Scientists have created ellular backpacksthat could carry therapeutic agents to the site of inflammation and then release them.
Inflammation is a normal way for the body to respond to injury or infection. The swelling, heat,
or even tissue death. any diseases result in inflammation, says Samir Mitragotri, professor of chemical engineering at University of California, Santa barbara,
Whether inflammation is a byproduct of the disease or the inflammation is the disease, it is a common indicator of a problem with the system. f we could target the common denominator,
whether the inflammation is coming from cancer or arthritis, we could deliver the drug there,
says Mitragotri, who specializes in targeted drug delivery. By taking advantage of natural body processes, researchers at UC Santa barbara and MIT have developed a method of targeting inflamed tissues
hold therapeutic agents that can be released at the site of the inflammation. These polymeric discs are coated on one side with a single layer of an antibody that can bind to receptors on the monocyte surface.
you and your doctor can make a plan on how to reverse it through diet, supplements,
or other therapies,"says Adam Murphy. Low Vitamin d linked to aggressive prostate cancer The development of effective cellular backpacks has broad potential,
say the researchers. asically the main benefit is that you can deliver the drug in a more effective dose,
which often has a narrow therapeutic range: too little and the treatment is not effective, too much and it can be lethal.
Not only can targeted therapy ensure other body systems remain unaffected, Mitragotri explains, but it could also allow for higher doses of drug to the site,
if your brain didn#t cycle A study with mice shows how the mammalian brain is able to maintain a constant state of up and downhile under anesthesia, during slow-wave sleep,
in a deal that expands the buyer gastrointestinal (GI) disorders and rare-disease portfolios, as well as its global footprint.
a parathyroid hormone (rhpth 1-84) that if approved would be the first bioengineered hormone replacement therapy for hypoparathyroidism (HPT.
an injection drug indicated for long-term treatment of adults with short bowel syndrome (SBS) who need parenteral support.
would complement Shire existing stable of drugs for gastrointestinal diseases.""The acquisition of NPS Pharma is a significant step in advancing Shire's strategy to become a leading biotechnology company, Shire CEO Flemming Ornskov, M d,
The NPS Pharma organization will be a welcome addition to Shire as we continue to help transform the lives of patients with rare diseases."
and ensure we continue to transform the lives of patients with short bowel syndrome, hypoparathyroidism,
and a new indication for teduglutide, pediatric SBS. NPS Pharma is now conducting a global study for teduglutide in pediatric patients with SBS who are dependent on parenteral support.
NPS has licensed several of its products through partnerships with several biopharma giants. Amgen markets cinacalcet HCL as Sensipar in the U s. and as Mimpara in the EU;
and we believe it has great therapeutic potential.""Dr. Xue is the lead author in a paper (lysine-rich motif in the phosphatidylserine receptorpsr-1 mediates recognition
and hopefully move toward solving injuries,"said Dr. Hilliard. In the future, neurosurgery may be combined with molecular biology to deliver positive clinical outcomes
and perhaps treat conditions like spinal cord or nerve injuries, he said. During programmed cell death,
apoptotic cells flag themselves for elimination by moving a specific cell membrane component known as phosphatidylserine (PS) from the inner membrane to the cell surface,
"While biomedical researchers have had some successes in repairing peripheral nerves and nerve clusters outside the brain and spinal cord in humans,
Such nerve damage can cause partial or total paralysis. Xue, who first identified the PSR-1 receptor in 2003,
According to Dr. Xue, C. elegans is an ideal organism to use in the hunt for new therapeutics to treat nerve damage because of its relatively small,
but we feel these findings offer promise in seeking new and effective therapeutics. c
#Small Molecule Successfully Targets Telomerase to Destroy Cancer cells Scientists at the University of Texas Southwestern Medical center report that they have targeted telomeres with a small molecule called 6-thiodg that takes advantage of the cell's biological clock to kill cancer cells
and shrink tumor growth. Jerry W. Shay, Ph d.,professor and vice chairman of cell biology at UT Southwestern,
and colleague, Woodring E. Wright, M d.,Ph d.,professor of cell biology and internal medicine, found that 6-thio-2'-deoxyguanosine could stop the growth of cancer cells in culture and decrease the growth of tumors in mice.
