Science Daily — In some ways, certain tumors resemble bee colonies, says pathologist Tan Ince. Each cancer cell in the tumor plays a specific role, and just a fraction of the cells serve as "queens," possessing the unique ability to maintain themselves in an unspecialized state and seed new tumors. These cells can also divide and produce the "worker" cells that form the bulk of the tumor.
Pathologist Tan Ince transformed normal cells into these cancerous ones (whose membranes are stained green). The transformed cells retain their sheet-forming capabilities, resembling the tumor cells found in many patients. They also possess enormous potential to create and spread tumors. As many as one in ten is a cancer stem cell. (Credit: Tan Ince)
These "queens" are cancer stem cells. Now the lab of Whitehead Member Robert Weinberg has created such cells in a Petri dish by isolating and transforming a particular population of cells from human breast tissue. After being injected with just 100 of these transformed cells, mice developed tumors that metastasized (spread to distant tissues).
"The operational definition of a cancer stem cell is the ability to initiate a tumor, so these are cancer stem cells," declares Weinberg, who is also an MIT professor of biology.
Ince didn't set out to engineer these potent cells. As a post-doctoral researcher in the Weinberg lab and gynecologic pathologist at Brigham and Women's Hospital, he was simply trying to create breast cancer models that look like real human tumors under the microscope and behave like those seen in many patients.
In more than 90 percent of human breast tumors, cancer cells resemble those lining our body's cavities. A trained pathologist can spot the similarities under a microscope. But the cancer cells previously engineered from normal breast cells for laboratory studies looked different. Ince suspected that researchers were transforming the wrong type of cells.
Now an independent investigator at Brigham and Women's Hospital and an instructor at Harvard Medical School, Ince developed a recipe for a new chemically defined culture medium and managed to grow a different type of human breast cell that ordinarily dies in culture. He transformed it into a cancer cell by inserting specific genes through a standard procedure.
The engineered cells proved to be extremely powerful. When Ince injected more than 100,000 of them into a mouse with a compromised immune system, it quickly developed massive, deadly tumors. In initial experiments, a few tissue slices revealed a primary tumor structure that resembled that of cancer patients with metastases.
That prompted Ince to wonder whether the cancer cells he created would metastasize if the mouse lived longer. He repeated the experiment in other mice, reducing the number of cells in the injection to as few as 100 in hopes of slowing tumor growth. The cancer cells continued to seed tumors and those tumors metastasized. In sharp contrast, scientists must inject about 1 million cells to get a tumor when working with the cancer cell lines routinely used in the laboratory.
"In the process of making a model that reflects a tumor type common in patients, I created tumor-initiating cells," Ince explains. "That was a complete surprise."
"This work could provide a boon to researchers who study these elusive cancer stem cells by offering a bountiful source of them," maintains Weinberg. "Labs can easily grow the newly created cells for use in experiments."
The study, which appears in Cancer Cell on August 13, also offers clues about the trajectory of cancer cells. A normal cell is thought to evolve progressively toward a malignant state through a series of genetic mutations. The early alterations confer uncontrolled growth, while later alterations enable the cell to migrate and invade other tissues. Over the past decades, considerable effort has gone into discovering these tumor-initiating and metastasis-initiating genetic alterations.
The new study suggests, however, that some normal cells are more prone to become tumor-initiating cells and have a higher metastatic potential when they become cancer cells than other normal cells. The culture medium Ince created favors the growth of the human breast cells with high tumor-making and metastatic potential while the standard culture medium favors cells with low tumor-making potential. Although the two types are only slightly different, the cells behave completely differently after acquiring the same mutations.
Ince confirmed this behavioral difference by taking a single human breast tissue sample, splitting it in two and growing the cells in the two culture mediums, which select for different cells. Next, he transformed the two populations with the same tumor-initiating genes, injected them in mice and watched the result. The cells that were grown in the new culture medium were 10,000 times more potent as tumor initiators and were the only ones able to metastasize. Thus genes that were previously thought to only initiate tumors initiated metastasis, which is the main cause of cancer mortality in the clinic.
