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Melanoma Incidence and Mortality in Europe (Sorry - could not obtain a link)
New Estimates, Persistent Disparities
A.M. Forsea, V. del Marmol, E. de Vries, E.E. Bailey, A.C. Geller Dec 09, 2012 Authors & Disclosures
The British Journal of Dermatology. 2012;167(5):1124-1130. © 2012 Blackwell Publishing
Summary
Background Melanoma incidence and mortality in Europe are high but there are significant gaps in the epidemiological information available across the continent.
Objectives With the aim of enhancing the planning of educational programmes for reducing the melanoma burden in Europe, we analysed the most recent incidence and mortality data for Europe with a new focus on the regional disparities of melanoma reporting.
Methods GLOBOCAN 2008, the standard set of worldwide estimates of cancer incidence and mortality produced by the International Agency for Research on Cancer for 2008, was used to provide the estimated age-standardized rates (world standard population) of melanoma incidence and mortality in European countries and regions.
Results The estimated age-standardized incidence of melanoma (measured per 100 000 person-years) varies widely from 19·2 in Switzerland to 2·2 in Greece. The incidence rate of 4·3 of Central and Eastern Europe (CEE) is less than half of that of Western Europe. Melanoma mortality rates of 1·5 are similar in CEE and Western Europe, although rates vary with a high of 3·2 in Norway and a low of 0·9 in Greece. Over 20 000 deaths from melanoma were estimated in Europe in 2008, with CEE having the largest share (35·5%) among the four geographical European regions. Population-based data are lacking for significant parts of CEE, which must rely on estimates.
Conclusions The most recent estimates of melanoma incidence and mortality in Europe reveal sharp differences between European countries, possibly related to missed opportunities for early diagnosis and incomplete reporting of melanoma in Eastern Europe.
From the In Vivo blog
MD Anderson Cancer Center/GlaxoSmithKline – University of Texas’ MD Anderson Cancer Center has tapped GlaxoSmithKline to help it develop and commercialize an antibody discovered by scientists at the center. Anderson will handle preclinical activities, while GSK will be responsible for clinical development and commercialization. Under the deal announced Dec. 7, the cancer center will receive an undisclosed upfront payment as well as research funding and development milestones. Anderson indicated that the deal could result in $335 million in payments for the center, as well as royalties on any commercial products that are developed. The antibodies activate OX40, a protein that stimulates the immune response in T-cells against cancer. "This agreement is not only a testament to the vision shared by GSK and MD Anderson that successful clinical development of oncology drugs requires seamless integration of drug development expertise and deep biological knowledge," said Giulio Draetta, director of the Institute of Applied Cancer Science at Anderson, in a statement. - L.L.
HIV Infection, Testing, and Risk Behaviors Among Youths — United States
http://www.cdc.gov/mmwr/preview/mmwrhtml/mm6147a5.htm?s_cid=mm6147a5_w
In 2009, 6.7% of the estimated 1.1 million persons living with human immunodeficiency virus (HIV) infection in the United States were youths (defined in this report as persons aged 13–24 years); more than half of youths with HIV (59.5%) were unaware of their infection.
microRNA: Targets and Tools for Therapeutic Development
http://www.healthtech.com/mrn
Identifying mRNA, MicroRNA and Protein Profiles of Melanoma Exosomes
http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0046874
Discussion
In the present study, we first investigated the mRNA signatures of melanoma cells and their exosomes and compared these signatures with those of normal melanocytes and their exosomes. We found large numbers of differentially expressed mRNAs in melanocytes compared with melanocyte-derived exosomes, and in melanoma cells compared with melanoma-derived exosomes. This is consistent with previous findings in glioblastoma microvesicles and their donor cells [14]. Exosomal mRNAs may transfer or shuttle signals between cells, and may contribute to important biological functions in normal cells, as well as malignant transformation in tumor cells [14], [15].
