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Weekly Reports £¨102£©on International Trends of Cutting ¨Cedge Life Science Development
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1.      Cholesterol 'fuels' breast cancer
 
¡¾Text abstracts¡¿Health and science report, BBC News 29 November 2013 Last updated at 03:54 GMT
 
Cholesterol 'fuels' breast cancer
James Gallagher
 
A by-product of cholesterol can fuel the deadly growth and spread of breast cancer, according to a group of scientists.
It raises the prospect that taking cholesterol-lowering drugs called statins could prevent cancer.
The work, published in the journal Science, helps explain why obesity is a major risk factor for the disease.
However, cancer charities cautioned that it was too soon to advise women to take statins.
Obesity has been linked with many cancers including those of the breast, bowel and womb.
¡°The results from this early study are promising¡± Dr Hannah Bridges Breakthrough Breast Cancer.
The fat in overweight people can pump out hormones, such as oestrogen, which drive the growth of cancers.
A team at Duke University Medical Centre, in the US, showed that cholesterol was having a similar effect.
Cholesterol is broken down by the body into 27HC, which can mimic oestrogen and produce the same effect as the hormone in some tissues.
Experiments on mice showed that a high fat diet increased levels of 27HC in the blood and led to tumours that were 30% larger than in mice on a normal diet.
Tumours were also more likely to spread. And human breast cancer tissue grew more quickly in the laboratory when it was fed 27HC.
One of the researchers Prof Donald McDonnell said: "A lot of studies have shown a connection between obesity and breast cancer, and specifically that elevated cholesterol is associated with breast cancer risk, but no mechanism has been identified.
"What we have now found is a molecule - not cholesterol itself, but an abundant metabolite of cholesterol - called 27HC that mimics the hormone oestrogen and can independently drive the growth of breast cancer."
Treatment
The researchers say their findings raise the prospect that lowering cholesterol can lower the risk of breast cancer developing.
Statins are already taken by millions of people to cut the risk of heart disease. However, studies have already suggested statins can cut the risk of breast cancer.
A healthier diet is another way to cut levels of cholesterol in the bloodstream.
Dr Hannah Bridges, from leading charity Breakthrough Breast Cancer, says: "Up until now research into the links between cholesterol levels, use of statins and breast cancer risk has been inconclusive.
"The results from this early study are promising and if confirmed through further research could increase our understanding of what causes some breast cancers to develop."
Dr Emma Smith, from Cancer Research UK, said: "This study is intriguing as it shows for the first time a direct link between cholesterol and breast cancer in mice - but it's too early to say how this knowledge might help tackle breast cancer in the future.
"As things stand, until we know more about the effects of statins on cancer risk, the best ways to cut the risk of developing breast cancer are to stay a healthy weight, cut down on alcohol and keep active."
 
 
2.       Engineering Complex Tissues
 
¡¾Text abstracts¡¿Sci Transl Med 14 November 2012: Vol. 4, Issue 160, p. 160rv12
 
Engineering Complex Tissues
Anthony Atala1, F. Kurtis Kasper, & Antonios G. Mikos, et al.
 
Tissue engineering has emerged at the intersection of numerous disciplines to meet a global clinical need for technologies to promote the regeneration of functional living tissues and organs. The complexity of many tissues and organs, coupled with confounding factors that may be associated with the injury or disease underlying the need for repair, is a challenge to traditional engineering approaches. Biomaterials, cells, and other factors are needed to design these constructs, but not all tissues are created equal. Flat tissues (skin); tubular structures (urethra); hollow, nontubular, viscus organs (vagina); and complex solid organs (liver) all present unique challenges in tissue engineering. This review highlights advances in tissue engineering technologies to enable regeneration of complex tissues and organs and to discuss how such innovative, engineered tissues can affect the clinic.
 
 
3.      Mesenchymal progenitor cells derived from traumatized muscle enhance neurite growth
 
¡¾Text abstracts¡¿Journal of Tissue Engineering and Regenerative Medicine£¬Volume 7, Issue 6, pages 443¨C451, June 2013
Mesenchymal progenitor cells derived from traumatized muscle enhance neurite growth
Wesley M. Jackson, Peter G. Alexander, & Jamie D. Bulken-Hoover, et al.
 
The success of peripheral nerve regeneration is governed by the rate and quality of axon bridging and myelination that occurs across the damaged region. Neurite growth and the migration of Schwann cells is regulated by neurotrophic factors produced as the nerve regenerates, and these processes can be enhanced by mesenchymal stem cells (MSCs), which also produce neurotrophic factors and other factors that improve functional tissue regeneration. Our laboratory has recently identified a population of mesenchymal progenitor cells (MPCs) that can be harvested from traumatized muscle tissue debrided and collected during orthopaedic reconstructive surgery. The objective of this study was to determine whether the traumatized muscle-derived MPCs exhibit neurotrophic function equivalent to that of bone marrow-derived MSCs. Similar gene- and protein-level expression of specific neurotrophic factors was observed for both cell types, and we localized neurogenic intracellular cell markers (brain-derived neurotrophic factor and nestin) to a subpopulation of both MPCs and MSCs. Furthermore, we demonstrated that the MPC-secreted factors were sufficient to enhance in vitro axon growth and cell migration in a chick embryonic dorsal root ganglia (DRG) model. Finally, DRGs in co-culture with the MPCs appeared to increase their neurotrophic function via soluble factor communication. Our findings suggest that the neurotrophic function of traumatized muscle-derived MPCs is substantially equivalent to that of the well-characterized population of bone marrow-derived MPCs, and suggest that the MPCs may be further developed as a cellular therapy to promote peripheral nerve regeneration.
 
