Despite advances in analyzing tumor biology, choosing effective therapies for cancer patients remains difficult. This is partly because there are still no timely, foolproof ways to test whether a patient will respond to a particular treatment. Addressing this issue, two independent teams—one at the Fred Hutchinson Cancer Research Center in Seattle and another at MIT—have developed devices that can test a tumor’s response to multiple cancer drugs directly in the patient. Both devices are described today (April 22) in Science Translational Medicine.
If validated in human clinical studies, the devices—which are being further developed by spinoff companies—could be used before surgery to help identify the best course of individualized treatment for certain cancer patients.
Researchers at the University of Cambridge have grown functional "mini-lungs" using stems cells derived from the skin cells of patients with a debilitating lung disease. Not only can the development help them in coming up with effective treatments for specific lung diseases like cystic fibrosis, but the process has the potential to be scaled up to screen thousands of new compounds to identify potential new drugs.
Creating miniature organoids has been the focus of many a research group, as it allows scientists to better understand the processes that take place inside an organ, figure out how specific diseases occur and develop or even work towards creating bioengineered lungs.
The research team from the Wellcome Trust-Medical Research Council Cambridge Stem Cell Institute studied a lung disease called cystic fibrosis, which is caused by genetic mutation and shortens a patient's average lifespan. Patients have great difficulty breathing as the lungs are overwhelmed by thickened mucus.
To create working mini-lungs, the researchers took skin cells from patients with the most common form of cystic fibrosis and reprogrammed them to an induced pluripotent state (iPS), which allows the cells to grow into a different type of cell inside the body.
by Young-Ho Lee, Xiyong Liu, Fuming Qiu, Timothy R. O’Connor, Yun Yen, David K.
Members of the heterochromatin protein 1 family (HP1α, β and γ) are mostly associated with heterochromatin and play important roles in gene regulation and DNA damage response. Altered expression of individual HP1 subtype has profound impacts on cell proliferation and tumorigenesis. We analyzed the expression profile of HP1 family by data mining using a published microarray data set coupled with retrospective immunohistochemistry analyses of archived breast cancer biospecimens. We found that the patient group overexpressing HP1βmRNA is associated with poorly differentiated breast tumors and with a significantly lower survival rate. Immunohistochemical staining against HP1α, HP1β and HP1γ shows that respective HP1 expression level is frequently altered in breast cancers. 57.4 - 60.1% of samples examined showed high HP1β expression and 39.9 - 42.6 % of examined tumors showed no or low expression of each HP1 subtype. Interestingly, comparative analysis on HP1 expression profile and breast cancer markers revealed a positive correlation between the respective expression level of all three HP1 subtypes and Ki-67, a cell proliferation and well-known breast cancer marker. To explore the effect of individual HP1 on PARP inhibitor therapy for breast cancer, MCF7 breast cancer cells and individually HP1-depleted MCF7 cells were treated with PARP inhibitor ABT-888 with or without carboplatin. Notably, HP1β-knockdown cells are hypersensitive to the PARP inhibitor ABT-888 alone and its combination with carboplatin. In summary, while increased HP1β expression is associated with the poor prognosis in breast cancer, compromised HP1β abundance may serve as a useful predictive marker for chemotherapy, including PARP inhibitors against breast cancer.
The immune system can remember a previously experienced pathogen and can evoke an enhanced response to reinfection that depends on memory lymphocyte populations. Recent advances in tracking antigen-experienced memory B cells have revealed the existence of distinct classes of cells that have considerable functional differences. Some of these differences seem to be determined by the stimulation history during memory cell formation. To induce rapid recall antibody responses, the contributions of other types of cells, such as memory T follicular helper cells, have also now begun to be appreciated. In this Review, we discuss these and other recent advances in our understanding of memory B cells, focusing on the underlying mechanisms that are required for rapid and effective recall antibody responses.
CD95 (Fas/APO-1) and its ligand, CD95L, have long been viewed as a death receptor/death ligand system that mediates apoptosis induction to maintain immune homeostasis. In addition, these molecules are important in the immune elimination of virus-infected cells and cancer cells. CD95L was, therefore, considered to be useful for cancer therapy. However, major side effects have precluded its systemic use. During the last 10 years, it has been recognized that CD95 and CD95L have multiple cancer-relevant nonapoptotic and tumor-promoting activities. CD95 and CD95L were discovered to be critical survival factors for cancer cells, and were found to protect and promote cancer stem cells. We now discuss five different ways in which inhibiting or eliminating CD95L, rather than augmenting, may be beneficial for cancer therapy alone or in combination with standard chemotherapy or immune therapy.
EPFL scientists Aurélie Pala and Carl Petersen have observed and measured synaptic transmission in a live animal for the first time, using optogenetics* to stimulate single neurons in the mouse barrel cortex (which processes sensory information from the mouse’s whiskers). They shined blue light on the neurons containing a gene-based light-sensitive protein, activating the neurons to fire. Then using microelectrodes, they measured resulting electrical signals in neighboring interneuron cells.
