#Urine test for early stage pancreatic cancer possible after biomarker discovery A team at Barts Cancer Institute, Queen Mary University of London, has shown that the three-protein'signature'can both identify the most common
--and distinguish between this cancer and the inflammatory condition chronic pancreatitis, which can be hard to tell apart.
while patients suffering from chronic pancreatitis had significantly lower levels than cancer patients. When combined, the three proteins formed a robust panel that can detect patients with stages I-II pancreatic cancer with over 90 per cent accuracy.
when the cancer has already spread. This means they are not eligible for surgery to remove the tumour--currently the only potentially curative treatment.
The five-year survival rate for pancreatic cancer in the UK is the lowest of any common cancer, standing at 3 per cent.
if the 3-biomarker signature is present during the latency period--the time between the genetic changes that will cause the cancer to develop and the clinical presentation."
"For a cancer with no early stage symptoms, it's a huge challenge to diagnose pancreatic cancer sooner,
"says co-author and Director of Barts Cancer Institute, Professor Nick Lemoine.""With pancreatic cancer, patients are diagnosed usually
when the cancer is already at a terminal stage, but if diagnosed at stage 2,
Early diagnosis is an important part of our overall efforts against this aggressive cancer, alongside developing new treatments to tackle the disease once diagnosis is made.
whether liver cancers tend to originate in these replicating cells, as opposed to more mature hepatocytes,
#Scientists determine how antibiotic gains cancer-killing sulfur atoms In a discovery with implications for future drug design,
This new discovery could open the way to incorporating sulfur into other natural products, potentially advancing new therapies for indications beyond cancer."
A number of compounds that contain sulfur have proven useful in the treatment of conditions ranging from acne and eczema to arthritis and cancer."
Researchers at the Center for Molecular biology of Heidelberg University, the German Cancer Research center and the Heidelberg Institute for Theoretical Studies collaborated on the project,
Dr. Bernd Bukau, Director of the Center for Molecular biology of Heidelberg University (ZMBH), who is also a researcher at the German Cancer Research center (DKFZ.
However, from a clinical standpoint, this discovery could lead to more effective cancer immunotherapies, better drugs for autoimmune conditions and new ways to expedite recovery from sepsis.
While immunotherapies might fight cancer, they may also open the door to opportunistic infections.""This was shown in mice which,
The finding was confirmed in samples from patients receiving high-dose interleukin 2 therapy to treat metastatic melanoma."
"In addition to illuminating how T cells respond to cancer immunotherapy, the study also provides insights into autoimmune disorders.
which means that melanoma is identified in all cases where it is ruled present, and out in 90.9%of cases where it is not."
"Skin malignant melanoma is a particularly aggressive cancer associated with quick blood vessel growth which means early diagnosis is vital for a good prognosis.
#New synthetic tumor environments make cancer research more realistic University of Illinois researchers have developed a new technique to create a cell habitat of squishy fluids, called hydrogels,
and grow into a tumor. They were able to observe how differently cells act in the three-dimensional, gel-like environment,
and expensive mouse avatars that are created by injecting human tumor cells into mice.""This is really the first time that it's been demonstrated that you can use a rapid methodology like this to spatially define cancer cells and macrophages,
and finds out they've been diagnosed with some sort of solid tumor, "Kilian said.""You take a biopsy of those cells,
we could be taking samples of different components of a cancer patient's mammary gland and building a model of their tissue to use as a personalized drug screening platform.
But in diseases such as breast cancer, the breakdown of this order has been associated with the rapid growth and spread of tumors."
it sets the stage for cancer.""But studying how the cells of complex tissues like the mammary gland self-organize,
but also to experiment with specifically adding in a single cell with a known cancer mutation to different parts of the organoid to observe its effects.
or more cells expressing low levels of the cancer gene Rasg12v affected the cells around them.
or structural changes in mammary glands can lead to the breakdown of tissue architecture associated with tumors that metastasize,
Such mutations have been linked not only with cancer but a host of other illnesses, including autism and schizophrenia.
Researchers can learn a lot by analyzing CNVS in bulk samples--from a tumor biopsy for example--but they can learn more by investigating CNVS in individual cells."
"You may think that every cell in a tumor would be the same, but that's actually not the case,"says CSHL Associate professor Michael Schatz."
"We're realizing that there can be a lot of changes inside even a single tumor, "says Schatz."
"If you're going to treat cancer, you need to diagnose exactly what subclass of cancer you have."