 
 
4.      Diabetes Shrinks the Brain
 
¡¾Text abstracts¡¿Sci Transl Med 4 December 2013: Vol. 5, Issue 214, p. 214fs42
 
Diabetes Shrinks the Brain
Ania M. Jastreboff
 
People with pre-diabetes and type 2 diabetes suffer from an accelerated decline in brain size and mental capacity in as little as two years according to new research presented at the joint International Congress of Endocrinology/European Congress of Endocrinology in Florence, Italy.
An Australian research team led by Associate Professor Katherine Samaras (Garvan Institute of Medical Research) found that the aging brain is vulnerable to worsening blood sugar levels even before type 2 diabetes is diagnosable.
While some brain volume loss is a normal part of aging, the researchers found that elderly people with blood sugar levels in flux, as well as type 2 diabetes, lost almost two and a half times more brain volume than their peers over two years. The reduction in size of the frontal lobe -- associated with higher mental functions like decision-making, emotional control, and long term memory -- has a significant impact on cognitive function and quality of life.
 
 
 
5.      Restricting Bone Metastasis
 
¡¾Text abstracts¡¿Sci. Signal., 26 November 2013£¬Vol. 6, Issue 303, p. ec287
 
Restricting Bone Metastasis
Leslie K. Ferrarelli
 
Just as no two types of soil are the same, the "seed and soil" theory of metastasis suggests that the different microenvironments of various organs can either inhibit or promote the growth of disseminated tumor cells (DTCs), explaining why cancers seem to have preferred metastatic sites.
Bragado et al. used a mouse xenograft model to show that strong signaling by transforming growth factor¨C¦Â2 (TGF-¦Â2) in the bone marrow induced the dormancy of disseminated human squamous carcinoma cells, whereas weak TGF-¦Â2 signaling in the lungs was permissive to metastatic growth. In situ confocal microscopic analysis of the dissemination of green fluorescent protein (GFP)¨Ctagged HEp3 cells (a human squamous carcinoma cell line from primary tumors formed in mice) revealed that secondary tumors were localized primarily to the lungs (80%) rather than the bone marrow (28%) or liver and spleen (5%). Whereas the number of DTCs in the bone marrow remained constant for at least 4 weeks after surgical removal of the primary tumor and the bone marrow DTCs showed poor proliferation when transplanted into culture, the number of DTCs in the lungs increased substantially within 2 weeks and thrived in culture. In agreement with their respective proliferative capacity, HEp3 cell cultures derived from either the lung or the primary tumor had low abundance of the cyclin-dependent kinase inhibitor p27 and a high ratio of the mitogen-activated protein kinase (MAPK) extracellular signal¨Cregulated kinases 1 and 2 (ERK1/2) to the MAPKs p38¦Á and p38¦Â (p38¦Á/¦Â) abundance. In contrast, bone marrow¨Cderived HEp3 cells had high p27 abundance and a low ERK:p38¦Á/¦Â ratio. Bone marrow¨Cderived DTCs also had increased expression of the tumor suppressor genes p53 and DEC2, as well as of TGF-¦Â2, but not of TGF-¦Â1 or TGF-¦Â3. Knockdown of MAPK14 (encoding p38¦Á), DEC2, p53, and TGF¦ÂR1 [encoding TGF-¦Â receptor I (TGF-¦ÂRI)] in the HEp3 initially introduced in the mice resulted in increased DTCs in the bone marrow after the primary tumors were removed. Alternatively, systemic pharmacological inhibition of TGF-¦ÂRI, TGF-¦ÂRIII, or p38¦Á/¦Â in the mice after removal of the primary tumor increased DTCs in the bone marrow. HEp3 cells treated with either medium conditioned by isolated lung cell cultures and supplemented with TGF-¦Â2 or medium conditioned by isolated bone marrow cells had decreased tumorigenicity when injected into mice. Depleting TGF-¦Â2 from the bone marrow¨Cconditioned medium prevented activation of p38 and inhibition of HEp3 tumorigenicity in mice. In contrast, treating bone marrow¨Cderived DTCs with TGF-¦Â1 before injection into the mice increased their tumorigenicity. The findings suggest that TGF-¦Â2 secreted from the bone marrow functioned as a dormancy signal for squamous carcinoma cells.
 
 
 

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