They also used an advanced imaging technique (two-photon microscopy) that allowed them to look deep into the brain of the live mouse and identify the type of each interneuron they were studying.
The data showed that the neuronal transmissions from the light-sensitive neurons differed depending on the type of interneuron on the receiving end. Only a few studies have directly investigated synaptic transmission between specific neocortical neurons in vivo, presumably due to the technical difficulties in obtaining intracellular recordings from connected pairs of neurons in vivo, the authors say in their (open-access) paper in Neuron.
The research overcomes a limitation of in vitro (lab) studies, where associated biomolecules are different from those in a live animal, and where cutting neural tissue for lab work also introduces artifacts, the researchers suggest. “This is a proof-of-concept study,” says Pala, who received her PhD for this work. “Nonetheless, we think that we can use optogenetics to put together a larger picture of connectivity between other types of neurons in other areas of the brain.”
The scientists are now aiming to explore other neuronal connections in the mouse barrel cortex. They also want to try this technique on awake mice, to see how switching neuronal activity on and off with a light can affect higher brain functions.
* Optogenetics works by inserting the gene of an light-sensitive protein into live neurons, from a single cell to an entire family of them. The genetically modified neurons then produce the light-sensitive protein, which sits on their outside, the membrane. There, it acts as an electrical channel – something like a gate. When light is shone on the neuron, the channel opens up and allows electrical ions to flow into the cell; a bit like a battery being charged by a solar cell. The addition of electrical ions changes the voltage balance of the neuron, and if the optogenetic stimulus is sufficiently strong it generates an explosive electrical signal in the neuron
Persistent hepatitis C virus (HCV) infection causes chronic liver diseases and is a global health problem. Although the sustained virologic response rate in the treatment of genotype 1 using new triple therapy (pegylated-interferon, ribavirin, and telaprevir/boceprevir) has been improved by more than 70%, several severe side effects such as skin rash/ageusia and advanced anemia have become a problem. Under these circumstances, a new type of anti-HCV oral drug with few side effects is needed. Our recently developed HCV drug assay systems, including the HuH-7 cell line-derived OR6 and AH1R, and the Li23 cell line-derived ORL8 and ORL11, allow genome-length HCV RNAs (several strains of genotype 1b) encoding renilla luciferase to replicate efficiently. Using these systems as anti-HCV candidates, we have identified numerous existing medicines that can be used against HCV with few side effects, such as statins and teprenon. To obtain additional anti-HCV candidates, we evaluated a number of oral health supplements, and found that the capsule but not the liquid form of Cordyceps militaris (CM) (Ascomycotinanorth, North Chinese caterpillar fungus), which is used as a Chinese herbal medicine, exhibited moderate anti-HCV activity. In combination with interferon-α or ribavirin, CM exhibited an additive inhibitory effect. Among the main components of CM, cordycepin, but not ergosterol, contributed to the anti-HCV activity of CM. In consideration of all these results, we suggest that CM would be useful as an oral anti-HCV agent in combination with interferon-α and/or ribavirin.
Pasquale Valente's insight:
"cordyceps militaris would be useful as an oral anti-HCV agent in combination with interferon-α and/or ribavirin"
Most people intuitively understand that exercise can improve your mood, but it was only last week that scientists figured out how it works. Their findings are of enormous importance to everybody who experiences stress at work.
According to a recent article in the New York Times, exercising causes your muscles to release a set of chemicals that block other chemicals the body releases in response to frequent stress.
In other words, constant stress brings you down, but consistent exercise lifts you up.
Scientists working in the area of pancreatic cancer research have uncovered a technique that sees cancerous cells transform back into normal healthy cells. The method relies in the introduction of a protein called E47, which bonds with particular DNA sequences and reverts the cells back to their original state.
The study was a collaboration between researchers at the Sanford-Burnham Medical Research Institute, University of California San Diego and Purdue University. The scientists are hopeful that it could help combat the deadly disease in humans.
"For the first time, we have shown that over-expression of a single gene can reduce the tumor-promoting potential of pancreatic adenocarcinoma cells and reprogram them toward their original cell type," says Pamela Itkin-Ansari, adjunct professor at Sanford-Burnham and lead author of the study. "Thus, pancreatic cancer cells retain a genetic memory which we hope to exploit."
(MedicalXpress)—Resting state networks (RSNs) in the brain are topographies of neural structures between which lag states propagate due to fluctuations of physical and other activities. Studying these networks reveals information about the functional connectivity of neural structures and regions. Results from various studies have confirmed that brain activity is spatially structured, linked to the representation of function, and has clinical relevance.
Functional connectivity is different from the brain's structural connectivity, which describes brain regions that are anatomically attached to each other. Regions with no structural connectivity can nonetheless have functional connectivity as nodes in a functionally connected RSN. Many common RSNs have been mapped in healthy subjects, and researchers believe that understanding the relationships between these networks can contribute to a fundamental model of brain function.
