and up to 10 times more mutations - forms of genetic damage that lead to cancer - compared with cells that lacked vitamin C altogether.

This finding is startling, said Anatoly Zhitkovich, an associate professor of medical science at Brown who oversaw the experiments. Outside cells, Zhitkovich said, vitamin C actually protects against the cellular damage caused by hexavalent chromium, the toxic chemical that starred as the villain in the true-to-life Hollywood drama, Erin Brockovich. In fact, vitamin C has been used as an antidote in industrial accidents and other instances when large amounts of chromium are ingested.

Vitamin C works protective wonders because it is a powerful antioxidant, blocking cellular damage from free radicals. Specifically, the vitamin rapidly "reduces," or adds electrons, to free radicals, converting them into harmless molecules. This electron transfer from vitamin C to chromium 6 produces chromium 3, a form of the compound that is unable to enter cells......... Posted by: Andria      Read more         Source

March 6, 2007, 4:35 AM CT

Measles Virus To Kill Multiple Myeloma

Mayo Clinic Cancer Center has opened a new Phase I clinical trial testing an engineered measles virus against multiple myeloma, a cancer of the bone marrow that currently has no cure. This is the third of a series of molecular medicine studies in patients testing the potential of measles to kill cancer.

This is the beginning of a long but exciting process, says Angela Dispenzieri, M.D., hematologist and lead researcher on the multiple myeloma clinical trial in the measles virus investigation. We are very hopeful that this will be a step toward helping our patients.

Mayo Clinic Cancer Center is the only institution in the world currently pursuing using engineered measles viruses for cancer treatment. It has shepherded the research from basic laboratory science to therapies being tested today in several tumor types, including glioblastoma multiforme (a brain tumor), recurrent ovarian cancer and now multiple myeloma.

The measles viruses being used for these studies were constructed by inserting additional genes into the measles vaccine strain.

Many cancers, including multiple myeloma, overexpress a protein, CD46, which allows them to evade destruction by the immune system. Laboratory strains of measles virus seek out this protein and use it as a receptor by which to enter the cancer cells. Upon entry, the virus spreads, infecting nearby tumor cells and fusing them together, increasing cancer cell death......... Posted by: Andria      Read more         Source

March 1, 2007, 9:50 PM CT

Insights Into Osteosarcoma In Cats And Dogs

Scientists at the University of Illinois have observed that a molecular pathway known to have a role in the progression of bone cancer in humans is also critical to the pathology of skeletal tumors in dogs and cats. Their work could lead to advances in the palliative care of companion animals afflicted with osteosarcoma.

The research team, which included U. of I. pathobiology professor Anne Barger, examined the homeostatic role of an enzyme, receptor activator of nuclear factor kappa-B (known as RANK), and two key modulators of its activity: RANK ligand (RANK-L) and osteoprotegrin (OPG). RANK is one of a family of receptors that regulates bone and immune homeostasis. In health, RANK, RANK-L and OPG together keep the continual process of bone growth and resorption in balance.

Bone tumors presumably derail this homeostatic process, however, by upregulating RANK-L expression. RANK-L binds to RANK, stimulating the production and activation of osteoclasts (bone cells that increase the breakdown of bone tissue).

OPG counter-regulates RANK-L by blocking its ability to bind to RANK.

Eventual therapeutic interventions may make use of OPG or other RANK-L inhibitors to slow the process of bone destruction in skeletal tumors in cats and dogs, Barger said. Eventhough not a cure, this could reduce the pain and other complications linked to bone cancer. Such therapies have proven effective at reducing pathologic bone loss in human bone cancer patients......... Posted by: Andria      Read more         Source

February 27, 2007, 8:26 PM CT

The Girl Who Kept On Smiling

Read this story of a brave girl:

A brave 16-year-old who gave up being treated for leukaemia to spend what time she had left with her family, has died.

Josie Grove lost her two-and-a-half year battle at home and surrounded by her closest relatives on Monday afternoon.

Her parents, Cliff, 46, and Jacqui, 44, said she wanted to be remembered for her smile.

A brave 16-year-old who gave up being treated for leukaemia to spend what time she had left with her family, has died.

Josie Grove lost her two-and-a-half year battle at home and surrounded by her closest relatives on Monday afternoon.

Her parents, Cliff, 46, and Jacqui, 44, said she wanted to be remembered for her smile......... Posted by: Andria      Read more         Source