Drs. Shay and Wright are co-senior authors of the study nduction of Telomere Dysfunction Mediated by the Telomerase Substrate Precursor 6-Thio-2deoxyguanosineappearing in Cancer Discovery. reatment with 6-thio
-dg resulted in rapid cell death for the vast majority of the cancer cell lines tested,
6-thio-dg caused a decrease in the tumor growth rate superior to that observed with 6-thioguanine treatment.
In addition, 6-thio-dg increased telomere dysfunction in tumor cells in vivo. These results indicate that 6-thio-dg may provide a new telomere-addressed telomerase-dependent anticancer approach."
as well as tumor burden shrinkage in mice,"noted Dr. Shay, who is also associate director of the Harold C. Simmons Comprehensive Cancer Center.
Cancer cells are protected from apoptosis by telomerase, which ensures that telomeres do not shorten with every division.
Telomerase has therefore been the subject of intense research as a target for cancer therapy.
but these drugs have to be administered for long periods of time to successfully trigger cell death and shrink tumors,
because cells in any one tumor have chromosomes with different telomere lengths and any one cell's telomeres must be shortened critically to induce death. 6-thiodg is used preferentially as a substrate by telomerase
Telomerase is an almost universal oncology target, yet there are few telomerase-directed therapies in human clinical trials,
researchers noted.""Using telomerase to incorporate toxic products into telomeres is remarkably encouraging at this point,
"Since telomerase is expressed in almost all human cancers, this work represents a potentially innovative approach to targeting telomerase-expressing cancer cells with minimal side effects on normal cells,"continued Dr. Shay."
"We believe this small molecule will address an unmet cancer need in an underexplored area that will be rapidly applicable to the clinic
#Ultra-Fast Software Developed to Scan the Human genome Researchers at Nationwide Children's Hospital say they have developed an analysis pipeline that cuts the time it takes to search a person's genome for disease-causing variations from weeks to hours.
and $3 billion to sequence the first human genome,"notes Peter White, Ph d.,principal investigator and director of the biomedical genomics core at Nationwide Children's and the study's senior author."
%"At Nationwide Children's we have a strategic goal to introduce genomic medicine into multiple domains of pediatric research and healthcare.
Rapid diagnosis of monogenic disease can be critical in newborns, so our initial focus was to create an analysis pipeline that was extremely fast,
and Mental health (CAMH) in Toronto have found a possible link between inflammation in the brain and clinical depression.
and standard of care for mental health issues. The results from this study, published today in JAMA Psychiatry in an article entitled ole of Translocator Protein Density,
a Marker of Neuroinflammation in the Brain During Major depressive episodes showed that there was a 30%increase in inflammation among patients experiencing a major clinical episode."
"This finding provides the most compelling evidence to date of brain inflammation during a major depressive episode,
"says Jeffrey Meyer, M d.,Ph d.,of CAMH's Campbell Family Mental health Research Institute and senior author of the study."
Currently, there are no therapies that address inflammation as part of regimen to treat depression and the CAMH team believes that using anti-inflammatories as a treatment option needs to be explored further. his finding provides the most compelling evidence to date of brain inflammation,
because it implies that therapeutics that reduce microglial activation should be promising for MDE, the paper concludes c
and placental barriers act as critical ramparts to infections from microbial pathogens, yet some have evolved mechanisms to breach the cellular obstacles that lie in their path.
Unlocking the underlying mechanisms of host barrier permissiveness to microbes is critical to understanding the etiology of many infectious diseases.
The common foodborne bacteria Listeria monocytogenes (Lm) can survive and proliferate within the intestinal lumen of the host,
causing meningitis and encephalitis, as well as the placental barrier, resulting in severe neonatal infection or miscarriage.