One of the tremendous advantages of functional magnetic resonance imaging (fMRI) is the ability to study brain functional activity without the need for subjects to perform complex tasks. Using fMRI to study resting-state functional connectivity yields a wealth of information about different stages of consciousness and patterns of synchronous activity. One of the neurological features that has emerged from such research is the existence of lags in intrinsic activity as represented by fluctuations of the blood-oxygen level-dependent signals (BOLDs), which are temporally synchronous within the somatomotor system.
Last year, researchers at the departments of radiology and neurology at Washington University published an analysis demonstrating that, contrary to the belief that BOLDs were synchronous with resting state networks (RSNs), the lag topography of BOLDs and RSNs is actually orthogonal. Additionally, they established that BOLDs are not attributable to hemodynamic factors and have neural origin.
By examining more than 3,600 postmortem brains, researchers at Mayo Clinic's campuses in Jacksonville, Florida, and Rochester, Minnesota, have found that the progression of dysfunctional tau protein drives the cognitive decline and memory loss seen in Alzheimer's disease. Amyloid, the other toxic protein ...
Strokes, heart attacks, and traumatic brain injuries are separate diseases with certain shared pathologies that achieve a common end: cell death and human injury due to hypoxia, or lack of oxygen.
In these diseases, a lack of blood supply to affected tissues begins a signaling pathway that ultimately halts the production of energy-releasing ATP molecules — a death sentence for most cells.
By employing derivatives of humanin, a naturally occurring peptide encoded in the genome of cellular mitochondria, researchers at Ben Gurion University of the Negev are working to interrupt this process,
Whereas it took 13 years and cost US$3 billion to sequence a human genome for the first time, senior author Peter White notes that now "even the smallest research groups can complete genomic sequencing in a matter of days." The chokepoint lies in the next step: calibrating and analyzing the billions of generated data points for genetic variants that could lead to diseases.
The interleukin-20 (IL-20) subfamily of cytokines comprises IL-19, IL-20, IL-22, IL-24 and IL-26. These cytokines are all members of the larger IL-10 family, but have been grouped together to form the IL-20 subfamily based on their usage of common receptor subunits and similarities in their target-cell profiles and biological functions. Members of the IL-20 subfamily facilitate the communication between leukocytes and epithelial cells, thereby enhancing innate defence mechanisms and tissue repair processes at epithelial surfaces. In this Review, we describe the cellular sources and targets of the IL-20 subfamily cytokines, and we detail how their expression is regulated. Much of our understanding of the unique biology of this group of cytokines is still based on IL-22, which is the most studied member of the IL-20 subfamily. Nevertheless, we attempt a broader discussion of the emerging functions of IL-20 subfamily cytokines in host defence, inflammatory diseases, cancer and metabolism.
Dialysis machines are needed by patients with renal (kidney) failure to clean their blood of wastes produced by the body. In 2008, Dr. Victor Gura, an internationally known kidney specialist at Cedars-Sinai Medical Center, proposed the first miniature portable dialysis machine.. An Alternative to Conventional Dialysis
The US Food & Drug Administration’s (FDA) fasttrack program, Innovation Pathway, streamlines the approval process for breakthrough technologies. In 2012, the “Wearable Artificial Kidney” (WAK), promoted by the Wearable Artificial Kidney Foundation, Inc., was awarded fast-track status, along with two other renal projects.
Coronary heart disease (CHD) kills more than 385,000 people in the United States each year, and more than half of those who die suddenly have no previous symptoms.
A new blood test that could reduce CHD-related illness and mortality by predicting the risk of future heart disease has been cleared by the US Food and Drug Administration (FDA). The PLAC Test for Lp-PLA2 screens for cardiovascular inflammation which can lead to a build up of rupture-prone plaque and result in a heart attack or stroke.
Statins form the pharmacologic cornerstone of the primary and secondary prevention of atherosclerotic cardiovascular disease. In addition to beneficial cardiovascular effects, statins seem to have multiple non-cardiovascular effects. Although early concerns about statin induced hepatotoxicity and cancer have subsided owing to reassuring evidence, two of the most common concerns that clinicians have are myopathy and diabetes. Randomized controlled trials suggest that statins are associated with a modest increase in the risk of myositis but not the risk of myalgia. Severe myopathy (rhabdomyolysis) is rare and often linked to a statin regimen that is no longer recommended (simvastatin 80 mg). Randomized controlled trials and meta-analyses suggest an increase in the risk of diabetes with statins, particularly with higher intensity regimens in people with two or more components of the metabolic syndrome. Other non-cardiovascular effects covered in this review are contrast induced nephropathy, cognition, cataracts, erectile dysfunction, and venous thromboembolism. Currently, systematic reviews and clinical practice guidelines indicate that the cardiovascular benefits of statins generally outweigh non-cardiovascular harms in patients above a certain threshold of cardiovascular risk. Literature is also accumulating on the potential non-cardiovascular benefits of statins, which could lead to novel applications of this class of drug in the future.
Researchers from the Broad Institute of MIT and Harvard, Harvard Medical School and Harvard-affiliated hospitals have uncovered an easily detectable, “pre-malignant” state in the blood that significantly increases the likelihood that a person will go on to develop blood cancers such as leukemia, lymphoma or myelodysplastic syndrome.
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