One interesting aspect of our findings was that when we examined the correlation of mRNA expression in cells compared with their exosomes, we noticed that melanoma cell-derived exosomes have a closer relationship with their originating melanoma cells than normal melanocyte-derived exosomes did with their originating non-cancer cells. This suggests that cancer-derived exosome mRNA profiles may more closely reflect mRNA profiles in cancer cells themselves, which would imply the potential of using exosomes as a biomarker for melanoma. By comparing mRNA profiles in melanoma exosomes with normal melanocyte-derived exosomes, we found that even though there are various biological processes and ontologies of those differentially expressed exosome mRNAs, many are linked to the advancement of melanoma. Indeed, several studies have shown that tumor exosomes have the ability to transport RNAs to promote tumor growth [14]. This finding also suggests the potential of using exosome profiles as biomarkers not only of the presence of disease, but also disease progression and response to therapy.
We then investigated miRNA signatures in melanoma cells and their exosomes and compared these signatures with those from normal melanocytes and their exosomes using miRNA arrays. We discovered that there are some differentially expressed miRNAs in melanocytes compared with melanocyte-derived exosomes, and also between melanoma cells compared with melanoma-derived exosomes. We also determined that many of these miRNA have important functions in cellular growth and proliferation, cellular development, cellular movement, and cell death. Our findings confirm earlier studies showing that miRNAs in exosomes have important biological functions [14]–[17]. An important finding from our study came from looking at the correlation of miRNA expression in cells compared with exosomes. Both melanoma cell-derived and normal melanocyte-derived exosomes miRNA profiles were strongly correlated with their originating cells. However, there was much weaker correlation between miRNA expression in melanoma exosomes compared with miRNA expression in normal melanocyte-derived exosomes. This strongly suggests that there are distinctive miRNA profiles between melanoma exosomes and normal melanocyte exosomes, which confirms the rationale behind many of the current studies investigating the usefulness of exosomal miRNA as tumor biomarkers in diseases, such as lung cancer and ovarian cancer [9], [18]. Our data show that differential expression of exosomal miRNA is more focused than mRNA expression. Furthermore, when we looked at the regression analysis of mRNA signals and miRNA signals between A375 and HEMa-LP exosomes, we showed that the difference of miRNA signals between A375 and HEMa-LP exosomes is much larger than that of mRNA signals. It is likely that this would be another advantage of using exosomal miRNA signatures in biomarker studies, instead of sophisticated and unbalanced mRNA data.
Through our proteomic approach, we identified exosomal proteins that are known to be associated with cell adhesion, migration, and invasion in melanoma. Some of these proteins have been identified by other researchers in similar studies. For example, Mears et al. compared the protein profiles of two melanoma cell lines, MeWo and SK-MEL-28 cells, with their exosomes [36]. They discovered several novel melanoma exosomal proteins, such as p120 catenin, radixin, and immunoglobulin superfamily member 8 (PGRL). Among the list of exosomal proteins they identified were syntenin 1 and annexin A2, which are also on our list of identified differentially expressed exosomal protein [36]. Although most reports have determined that syntenin-1 enhances melanoma cell migration, invasion and metastasis [37], [38], several discrepant findings have been observed about the role of syntenin-1 depending on the specific cellular environment investigated [39]. In our study, we observed that syntenin-1 protein expression was reduced in melanoma exosomes compared to normal melanocyte-derived exosomes. This is in line with findings in a B16 mouse melanoma model that show syntenin-1 has lower expression levels in melanoma secrotomes, but cells exhibit a greater capacity for cell invasion [23].