Researchers at the Pasteur institute in Paris have discovered the protein pathways that are responsible for allowing Listeria to circumvent host barriers.
The results from this study were published today in the Journal of Experimental Medicine within an article entitled I3-kinase activation is critical for host barrier permissiveness to Listeria monocytogenes Listeria relies on two surface proteins called
Marc Lecuit, M d.,Ph d.,Head of the Biology of Infections Unit at the Pasteur institute and senior author on the study,
results illustrate how microbial pathogens have evolved to invade mammalian tissues, taking advantage of both similarities and differences of host barriers.
They also suggest that the absence of placental constitutive PI3-K activity may reinforce its barrier function toward pathogens
funded by the Movember Foundation and conducted by scientists at The Institute of Cancer Research (ICR) in London,
in addition to uncovering a gene that may aid tumors in promoting resistance to existing drug therapies.
According to the authors, this is the first study of its kind to use whole-exome sequencing to probe testicular germ cell tumors,
and reveals some potentially important clues as to how the disease could be treated more effectively, stated Paul Workman, Ph d.,chief executive of ICR.
examined tumor samples from 42 patients with testicular cancer. They report previously unidentified chromosome duplications and confirmed data from earlier findings that associated these tumors with the KIT gene,
which has been linked to an array of other cancerous tissues.""Our study is the largest comprehensive sequencing study of testicular tumors published to date,
describing their mutational profile in greater detail than has been possible using previous technologies, says Clare Turnbull, Ph d.,senior author and team leader in predisposition and translational genetics at ICR.
Their preliminary finding of a link between XRCC2 and platinum drug resistance was validated once they sequenced a sample from an additional platinum-resistant tumor. e have identified new potential driver mutations for this type of cancer
whose cancer progresses in spite of the best available treatments,"said Dr. Turnbull Despite the fact that testicular cancer responds well to chemotherapy,
This study provides essential general knowledge concerning testicular germ line cell tumor development but more importantly, valuable insight into the genetic underpinnings as to why certain patients develop resistance to chemotherapy h
The goal of the new procedure is to avoid the transmission of mitochondrial diseases. Under the decision, the embryo would receive nuclear DNA from its mother and father along with healthy MITOCHONDRIAL DNA from a female donor.
Researchers at the Wellcome Trust Centre for Mitochondrial Research at Newcastle University estimate that about 2, 500 women of childbearing age in Britain carry mitochondrial disease.
We have great sympathy for families affected by mitochondrial disease and are opposed not in principle to mitochondrial replacement.
A committee of the Institute of Medicine (IOM) yesterday called for the sharing of supporting data for clinical trials results within six months after publication, with a full analyzable data set shared no later than 18 months
Also yesterday, Johnson & johnson (J&j) joined the Yale Open data Access (YODA) Project in agreeing to share data from clinical trials for medical devices and diagnostics.
or deny requests from investigators for de-identified patient data associated with the pharmaceutical, medical device,
professor of medicine and leader of the YODA Project. e hope this action serves as a catalyst to others to join the momentum on open science.
The European Medicines Agency in October issued a more expansive data sharing policy last October, though not the full open-access sought by advocates.
or otherwise harm public health? whether through inadvertent errors in data analysis or, in the U s.,the prospect of monetary gain through qui tam lawsuits, the report stated.
and therapies and that sustains patientswillingness to participate in them, said committee chair Bernard Lo, president of the Greenwall Foundation,
a funder of bioethics research. ur recommendations attempt to balance the interests of different stakeholders with the public interest in having the best information possible regarding the effectiveness and safety of therapies.
as well as disease-focused patient advocacy groups, regulators, and overseers such as institutional review boards, research ethics committees, investigators, their research institutions or universities, journals,
#New Microchip Design Captures Circulating Tumor Cells Circulating tumor cells (CTCS) represent the metastatic seed that can break away from the primary tumor site,
and spread to other parts of the bodyften causing more pathological symptoms than the primary cancer from which the CTCS were derived.
which could yield important new insights into how different cancers spread.""Very little is known about CTC clusters and their role in the progression and metastasis of cancer.