"Tan has demonstrated that a critical determinant of eventual metastasis is the identity of the normal cell type that preexists in the breast and becomes the object of mutation and selection," Weinberg says.
This research is funded by the Breast Cancer Research Foundation and the National Institutes of Health.
US House Oversight and Foreign Affairs Committees today asked Bush administration to explain the failure of US-funded "abstinence and be faithful" HIV prevention programs for youth.
Oversight Committee Chairman Henry A. Waxman, Foreign Affairs Committee Chairman Tom Lantos, and Congresswoman Barbara Lee wrote to US Global AIDS Coordinator Mark Dybul to ask how his office will respond to a recent evaluation which found that the US$15 billion dollar programs failed to serve the needs of young people who are or may become sexually active.
Independent evaluators found that most programs lacked adequate information about partner reduction, fidelity, condom use, and cross-generational and transactional sex.
Most programs did not contain age-appropriate content, especially for older youth, and failed to refer participants appropriately to more comprehensive programs, the evaluators reported.
The USAID funded study showed that while sex with adult men is a significant factor in HIV risk for adolescent girls, contributing to higher rates of infection among girls than boys the same age, few of the curricula had specific skill-based lessons to deal with issues of gender inequality, including cross-generational and commercial sex.
"Incorporating focused lessons on important gender-based issues, including cross-generational and transactional sex, is likely to be more effective than only promoting abstinence and ignoring issues of power imbalance that put youth at risk of coercive and unwanted sex," the evaluators pointed out.
Waxman, Lantos and Lee asked Dybul to describe how you plan to respond to the findings and recommendations of this report as they relate to the needs of sexually active youth.
If claims made by scientists come out true then days are not far away when they will come out with a portent weapon to cure patients with HIV infection, as a new study shows them way to remove the virus from infected cells, bringing a glimmer of hope for the more than 40 million people infected worldwide.
Actually, researchers have engineered an enzyme that attacks the DNA of the HIV virus, cutting it out of the infected cells.
Throwing more light on the hope, which this study has sprouted Alan Engelman of Harvard University’s Dana-Farber Cancer Institute, writes:
A customized enzyme that effectively excises integrated HIV-1 from infected cells in vitro might one day help to eradicate (the) virus from AIDS patients.
Well, it would be too premature to become very enthusiastic about this new finding as the enzyme is still far from being ready to use and hasn’t even been tested in animals yet. However, one thing could certainly be said that this new way would revolutionize the way HIV-infected patients are treated.
In major breakthrough, researchers from the University of Dana-Farber Institute, at Harvard University in Massachusetts, have found a protein called; p53 that they believe could help protect against skin cancer along with tanning your skin.
Actually, protein p53 is activated when the sun’s ultraviolet rays damage DNA. As a result, alpha-MSH (a hormone that makes the pigment melanin) is produced, which assists in the tanning of skin.
I see this finding as a significant one because it raises hope of better treatment for patients with melanoma skin cancer, the fastest-increasing form of cancer in the world. Moreover, it provides researchers with a strong base upon which they may find way to tan skin without the use of the Sun or artificially made products.
Cancer particularly of the stomach, colon and liver is listed among the top 20 causes of mortality around the world. With a lot of research into newer and newer drugs to tackle it, science has bought to the forefront the role of naturally-occurring compounds from plants and more recently from animals in aborting the progression of cancer. 
One such compound which has caught the attention of members of scientific community is conjugated linoleic acid (CLA). Typically CLA is a fatty acid and has been shown to be similar to a fatty acid - linoleic acid. However, CLA has been found to be beneficial as opposed to linoleic acid since it prevents the progression of cancer unlike linoleic acid, which has been found to promote cancer.
The sources of CLA in nature are meat and dairy products obtained from grazing animals, particularly feeding more on grass rather than grains. In the market however, diet supplements available contain synthetic CLA with meager health benefits as compared to the naturally occurring compound. Earlier studies into health benefits of CLA have shown that it is effective against diabetes and obesity as well.
