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Weekly Reports £¨107£©on International Trends of Cutting ¨Cedge Life Science Development
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1.      'Sticky balls' may stop cancer spreading
¡¾Text abstracts¡¿Health and science reporter, BBC News
 
'Sticky balls' may stop cancer spreading
James Gallagher
 
Cancer-killing "sticky balls" can destroy tumour cells in the blood and may prevent cancers spreading, early research suggests.
The most dangerous and deadly stage of a tumour is when it spreads around the body.
Scientists at Cornell University in the US have designed nanoparticles that stay in the bloodstream and kill migrating cancer cells on contact.
They said the impact was "dramatic" but there was "a lot more work to be done".
One of the biggest factors in life expectancy after being diagnosed with cancer is whether the tumour has spread to become a metastatic cancer.
"About 90% of cancer deaths are related to metastases," said lead researcher Prof Michael King.
Continue reading the main story
¡°The results are quite remarkable¡±Prof Michael King, Lead researcher. On the trail, the team at Cornell devised a new way of tackling the problem.
They attached a cancer-killing protein called Trail, which has already been used in cancer trials, and other sticky proteins to tiny spheres or nanoparticles.
When these sticky spheres were injected into the blood, they latched on to white blood cells.
Tests showed that in the rough and tumble of the bloodstream, the white blood cells would bump into any tumour cells which had broken off the main tumour and were trying to spread.
The report in Proceedings of the National Academy of Sciences showed the resulting contact with the Trail protein then triggered the death of the tumour cells.
Prof King told the BBC: "The data shows a dramatic effect: it's not a slight change in the number of cancer cells.
"The results are quite remarkable actually, in human blood and in mice. After two hours of blood flow, they [the tumour cells] have literally disintegrated."
He believes the nanoparticles could be used used before surgery or radiotherapy, which can result in tumour cells being shed from the main tumour.
It could also be used in patients with very aggressive tumours to prevent them spreading.
However, much more safety testing in mice and larger animals will be needed before any attempt at a human trial is made.
So far the evidence suggests the system has no knock-on effect for the immune system and does not damage other blood cells or the lining of blood vessels.
But Prof King cautioned: "There's a lot of work to be done. Various breakthroughs are needed before this could be a benefit to patients."
 
2.      Enhanced Telomere in Pluripotent Cells Reprogrammed via Nuclear Transfer Relative to Induced Pluripotent Stem Cells
¡¾Text abstracts¡¿Cell Stem Cell, Volume 14, Issue 1, 27-39, 21 November 2013
 
Enhanced Telomere in Pluripotent Cells Reprogrammed via Nuclear Transfer Relative to Induced Pluripotent Stem Cells
 
Although somatic cell nuclear transfer (SCNT) and induction of pluripotency (to form iPSCs) are both recognized reprogramming methods, there has been relatively little comparative analysis of the resulting pluripotent cells. Here, we examine the capacity of these two reprogramming approaches to rejuvenate telomeres using late-generation telomerase-deficient (Terc−/−) mice that exhibit telomere dysfunction and premature aging. We found that embryonic stem cells established from Terc−/− SCNT embryos (Terc−/− ntESCs) have greater differentiation potential and self-renewal capacity than Terc−/− iPSCs. Remarkably, SCNT results in extensive telomere lengthening in cloned embryos and improved telomere capping function in the established Terc−/− ntESCs. In addition, mitochondrial function is severely impaired in Terc−/− iPSCs and their differentiated derivatives but significantly improved in Terc−/− ntESCs. Thus, our results suggest that SCNT-mediated reprogramming mitigates telomere dysfunction and mitochondrial defects to a greater extent than iPSC-based reprogramming. Understanding the basis of this differential could help optimize reprogramming strategies.
 