This unique technology presents an exciting opportunity to capture these exceptionally rare groups of cells for further analysis in a way that is minimally-invasive,
. director at the National Institute of Biomedical Imaging and Engineering who helped find the current study."
"This is the kind of breakthrough technology that could have a very large impact on cancer research."
"The findings from this study were published recently in Nature Methods through an article entitled"A microfluidic device for label-free, physical capture of circulating tumor cell clusters."
and melanoma cancers. The researchers observed CTC clusters ranging from 2-19 cells among 300%of the patients."
"said senior author Mehmet Toner, Ph d.,professor of surgery and health sciences and technology at Harvard Medical school,
Massachusetts General Hospital. he fact that we saw clusters in this many patients is really a remarkable finding."
Dr. Toner and his colleagues went on to test the technique in a small trial of 60 patients with metastatic cancer.
31%of prostate and 30%of melanoma patientsuggestive of a greater role for CTC clusters in metastatic cancers than previously thought.
Interestingly, the data from this small study also showed a rare presence of non-tumor derived immune cells within clusters,
"Given the increasing number of cancer therapies that engage the immune system, the ability to monitor tumor-immune cell interactions via the blood could be of great value."
"Dr. Toner and his colleagues anticipate that the Cluster-Chip will have an increasingly important role in stimulating new research on CTC cluster biology,
and to develop even better technologies to understand their biology in cancer metastasis. t
#Inexpensive Technique Developed to Manufacture Nanofibers Scientists at the University of Georgia say they have developed an inexpensive way to manufacture nanofibers,
Thousands of times thinner than the average human hair, nanofibers are used by medical researchers to create advanced wound dressings and for tissue regeneration
drug testing, stem cell therapies, and the delivery of drugs directly to the site of infection."
"The process we have developed makes it possible for almost anyone to manufacture high-quality nanofibers without the need for expensive equipment,
Nanofibers can also be loaded with proteins, nanotubes, fluorescent materials and therapeutic agents.""We can use almost any kind of polymer with this platform,
These people accumulate numerous self-inflicted injuries, often leading to reduced lifespan. Using detailed genome mapping
The team looked at nerve biopsies taken from the patients to see what had gone wrong and found that particular pain-sensing neurons were absent.
From these clinical features of the disease, the team predicted that there would be a block to the production of pain-sensing neurons during the development of the embryo.
and may hold promise as a target for new pain therapeutics, wrote the investigators.""The ability to sense pain is essential to our self-preservation,
"says Geoff Woods, M d, from the Cambridge Institute for Medical Research at the University of Cambridge,
#New Gene Subgroup Driving Aggressiveness in Prostate Cancer Identified Prostate cancer is the most commonly diagnosed malignancy among males within developed countries.
Most often the majority of prostate cancer is thought of as an organ-confined disease with little genetic variation.
However, data in recent years is beginning to bring into focus that many prostate tumors display substantial amounts of genetic heterogeneity, leading to differential mortality rates.
Now, prostate cancer researchers in Canada have sketched a molecular portrait providing a complete picture of
what they describe as a localized, multi-focal disease within the prostate gland, as well as identifying a new gene subgroup acting as a molecular driver for tumor progression. ur research shows how prostate cancers can vary from one man to anotherespite the same pathology under the microscopes well as how it can vary within one man who may have multiple
tumor types in his prostate, "explained Robert Bristow, M d.,Ph d.,clinician-scientist at Princess Margaret Cancer Centre,
Toronto and senior author on the study. hese sub-types may be important to determining the response to surgery or radiotherapy between patients."
"The findings from this study were published recently in Nature Genetics through an article entitled patial genomic heterogeneity within localized, multifocal prostate cancer.