Annexin A1 has also been shown to amplify the ability of cells to become invasive and to enhance melanoma dissemination [40]. It is a key regulator of pathological angiogenesis and physiological angiogenic balance [34]. Similarly, annexin A2 is upregulated in various tumors and has been shown to play multiple roles in regulating cellular function, including angiogenesis, proliferation, apoptosis, cell migration, invasion and adhesion [31]. In our study, we found that protein expression levels of annexin A1 were upregulated, whereas annexin A2 levels were downregulated in A375 melanoma exosomes. Grewal and Enrich have summarized the differences in various isoforms of annexin protein expression patterns, subcellular localization and mode of action. They suggest that annexins are likely to differentially contribute and cooperate in fine-tuning of the activity of epidermal growth factor receptor (EGFR), thus regulate the growth of a variety of tumor cells [41].
Our study also revealed several novel proteins differentially expressed in exosomes that have not previously been identified in this context. The protein with the greatest differential expression in melanoma exosomes is hyaluronan and proteoglycan link protein 1 (HAPLN1). HAPLN1 is an extracellular matrix mucopolysaccharide that has been previously shown to promote metastasis in cancer cells, including B16F10 melanoma [42], [43]. HAPLN1 is also involved in melanoma development and extracellular matrix remodeling during the process of melanoma cell migration and melanoma progression [35], [44]. Further research investigating the role of HAPLN1 in exosomes may uncover novel mechanisms to explain potential roles for exosomes in melanoma progression. Additionally, HAPLN1 may also prove to be important clinically, as it is a specific exosomal protein that could be the focus of future melanoma biomarker studies.
Some differentially expressed exosomal proteins have already been explored as potential biomarkers in melanoma patients [1]. For example, Logozzi et al. designed an in-house sandwich ELISA (Exotest) and found that plasma exosomes expressing CD63 or caveolin-1 were significantly increased in melanoma patients compared to healthy donors. They further determined that the number of caveolin-1 positive plasma exosomes was significantly greater than the number of CD63 positive exosomes in melanoma patients [1]. Since then, CD63 has become commonly accepted as an exosome marker. Obviously, combining our findings with those of others, together with additional clinical validations will be the best way to provide us with a panel of proteins that will enable us to make more precise predictions of prognosis for melanoma patients. Similar exosomal proteomics techniques have been applied by many researchers to diseases other than those involving tumors [45], such as neurodegenerative disorders [46] and kidney disease [20], which further suggests that exosomal proteomics might provide a powerful diagnostic tool for many diseases.
We are aware that studies such as ours that examine exosomal mRNA, miRNA, and protein profiles produce large amounts of data. Indeed, our mRNA expression profile resulted in identification of thousands of disparate differentially expressed genes. However, we were able to focus this information better when combining miRNA and protein profiles. Proteins are the end-point molecules that execute biological functions after undergoing several sophisticated genetic processes, including transcription, translation and post-translational/post-transcriptional modifications. Our findings lead us to suggest that combining miRNA and protein profiles is a superior approach to identify future exosomal biomarker of disease. One example of how our data can be combined to provide potential new avenues of mechanistic melanoma research and biomarker studies is to look at interactions of highly differentially expressed proteins and miRNAs. In our study, HAPLN1, hsa-miR-23, and hsa-miR-21 were the three molecules at the top of our differentially expressed lists. TargetScan identified that HAPLN1 is targeted by hsa-miR-23, but HAPLN1 can also trigger upregulation of miR-21, which was previously shown to serve an essential role in the malignant progression of human gliomas [47]. Identifying how these three molecules interact in melanoma to contribute to metastasis and disease progression could potentially reveal new avenues of targeted therapy or biomarkers useful in diagnosis and prognosis.