The research pertaining to CLA is still in its nascent stages and there is a long way to go before its long term beneficial effects to human health are established however, the few trials conducted so far look quite promising particularly in tackling some of the common cancers like breast and colon cancers.
With a lot of naturally-occurring compounds exhibiting the potential to tackle cancer more avenues for cancer research and treatment should be explored.
t is easy to pop vitamin-pills to get the nutrients we need while ignoring the incredible package nature provides us in the form of fruits. Try to include fruits in your everyday diet as they are a wonderful source of nutrients. It is nature’s way of providing you a great defense for fighting diseases.
Today, let’s check out what Apricots have in store for us.
These lovely, yummy orange colored Apricots are rich with vitamin A, vitamin C, iron, fiber, potassium and antioxidants; Apricots also make it to the top ten beta-carotene sources.
Fights cancer: Dried apricots are an excellent source of lycopene, the cartenoid that fights prostrate and breast cancer. The beta-carotene in the apricots reduces the risk of stomach and intestinal cancers. Health experts suggest having about 30 dried apricots a day should help you get these benefits.
Good for heart: Since apricots are rich in potassium, it helps control the blood pressure and thereby preventing heart diseases. The fiber content helps reduce cholesterol and the chances of clogging your arteries.
Great for vision: In a data reported in the Archives of Opthamology, it was found that three or more servings of this fruit actually reduces the risk of age-related macular degeneration (ARMD), the primary causeof vision loss in older adults. This means apricots are good for your eyes.
Secret to long life: If you enjoy life and are looking to hit the century mark, then apricots must be a part of a regular diet. Since they fight all age -related diseases like memory loss, high blood pressure, heart diseases, ARMD, cancer and cholesterol, and Alzheimer’s disease, you are naturally healthy and are sure to celebrate your 100th birthday.
Eat them fresh or dried; toss them in your salad or your deserts. Eat them anyway and reap in the benefits!
Efforts of health experts to bring down the number of patients with dementia may face severe setback with England fast heading to be the fattest nation on the planet.
Experts estimate that if obesity goes on soaring like this, then around 2.5 million Britons would be suffering from dementia or other brain distorting diseases by 2051 because several studies have linked middle-age obesity to dementia in later life. Actually, obesity stirs up higher blood pressure and cholesterol and both these things are known to increase the chances of dementia by interrupting the blood supply to the brain. Confirming this fact, further Neil Hunt, chief executive of the Alzheimer’s Society, said:
It was now unarguable that blood pressure, cholesterol levels and other factors associated with an increased risk of heart disease played an important role in the onset of dementia.
Keeping this fact in mind, it could be said that situation is bound to go from worse to worst, as an estimate states that in the coming few years, about 14 million of the British individuals, from the youngest to the oldest are likely to turn obese by 2010.
This would be a further blow to Britain’s health machinery, as already there are around 700,000 people with Alzheimer’s disease with number of people with dementia likely to touch 1.5 million marks in the next 40 years.
This would be a further blow to Britain’s health machinery, as already there are around 700,000 people with Alzheimer’s disease with number of people with dementia likely to touch 1.5 million marks in the next 40 years. If we look at this situation in wider aspect, then we could say that dementia situation is likely to take a serious turn around the globe in the coming years, which already costs around $315 billion worldwide annually with total number of people with dementia soars up to more than 29 million.
This is quite a serious issue, which needs to be addressed earnestly because threat of dementia is not the only one that swells with rise in obesity but many other problems like diabetes, cardiovascular disease and even cancer also get aggravated due to this.
Researchers at the Ohio State University Comprehensive Cancer Center have discovered the first inherited gene mutation that increases the risk for chronic lymphocytic leukaemia.
Chronic lymphocytic leukaemia (CLL), a cancer of the lymphocytes, is the most common type of leukaemia. It is a blood and bone-marrow disease and mainly affects people over 60. And it occurs more often in men than women.