Specifically, the study involved the molecular profiling of 74 patients with relatively high aggressiveness scores.
From this group, whole genome sequencing was performed on samples from five patients whose prostates were removed surgically.
The investigators carefully analyzed the genetic backgrounds of each tumor sample, assigning individual aggression scores to the discreet cancer foci regions they identified.
The data revealed that even small cancers within the prostate can contain very aggressive cells capable of varying long term disease prognosis.
Dr. Bristow and his colleagues identified two members of the MYC oncogene family that played essential roles in tumor development.
The researchers identified C-MYC as being the driver of aggressiveness for the disease and L-MYC,
which has already been implicated in lung cancer development, playing a critical role in tumor progression.""This discovery of a new prostate cancer-causing gene gives researchers a new avenue to explore the biology of the disease
and improve treatment,"stated Paul Boutros, Ph d, . principal investigator at the Ontario Institute for Cancer Research and lead author on the current study."
"By showing that mutations in prostate cancer vary spatially in different regions of a tumor,
this study will aid in the development of new diagnostic tests that will improve treatment by allowing it to be personalized further."
Dr. Bristow thinks that this study takes an important step forward in identifying new biomarkers for prostate cancer and developing novel treatment options for patients."
"Our findings suggest we are getting closer to subtyping prostate cancer based on which gene is present to determine a patients'disease aggression in terms of the risk of spread outside the prostate gland at time of treatment,
said Dr. Bristow. n developing this research tool into a clinical test within three years,
we hope to inform doctors and patients about specialized treatments for each prostate cancer patient. e
when oncologists at Memorial Sloan-Kettering Cancer Center (MSK) refused to prescribe Zaltrap (ziv-aflibercept) for metastatic colorectal cancer due to its initial $11, 000-per-month cost.
Cancer was the third most expensive category of specialty drugs last year measured per-member-per year, according to Express Scripts;
Multiple sclerosis (MS) was second, and inflammatory conditions such as rheumatoid arthritis (RA), the priciest. However, cancer accounts for 32%of drugs costing more than $100, 000 a year,
and is among a handful of key drivers of rising costs here are drugs in cancer that may give five months of life in one indication and 12 days of life in another.
Yet payers are being asked to pay the exact same amount for both, Henry said June 3. hen you get to the point where you have orphan drug pricing for non-orphan drugs,
Germany Institute for Quality and Efficiency in Health care (IQWIG) applies eference pricing setting reimbursements for new drugs at the same level as the best existing comparator unless the new drugs show superiority to that comparator;
director of MSK Center for Health policy and Outcomes, told GEN. Last year, Dr. Bach published a commentary in Journal of the American Medical Association supporting indication-based pricing for cancer drugs.
As for pricing rare-disease drugs higher, Dr. Bach added: dispassionate economist would say that inefficient.
a life sciences and healthcare industry consultant, told GEN. Express Scripts is hoping to repeat the success it enjoyed last year in hepatitis C. In December 2014,
the company immediately added Abbvie Viekira Pak to its National Preferred Formulary as the exclusive option for patients with genotype 1 hepatitis Cust three days after the FDA approved the drug.
Express Scriptsindependent Pharmacy & Therapeutics Committee concluded that Viekira Pak was at least clinically equivalent to two Gilead sciences drugs, Harvoni (ledipasvir and sofosbuvir) and Sovaldi (sofosbuvir.
and only covers Sovaldi for non-genotype 1 hepatitis C. ur clients will save more than $1 billion this year on hepatitis C medications,
and we will financially guarantee that their patients will adhere to their therapy. Due to the industry-wide ripple effect of our decision,
000-a-pill pricing by noting that the cost of Sovaldi is lower than the cost of complications associated with hepatitis C treatment, such as liver damage or liver failure.