Another novel finding of our study is that normal melanocytes can acquire invasiveness through the internalization of melanoma exosomes. Our data suggest that mRNA and miRNA within melanoma exosomes may be actively transported into normal melanocytes and induce normal melanocyte invasion ability. Pre-treatment of melanoma exosomes with DNase and RNase A didn’t affect the invasion ability of normal melanocytes rendered by melanoma exosome transfer. This excludes the possibility that DNA or RNA molecules in the cell supernatant might mediate this induced normal melanocyte invasion ability. It is exosome transportation that confers normal melanocytes’ invasion ability. Pre-treatment of Protease K abolished the normal melanocytes’ invasion ability rendered by the melanoma exosomes. The reason might be that Protease K disrupt the exosome membrane structure and affect the exosome transmission. A protein synthesis inhibitor was also able to inhibit normal melanocytes’ invasion ability acquired through uptake of melanoma exosomes. This further suggests that the whole process of exosome uptake, molecule transmission, and promotion of invasion requires new protein synthesis.
Although it seems unlikely that circulating exosomes impart a malignant phenotype to normal melanocytes in vivo, it demonstrates the principle that potent intercellular signaling via melanoma exosomes may alter disease progression and metastatic potential. Our findings are in accordance with results from other researchers showing that exosomes can transport RNA and proteins to other cells in order to promote tumor growth [14]. Exosomes released from melanoma cells can also prepare sentinel lymph nodes for tumor metastasis [48]. We attempted to use cytochalasin D to inhibit exosome uptake by HEMa-LP cells to further study the underlying mechanisms; however, cytochalasin D is toxic to the HEMa-LP cells (data not shown). This prevented us from obtaining useful data. Detailed mechanistic studies are needed to clarify how the uptake of exosomes contributes to melanoma progression.
We also compared our method of combination of ultrafiltration and ultracentrifugation with another exosome isolation method, Exoquick-TC precipitation, to assess whether there were differences in the ability of the exosomes to induce migration/invasion. Exosomes isolated by Exoquick-TC precipitation were not able to affect the normal melanocyte invasion ability. The reason for a discrepancy between the effects of exosomes isolated by different methods might be that Exoquick-TC precipitation couldn’t enrich enough exosomes. Indeed, we observed that sufficient exosomes are essential for the effective enhancement of normal melanocyte invasion ability (unpublished data).
We expected that after exosomes are taken up by normal melanocytes, those highly expressed genes in melanoma exosomes might also then be highly expressed in normal melanocytes. However, when assessing the gene expression changes of normal melanocyte after the uptake of melanoma cell-derived exosomes, we found minimal differential expression of those genes that were highly expressed in melanoma exosomes. We have considered two possible explanations for this finding. One is that, even though the invasive melanocytes significantly increased compared with control melanocytes, the portion of invasive melanocytes were a small part of the total melanocytes (about 10%, Fig. 6C). The other reason is that after exosomes transfer into melanocytes, there were multiple cellular processes and signal pathways that would need to act cooperatively in order to alter cellular gene expression to reflect the original highly expressed genes in melanoma exosomes. The best approach to identify the differentially expressed genes in normal melanocytes after the upake of exosomes would be through microarray screening. Microarray screening may also help to clarify the mechanisms of increased invasion ability of normal melanocyte after taking-up melanoma exosomes. This is one of our future research interests.
Since this work was based on two melanoma cell lines compared with two normal melanocyte cell lines, we understand that our differentially expressed mRNAs, miRNAs, and protein profiles cannot be universally applied to other melanoma cell lines. However, these data provide us with initial candidate molecules that may be important in melanoma tumorigenesis and tumor progression. Further exploration into the role of these molecules contained in melanoma exosomes is likely to unveil detailed molecular mechanisms of melanoma progression. Similarly, it is likely that samples from melanoma patients will also provide expression profiles that have some variation with cell lines. However, further investigation of exosomal profiles using clinical samples may lead to clinical translation using these profiles as disease biomarkers, or even through identification of new therapeutic targets.
In conclusion, to the best of our knowledge, this is the first comprehensive attempt to reveal the whole mRNA, miRNA and proteome of melanoma exosomes compared with normal melanocyte exosomes. Our study provides a starting point for future more in-depth explorations of tumor-derived exosomes. This exosome research will aid in understanding the molecular biology of melanoma, and may also define targets that can be translated into clinical applications as non-invasive biomarkers or as therapeutic targets for melanoma patients.
