plus 3, Spices may help prevent breast cancer - Democratic Underground.com |
- Spices may help prevent breast cancer - Democratic Underground.com
- TGFb growth factor controls spread of cancer cells - News-Medical.Net
- Stress could increase breast cancer risk - Daily News and Analysis
- Potential New 'Twist' In Breast Cancer Detection - Redorbit.com
| Spices may help prevent breast cancer - Democratic Underground.com Posted: 07 Dec 2009 10:52 PM PST Spices may help prevent breast cancer
Current chemotherapies do not work against these cancer stem cells, which is why cancer recurs and spreads. Eliminating the cancer stem cells may be the key to controlling cancer, says Dr. Madhuri Kakarala, clinical lecturer in internal medicine at the University of Michigan Medical School and a research investigator at the VA Ann Arbor Healthcare System. Researchers at the university's cancer center found that when the dietary compounds curcumin, derived from the Indian spice turmeric, and piperine, derived from black peppers, were applied to breast cells in culture at the equivalent of about 20 times the potency of what could be consumed through diet, they decreased the number of stem cells while having no effect on normal differentiated cells. "If we can limit the number of stem cells, we can limit the number of cells with potential to form tumors," Kakarala, the study's lead author, said in a statement. This content has passed through fivefilters.org.  This posting includes an audio/video/photo media file: Download Now |
| TGFb growth factor controls spread of cancer cells - News-Medical.Net Posted: 06 Dec 2009 09:56 PM PST The spread, or metastasis, of individual breast cancer cells from the main tumor into the blood circulation to the lungs and other body tissues and organs is under the control of a growth factor abbreviated TGFb, according to a study with laboratory mice that will be presented at the American Society for Cell Biology (ASCB) 49th Annual Meeting, Dec. 5-9, 2009 in San Diego. These messenger genes may be a promising target for drugs to block the metastatic breast cancer route, said Erik Sahai, Ph.D., of Cancer Research UK in London. "The results helped us to find the set of genes that are behind the spread of breast cancer -- and that the genes need to be first turned on and then off in order for single cancer cells to be able to 'relocate,'" Sahai said. Sahai's presentation at the ASCB conference follows the Oct. 2009 publication of the study in Nature Cell Biology. In their studies with laboratory mice with breast cancer, Sahai and his colleagues determined that the control switch is the TGFb (transforming growth factor beta) that previous research had shown to regulate normal cell growth and movement. Using an advanced microscopy and analysis technique, the Cancer UK scientists documented the movement of the cancer cells from the mouse's primary tumor site. Because the cancer cells were tagged with a "reporter" protein that glowed blue when the TGFb cell messenger system was active, the researchers were able to determine that single breast cancer cells broke away from the main tumor and entered the blood system when TGFb first turned on the messenger genes in the cancer cells and then turned them off. But, when TGFb was inactive, clumps, not individual, breast cancer cells broke away from the main tumor. Because these clumps can spread only through the lymphatic system, the metastasis was local, not through the blood. The spread of individual cancer cells is more life-threatening than is the metastasis of a group of cells. While single cells can travel through the blood circulation to sites throughout the body, groups of cancer cells are limited the lymphatic system, which keeps them local. Advanced microscopy and analysis, said Sahai, allows researchers to investigate cell signaling "live" while observing individual cancer cells make the crucial transition to metastasis. It gives science a closer look at a process that has been largely hidden. "Surprisingly little is known about the way cancer cells spread through the body because it is so incredibly difficult to study," said Sahai. "In a medium-sized tumor there could be a billion cells -- and only a small proportion might break away and spread. So it is like trying to find -- and understand -- a moving needle in a very big haystack." Source: American Society for Cell Biology This content has passed through fivefilters.org. |
| Stress could increase breast cancer risk - Daily News and Analysis Posted: 08 Dec 2009 03:02 AM PST Washington: Social isolation and related stress could be a factor in increasing human breast cancer risk, says a study. Researchers at the University of Chicago based their study on a rat model to identify environmental mechanisms contributing to cancer risk. Lead author Gretchen Hermes, a former researcher at the University and now a resident in psychiatry at the Yale University School of Medicine, found that isolation and stress result in a 3.3-fold increase in the risk of developing cancer among rats with naturally occurring mammary tumors. Martha McClintock, a psychologist at the University of Chicago and an author of the paper, said: "We need to use these findings to identify potential targets for intervention to reduce