Cancer treatments marketed by eight companies accounted for six of the Top 25 Best-selling Drugs of 2014 as listed by GEN,
and its Genentech subsidiary from marketing the top three cancer treatments: Rituxan (rituximab, co-marketed with Biogen and ranked#4), Avastin (bevacizumab;#
Genentech provided its medicines to more than 180,000 people last year for free or reduced cost. Willson noted that the Genentech Access to Care Foundation recently changed its financial criteria with the goal of helping more people, n recognition of the changing healthcare environment and the increasing number of people with high out
e understand that the cost of medicines can be challenging for some patients, Novartis said. he majority of CML patients in the U s. pay less than $100 out of pocket per month for our CML treatments,
and we are committed to ensuring that patients have access to their medicines. To that end, Novartis said,
its patient assistance program provides the company medicines for free or at a reduced cost to those who can afford them,
The company CML medicines have been provided free to an average of 5 000 uninsured or underinsured patients in the U s. annually for the past six-and-a-half yearsore than $1 billion in free medicine. ecause the cost of drugs is one of the few transparent healthcare costs,
drugs get much public attention, yet are only a small percentage of spending and demonstrate remarkable rewards,
Peter B. Bach, M d.,MAPP, director of MSK Center for Health policy and Outcomes cautioned that some alternative pricing programs have helped developers skirt the prior-authorization rules of payers.
yet developers can win payer approval for a costlier medicine by agreeing to allow limited-time use,
The scientists believe their research paves the way to an entirely new approach for finding a drug that can cure
or at least slow the progression of such neurodegenerative diseases as ALS, Alzheimer's, Parkinson's, and Huntington's diseases.
and trigger the disease, said Alex Parker, Ph d.,CHUM researcher and associate professor in the department of neuroscience at the University of Montreal.
Amyotrophic lateral sclerosis is a neuromuscular disease that attacks neurons and the spinal cord. Those affected gradually become paralyzed and typically die less than five years after the onset of symptoms.
the person develops the disease. Scientists introduced a mutated human gene (TDP-43 or FUS) into C. elegans.
and suffered far less paralysis, she added. This study highlights a never previously suspected mechanism:
that system triggers a misguided attack against the worm's own neurons. he worm thinks it has a viral or bacterial infection and launches an immune response.
This makes the TIR-1 protein (or SARM1 in humans) an excellent therapeutic target for development of a medication.
because we caused the disease. This allows us to administer treatment very early in the worm's life.
But ALS is a disease of aging, which usually appears in humans around the age of 55.
But we have demonstrated clearly that blocking this key protein curbs the disease's progress in this worm
Now, a collaboration of researchers from UT Southwestern Medical center, Case Western Reserve University, and the University of Kentucky has identified an enzyme they say regulates tissue regeneration.
The scientists believe that the inhibition of this enzyme could accelerate tissue recovery from injury, disease,
"Patients undergoing bone marrow transplants and patients with colitis may benefit from this approach, "stated co-author James Willson, M d,
. associate dean of oncology programs at UT Southwestern Medical center and co-author on the current study.""We propose that SW033291 will be useful in accelerating recovery of bone marrow cells following a bone marrow transplant
and may also be a treatment for colitis."The findings from this study were published recently in Science through an article entitled"Inhibition of the prostaglandin-degrading enzyme 15-PGDH potentiates tissue regeneration."
"15-PDGH is a key enzyme responsible for the biological inactivation of a group of signaling molecules, called eicosanoids,
"explained co-author Dr. Joseph Ready, Ph d.,professor of biochemistry and member of the Simmons Cancer Center at UT Southwestern Medical center.
the collaborators wanted to investigate the therapeutic potential of 15-PGDH inhibitors in tissue regeneration.
our observations identify 15-PGDH as a therapeutic target and provide a chemical formulation, SW033291, that is an active 15-PGDH inhibitor in vivo and that potentiates repair in multiple tissues.
SW033291 or related compounds may merit clinical investigation as a strategy to accelerate recovery after bone marrow transplantation and other tissue injuries. e
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