Nephroplus Ties Up With Medicity Hospitals to Launch 11 Dialysis Units in South India
http://ehealth.eletsonline.com/2012/10/nephroplus-ties-up-with-medicity-hospitals-to-launch-11-dialysis-units-in-south-india/
The state of kidney care in India is still in shambles as more than 1/3 of dialysis patients get infected with life threatening HIV, hepatitis C and hepatitis B infections during dialysis.
Panel recommends routine HIV tests for teens, adults
http://www.usatoday.com/story/news/nation/menshealth/2012/11/19/hiv-tests-teens-adults/1712683/
"In a broad new expansion of HIV screening, an influential government panel now says everyone ages 15 to 65 should be tested for the virus that causes AIDS."
FDA approves Promacta for patients with chronic HCV, thrombocytopenia
November 20, 2012
http://www.healio.com/hepatology/chronic-hepatitis/news/online/%7BB262ADBD-9DB6-477A-B006-8A26067C19F6%7D/FDA-approves-Promacta-for-patients-with-chronic-HCV-thrombocytopenia
Growing concerns over 'in the air' transmission of Ebola
http://www.bbc.co.uk/news/science-environment-20341423
Cancer Exosomes Trigger Fibroblast to Myofibroblast
Differentiation
http://cancerres.aacrjournals.org/content/70/23/9621.full.pdf
SCIENTISTS AT IRB BARCELONA DISCOVER A KEY PROCESS THAT ALLOWS COLON CANCER TO METASTASIZE
http://www.irbbarcelona.org/index.php/en/news/irb-news/scientific/scientists-at-irb-barcelona-discover-a-key-process-that-allows-colon-cancer-to-metastasize
HANS CLEVERS: “EVERY DAY NEW RESEARCH IS SHOWING US THAT MANY TYPES OF CANCERS ARE FED BY TUMOUR STEM CELLS"
http://www.irbbarcelona.org/index.php/en/news/irb-news/corporative/hans-cleversevery-day-new-research-is-showing-us-that-many-types-of-cancers-are-fed-by-tumour-stem-cells
Marine animals inspire researchers to invent a device that can detect, capture and release rare cancer cells
http://www.eurekalert.org/pub_releases/2012-11/bawh-car110912.php
Detection, analysis of 'cell dust' may allow diagnosis, monitoring of brain cancer
A novel miniature diagnostic platform using nuclear magnetic resonance technology is capable of detecting minuscule cell particles known as microvesicles in a drop of blood. Detecting microvesicles shed by cancer cells could prove a simple means for diagnosing cancer or monitoring treatment response.
http://www.massgeneral.org/about/pressrelease.aspx?id=1519
Hepatitis Drug Derailed by Deal
http://online.wsj.com/article/SB10001424127887324073504578107421424680236.html
Therapeutic Potential of RNA Interference
A New Molecular Approach to Antiviral Treatment for Hepatitis C
M. Motavaf, S. Safari, S. M. Alavian Nov 09, 2012Authors & Disclosures
J Viral Hepat. 2012;19(11):757-765. © 2012 Blackwell Publishing
Hepatitis C virus (HCV) infection remains a major cause of chronic liver disease with an estimated 170 million carriers worldwide. Current treatments have significant side effects and have met with only partial success. Therefore, alternative antiviral drugs that efficiently block virus production are needed. During recent decades, RNA interference (RNAi) technology has not only become a powerful tool for functional genomics but also represents a new therapeutic approach for treating human diseases including viral infections. RNAi is a sequence-specific and post-transcriptional gene silencing process mediated by double-stranded RNA (dsRNA). As the HCV genome is a single-stranded RNA that functions as both a messenger RNA (mRNA) and replication template, it is an attractive target for the study of RNAi-based viral therapies. In this review, we will give a brief overview about the history and current status of RNAi and focus on its potential application as a therapeutic option for treatment for HCV infection.