The study revealed that the inherited mutation greatly reduces the gene’s protective activity. Furthermore, a second kind of change occurs later that turns the gene off altogether, leading to leukaemia. This latter alteration is a chemical change called DNA methylation and it is not inherited. Healthy cells use this process to silence unneeded genes. But abnormal DNA methylation can turn off genes that control cell growth, and that lead to tumour growth.
John C. Byrd, professor of internal medicine and a CLL specialist, said
“Our findings identify for the first time a gene that appears to be associated with hereditary CLL,”
“They also show the importance of the gene in the pathogenesis of CLL, and direct us to target this gene with therapies that might re-activate it.”
Researchers examined a family in which the father, four sons, a grandson, and a distant female relative developed this form of leukaemia. The mutation was identified in a gene called DAPK1. DAPK1 or death-associated protein kinase 1 is a tumour suppressor which helps trigger the death of cells before they become cancerous.
Albert de la Chapelle, professor of molecular virology, immunology and medical genetics and a researcher with the Ohio State human cancer genetics program, said
“This inherited change is remarkably subtle. It does not shut down the gene, but just lowers its expression somewhat. Recently, many cancer geneticists have come to believe that such subtle changes are common causes of cancer, and this is one of the first, strong examples of that principle,”
The findings could help identify people at risk for chronic leukaemia, but they also may provide new insights into the process of natural cell death. They may even lead to new strategies for treating the disease. The findings also provide evidence that some genes might contribute to cancer even when they are not silenced entirely.
American scientists have come up with a new method of treating cancer. They aspire to start clinical trials of the method, which has minimum risks of invasion, soon on individuals with prostate cancer.
The process, called irreversible electroporation (IRE), has been devised by Virginia Techbiomedical engineer Rafael V. Davalos and University of California bioengineering professor Boris Rubinsky.
Researchers have been cognizant for a long time now of electroporation increasing the permeability of a cell from none to a reversible opening to an irreversible opening. Since irreversible concept kills the cells, Davalos and Rubinsky used it to target cancer cells.
Davalos, recipient of the Hispanic Engineer National Achievement Award for Most Promising Engineer or Scientist in 2006, said:
IRE removes tumors by irreversibly opening tumor cells through a series of short intense electric pulses from small electrodes placed in or around the body
He further explained that this application creates permanent openings in the pores in the cells of the undesirable tissue which eventually result in the death of the cells eliminating the need to use potentially harmful chemotherapeutic drugs.
The researchers carried out a fruitful operation by using the IRE pulses in the livers of male Sprague-Dawley rats.
We did not use any drugs, the cells were destroyed, and the vessel architecture was preserved,
Davalos said.
Davalos and Rubinsky also told that the new process was more useful compared to the currently available methods for destroying tumors using heat or freezing, because these techniques may damage healthy tissue or leave malignant cells.
The researchers said that the process of IRE enabled them to adjust the electrical current and kill the targeted cells without affecting surrounding tissue or nearby blood vessels.
Th researchers held that IRE shows remarkable promise as a minimally invasive, inexpensive surgical technique to treat cancer. This method is expedient because it is not disturbed by local blood flow and can be supervised and checked by using electrical impedance tomography.
The researchers said that they would keep promoting the promising method to treat cancer, which is being featured in a special issue of Technology in Cancer Research and Treatment.
Indeed, this new development in cancer research may go a long way in negotiating the deadly ailment as it seems full of high potentials.
Scientists have developed a new type of nanoparticles that can aim, image and destroy tumor cells. This technology can also be used to develop means by which cancer can be cured.
The system contains gold nanoparticles which branching polymers called dendrimers. These dendrimers sprout out from the surface of the nanoparticles. These particles can be used to launch a multiprong attack against the tumors.
The arms of these dendrimers can carry many different molecules, including those that can fight cancer cells and even drugs that can slow their growth or destroy them completely.
Scientists aim that this method should be able to destroy the cancer cells without harming anything else in the body. Currently researchers are pursuing tests on animals and once the technology pass some more tests then it should be made available for human use.