cancer and other and its psychological and social risk factors. "In order to do that, we need to look at the problem from a variety of perspectives, including examining the sources of stress in neighbourhoods as well as the biological aspects of cancer development." Boffins also found that rats living in isolation experienced a 135% increase in the number of tumors and a more than 8,000% increase in their size. The impact of isolation was much larger than the impact another environmental source of tumor formation-the unlimited availability of high-energy food. The paper, "Social Isolation Dysregulates Endocrine and Behavioral Stress While Increasing Malignant Burden of Spontaneous Mammary Tumors," was published in the Proceedings of the National Academy of Sciences. This content has passed through fivefilters.org. |
| Potential New 'Twist' In Breast Cancer Detection - Redorbit.com Posted: 05 Dec 2009 12:03 PM PST Posted on: Saturday, 5 December 2009, 14:10 CST Mouse studies reveal new -- and better -- picture of stem cells that may fuel some breast cancers Working with mice, scientists at Johns Hopkins publishing in the December issue of Neoplasia have shown that a protein made by a gene called "Twist" may be the proverbial red flag that can accurately distinguish stem cells that drive aggressive, metastatic breast cancer from other breast cancer cells. Building on recent work suggesting that it is a relatively rare subgroup of stem cells in breast tumors that drives breast cancer, scientists have surmised that this subgroup of cells must have some very distinctive qualities and characteristics. In experiments designed to identify those special qualities, the Hopkins team focused on the gene "Twist" (or TWIST1) – named for its winding shape – because of its known role as the producer of a so-called transcription factor, or protein that switches on or off other genes. Twist is an oncogene, one of many genes we are born with that have the potential to turn normal cells into malignant ones. "Our experiments show that Twist is a driving force among a lot of other players in causing some forms of breast cancer," says Venu Raman, Ph.D., associate professor of radiology and oncology, Johns Hopkins University School of Medicine. "The protein it makes is one of a growing collection of markers that, when present, flag a tumor cell as a breast cancer stem cell." Previous stem cell research identified a Twist-promoted process known as epithelial-to-mesenchymal transition, or EMT, as an important marker denoting the special subgroup of breast cancer stem cells. EMT essentially gets cells to detach from a primary tumor and metastasize. The new Hopkins research shows that the presence of Twist, along with changes in two other biomarkers – CD 24 and CD44 – even without EMT, announces the presence of this critical sub-group of stem cells. "The conventional thinking is that the EMT is crucial for recognizing the breast cancer cell as stem cells, and the potential for metastasis, but our studies show that when Twist shows up in excess or even at all, it can work independently of EMT," says Farhad Vesuna, Ph.D., an instructor of radiology in the Johns Hopkins University School of Medicine. "EMT is not mandatory for identifying a breast cancer stem cell." Working with human breast cancer cells transplanted into mice, all of which had the oncogene Twist, the scientists tagged cell surface markers CD24 and CD44 with fluorescent chemicals. Following isolation of the subpopulation containing high CD44 and low CD24 by flow cytometry, they counted 20 of these putative breast cancer stem cells. They then injected these cells into the breast tissue of 12 mice. All developed cancerous tumors. "Normally, it takes approximately a million cells to grow a xenograft, or transplanted tumor," Vesuna says. "And here we're talking just 20 cells. There is something about these cells – something different compared to the whole bulk of the tumor cell – that makes them potent. That's the acid test – if you can take a very small number of purified "stem cells" and grow a cancerous tumor, this means you have a pure population." Previously, the team showed that 65 percent of aggressive breast cancers have more Twist compared to lower-grade breast cancers, and that Twist-expressing cells are more resistant to radiation. Twist is what scientists refer to as an oncogene, one that if expressed when and where it's not supposed to be expressed, causes oncogenesis or cancer because the molecules and pathways that once regulated it and kept it in check are gone. This finding – that Twist is integral to the breast cancer stem cell phenotype – has fundamental implications for early detection, treatment and prevention, Raman says. Some cancer treatments may kill ordinary tumor cells while sparing the rare cancer stem cell population, sabotaging treatment efforts. More effective cancer therapies likely require drugs that kill this important stem cell population. This study was supported by the Maryland Stem Cell Research Foundation. In addition to Vesuna and Raman, authors of the paper include Ala Lisok and Brian Kimble, also of Johns Hopkins. --- On the Net: This content has passed through fivefilters.org. |
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