Introduction
Hepatitis C virus (HCV) is a major cause of chronic liver disease and hepatocellular carcinoma. More than 170 million individuals are affected with this virus worldwide.[1]
The current HCV antiviral therapy for interferon/ribavirin is successful in approximately half of the G1 cases. With the addition of the new FDA- and EMA-approved NS3 protease inhibitors, boceprevir and telaprevir, the rate of sustained virologic response in G1 has improved to 70%, still leaving an unmet clinical need. RNAi has been shown to be a naturally occurring process of sequence-specific gene silencing in plants and vertebrates.[2]
This process is an RNA-dependent gene silencing process that is controlled by the RNA-induced silencing complex (RISC) and is initiated by short double-stranded RNA molecules (dsRNA) in a cell's cytoplasm. The dsRNA can either be chemically synthesized as small inferring RNA (siRNA) then directly transfected into cells or can be produced inside the cell by introducing vectors that express short-hairpin RNA (shRNA) precursors of siRNAs. The process of shRNA into functional siRNA involves cellular RNAi machinery that naturally process genome encoded microRNAs (miRNA) that are responsible for cellular regulation of gene expression by different mechanisms.[3] To date, hundreds of miRNAs have been identified as human genome. These are 22–24 nucleotides in length and downregulate gene expression by attaching themselves to messenger RNAs (mRNAs) and preventing them from being translated into proteins.[4]
Because of the functional similarities between miRNA and siRNA, which is involved in the inhibition of viruses and silencing of transposable elements in plants, insects, fungi and nematodes, exogenously introduction of siRNA into the target cells by various transfection methods may trigger the RNAi pathway against target gene. Many viruses, including HCV, produce a transitory double-stranded RNA during replication that can serve as RNA target for RNAi pathway. This makes HCV an attractive target for RNAi therapy. Whether it will ultimately be necessary is dependent on the outcome of current studies looking at the efficacy of interferon-free combination therapeutic regimes that include protease, polymerase and NS5A inhibitors.
New portable device enables RNA detection from ultra-small sample in only 20 minutes
http://www.riken.jp/engn/r-world/info/release/press/2012/121108/index.html
Organ on a chip? Scientists test drugs on tiny, artificial lung
http://news.yahoo.com/organ-chip-scientists-test-drugs-tiny-artificial-lung-004601848--finance.html
Exosomes and the Kidney: Blaming the Messenger.
http://www.unboundmedicine.com/medline/ebm/record/23113949/abstract/Exosomes_and_the_Kidney:_Blaming_the_Messenger_
Exosomes: Cell Garbage Can, Therapeutic Carrier, or Trojan Horse?
http://www.unboundmedicine.com/medline/ebm/record/23114790/abstract/Exosomes:_Cell_Garbage_Can_Therapeutic_Carrier_or_Trojan_Horse
Chronic myeloid leukemia (CML) exosomes promote angiogenesis in a Src-dependent fashion in vitro and in vivo
http://researchfestival.nih.gov/2012/posters.cgi?id=CELLBIO-11
[b"]This credentials exosomes and angiogenesis as molecular targets in CML via activation of Src both in leukemia and its microenvironment".
Research and Markets: MicroRNAs and Exosomes Market Report 2012
http://finance.yahoo.com/news/research-markets-micrornas-exosomes-market-094400445.html
A label-free electrical detection of exosomal microRNAs using microelectrode array
http://pubs.rsc.org/en/content/articlelanding/2012/CC/C2CC36111F
The genomic and proteomic content of cancer cell-derived exosomes
http://www.frontiersin.org/cancer_genetics/10.3389/fonc.2012.00038/abstract
Strategies for Rational and Personalized Cancer Biomarker Discovery
http://www.sciclips.com/sciclips/blogArticle.do?id=1021
Incidence of hepatitis C virus infection in patients on hemodialysis: A systematic review and meta-analysis.
http://www.ncbi.nlm.nih.gov/pubmed/23072424
"The incidence rate of hepatitis C virus infection among patients on hemodialysis was significantly high. Efforts should be taken to control hepatitis C virus infection in hemodialysis units, especially in developing countries."