3.      'Heat maps' find cervical cancer
 
'Heat maps' find cervical cancer
 
A new test that uses heat to examine blood can be used to detect cancer, according to US scientists.
The "plasma thermogram" examines the proteins inside blood, including those produced by tumours.
A study, in the journal Plos One, showed the test could detect cervical cancer and how advanced it was.
Cancer Research UK said thermograms might improve detection, but more evidence on the accuracy and reliability was needed.
Screening for cervical cancer currently involves a looking for abnormal cells in a smear test and detecting high-risk viruses that can cause the disease.
The study, at the University of Louisville, used the plasma thermogram technology to analyse blood samples.
The sample will respond differently to heat depending on the types of proteins contained in the blood. It results in a thermogram - like a fingerprint - of the protein content.
The system was tested on 67 women with different stages of the cervical cancer to see if it could detect the differences between the patients and healthy people.
Lead researcher Dr Nichola Garbett said: "We have been able to demonstrate a more convenient, less intrusive test for detecting and staging cervical cancer."
She said the test could be used to determine which cancers needed to be treated and which needed monitoring.
"Comparing blood samples of patients who are being screened or treated against those thermograms should enable us to better monitor patients as they are undergoing treatment and follow-up," she added.
"This will be a chance for us to adjust treatments so they are more effective."
Dr Emma Smith, from Cancer Research UK, said: "This new approach could lead to improvements in the way we detect, treat and monitor cervical cancer, but this was a very small study so it's not yet known if it will be accurate and reliable enough for wider use.
"Early changes that can lead to cervical cancer often disappear naturally, so having a test that gives doctors a better indication of the risk posed by abnormal cells detected during a smear test could prevent some women receiving unnecessary treatment."
 
4.      A Ligand-Independent VEGFR2 Signaling Pathway Limits Angiogenic Responses in Diabetes
¡¾Text abstracts¡¿Sci. Signal., 7 January 2014,Vol. 7, Issue 307, p. ra1
 
A Ligand-Independent VEGFR2 Signaling Pathway Limits Angiogenic Responses in Diabetes
Carmen M. Warren, Safiyyah Ziyad, Anaïs Briot et al.
 
Although vascular complications are a hallmark of diabetes, the molecular mechanisms that underlie endothelial dysfunction are unclear. We showed that reactive oxygen species generated from hyperglycemia promoted ligand-independent phosphorylation of vascular endothelial growth factor receptor 2 (VEGFR2). This VEGFR2 signaling occurred within the Golgi compartment and resulted in progressively decreased availability of VEGFR2 at the cell surface. Consequently, the responses of endothelial cells to exogenous VEGF in a mouse model of diabetes were impaired because of a specific deficiency of VEGFR2 at the cell surface, despite a lack of change in transcript abundance. Hyperglycemia-induced phosphorylation of VEGFR2 did not require intrinsic receptor kinase activity and was instead mediated by Src family kinases. The reduced cell surface abundance of VEGFR2 in diabetic mice was reversed by treatment with the antioxidant N-acetyl-L-cysteine, suggesting a causative role for oxidative stress. These findings uncover a mode of ligand-independent VEGFR2 signaling that can progressively lead to continuously muted responses to exogenous VEGF and limit angiogenic events.
 
5.       An Effective Approach to Prevent Immune Rejection of Human ESC-Derived Allografts
¡¾Text abstracts¡¿Cell Stem Cell, Volume 14, Issue 1, 121-130, 2 January 2014
 
An Effective Approach to Prevent Immune Rejection of Human ESC-Derived Allografts
 
Human embryonic stem cells (hESCs) hold great promise for cell therapy as a source of diverse differentiated cell types. One key bottleneck to realizing such potential is allogenic immune rejection of hESC-derived cells by recipients. Here, we optimized humanized mice (Hu-mice) reconstituted with a functional human immune system that mounts a vigorous rejection of hESCs and their derivatives. We established knockin hESCs that constitutively express CTLA4-Ig and PD-L1 before and after differentiation, denoted CP hESCs. We then demonstrated that allogenic CP hESC-derived teratomas, fibroblasts, and cardiomyocytes are immune protected in Hu-mice, while cells derived from parental hESCs are effectively rejected. Expression of both CTLA4-Ig, which disrupts T cell costimulatory pathways, and PD-L1, which activates T cell inhibitory pathway, is required to confer immune protection, as neither was sufficient on their own. These findings are instrumental for developing a strategy to protect hESC-derived cells from allogenic immune responses without requiring systemic immune suppression.
 

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