Antiviral therapy for prevention of hepatocellular carcinoma in chronic hepatitis C: systematic review and meta-analysis of randomised controlled trials
http://bmjopen.bmj.com/content/2/5/e001313.abstract
Tumor Exosomes Promote Metastatic Dissemination by Reprogramming Bone Marrow Cells
http://www.hematology.org/Publications/Hematologist/2012/8895.aspx
While the specifics are intriguing, more broadly, the study hints at the complexity of the cargo carried by tumor exosomes, suggesting an enormous potential to directly influence the biology of the tumor microenvornment. The experiments also identify another part of the multi-compartmental physiology of metastatic cancer by demonstrating that exosome trafficking alters the malignant phenotype and transcends conventional paracrine signaling by direct cytoplasmic transfer of a receptor tyrosine kinase. Even though experimentally feasible, global interference with exosome release as a constitutive cellular function is too broad a therapeutic target. Going forward, we can anticipate that discovery-driven proteomic or transcriptomic analyses will dissect the molecular events that result from vesicle trafficking in the tumor and bone marrow microenvironment and lead to the identification of more suitable therapeutic targets.
Peinado and colleagues provide persuasive evidence that tumor-derived exosomes promote melanoma metastasis by activating cells in the bone marrow and prompting the formation of a “pre-metastatic” niche. Questions remain unanswered about the mechanism by which c-kit/Tie-2–expressing cells shape the microenvironment in the metastatic target tissue and about other cellular processes that are affected by the exosome transfer process. Nevertheless, this imaginative study has both diagnostic and therapeutic implications and should stimulate further research into the role of exosomes and their cellular targets in the bone marrow during the evolution and progression of cancer.
Microfluidic Breakthroughs Offer New Options for Ease and Accuracy in Extraction of Rare Cells or Separating Blood
http://www.uc.edu/news/NR.aspx?id=16775
Antiviral therapy for prevention of hepatocellular carcinoma in chronic hepatitis C: systematic review and meta-analysis of randomised controlled trials
http://bmjopen.bmj.com/content/2/5/e001313.long
Plasmonic ELISA for the ultrasensitive detection of disease biomarkers with the naked eye
https://fileexchange.imperial.ac.uk/files/cb229a60c28/NNANO%202012%20186.pdf
Imperial College London
Studies Find Cancer Comes in More Shades Than Pink
http://www.bloomberg.com/news/2012-10-30/studies-find-cancer-comes-in-more-shades-than-pink.html
MicroRNAs and Thyroid Cancer
http://www.hindawi.com/journals/ije/si/613037/cfp/
Thank you very much for that.
Aethlon Medical Announces Issuance of Cancer Therapy Patent
http://aethlonmedical.investorroom.com/2012-10-25-Aethlon-Medical-Announces-Issuance-of-Cancer-Therapy-Patent
Projections of cancer prevalence in the United Kingdom, 2010–2040
http://www.nature.com/bjc/journal/v107/n7/full/bjc2012366a.html
"Increasing cancer survival and the growing/ageing population of the United Kingdom mean that the population of survivors is likely to grow substantially in the coming decades, as are the related demands upon the health service. Plans must, therefore, be laid to ensure that the varied needs of cancer survivors can be met in the future."
HCV Admissions Rise While HIV Ones Fall
http://beforeitsnews.com/healthcare/2012/10/hcv-admissions-rise-while-hiv-ones-fall-2442490.html
Connecting Patients With Experimental Drugs
http://online.wsj.com/article/SB10000872396390444592704578062640104322714.html