"Simultaneously employing different drugs to target different cancer subclasses could prevent remission, scientists have proposed. One powerful single-cell analytic technique for exploring CNV is whole genome sequencing.
The challenge is that, before sequencing can be done, the cell's DNA has to be amplified many times over.
He adds that CSHL has collaborations with many hospitals, notably Memorial Sloan Kettering Cancer Center and the North Shore-LIJ Health System,
"says Dan Theodorescu, MD, Phd, director of the University of Colorado Cancer Center.""Bill Petri and I had been social friends for years--Christmas parties, that kind of thing.
MD, Phd, chief of the Division of Infectious diseases & International Health at the University of Virginia led to the idea of applying an innovative cancer science technique to the study of infectious disease.
She took a library of cells that Dan had developed in his work with bladder cancer
"We do this all the time in cancer research, "Theodorescu says.""Commonly, we're looking for genes that,
but also proof that this cancer-science approach can be used to explore genetic mechanisms of resistance in the field of infectious disease,
#Pancreatic cancer subtypes discovered in largest gene expression analysis of the disease to date Dense surrounding tissue can block drugs from reaching pancreatic cancer tumors,
but it can also help prevent the cancer from spreading. Now a new study by UNC Lineberger Comprehensive Cancer Center researchers and collaborators helps explain the conflicting role of the surrounding tissue known as stroma.
In the study, the researchers revealed that based on molecular characteristics, there are two subtypes of pancreatic cancer stroma.
researchers reveal findings of both new subtypes of stroma and two subtypes of pancreatic cancer tumors.
while for some other cancers, we personalize treatment based on an individual patient's tumor genetics or other characteristics,"said the study's senior author Jen Jen Yeh, MD, a UNC Lineberger member and an associate professor and the vice chair for research in the UNC School of medicine Department of Surgery."
"The study reveals the most rigorously validated classification system for pancreatic ductal adenocarcinoma to date. Previous studies,
"The issue is that pancreatic cancer is a particularly difficult cancer to analyze because of its confounding stroma,
either promote or be a barrier to tumor spread, "Yeh said.""We are seeing two distinct types of stroma in patients."
"Their analysis also revealed two subtypes of pancreatic cancer tumors. One subtype, called"basal-like is linked to worse outcomes for patients.
"Basal-like tumors also trended toward a better response to adjuvant therapy.""If we know that your tumor is aggressive,
then it may be important to treat your whole body first with neoadjuvant therapy, which is given therapy prior to surgery,
as opposed to just trying to remove the tumor with surgery at the outset, "said Yeh, who,
"In addition, the basal-like subtype is very similar to basal breast and bladder cancers, which respond to therapies differently than other tumor subtypes,
so we are interested very in seeing whether or not this is true for pancreatic cancer as well.""Overall, the findings suggest that treatment decisions should be based on both a patient's stroma and tumor subtype.
Yeh said the researchers will be launching clinical trials to investigate how patients with the different subtypes respond to treatment."
"With this cancer, you don't have a lot of time to try different therapies. If a patient is given a therapy that is unsuccessful, that is time in
#New drug-like compounds may improve odds of men battling prostate cancer, researchers find Researchers at Southern Methodist University,
Dallas, have discovered three new drug-like compounds that could ultimately offer better odds of survival to prostate cancer patients.
and developed into medicines that target a protein in the human body that is responsible for chemotherapy resistance in cancers,
So far there's no approved drug on the market that reverses cancer chemotherapy resistance caused by P-glycoprotein
"The problem when a person has cancer is that the treatment itself is composed of cellular toxins--the chemotherapeutics that prevent the cells from dividing.
Usually upon the first chemo treatment the cancer responds well, and initially goes away. Ideally it doesn't come back,
"Sometimes, however, the cancer returns,"she said.""The reason often is that some of the cancer cells"learn,"after the first rounds of chemotherapy,
"As a result, P-gp causes resistance of the diseased cells to a majority of drugs currently available for the treatment of cancer,
commonly used to treat prostate cancer patients. Also, each was tested on a companion cell line already multi-drug resistant,
they were able to push back the sensitivity of the resistant cancer line to the level of the non-resistant one."
just as if the cancer was seeing the chemotherapy for the first time, "Vogel said. About 14 percent of men will be diagnosed over their lifetime with prostate cancer, according to the National Cancer Institute.
Survival is diagnosed highest if early before it has spread, the institute reports s
#New drug-like compounds may improve odds of men battling prostate cancer, researchers find Researchers at Southern Methodist University,
Dallas, have discovered three new drug-like compounds that could ultimately offer better odds of survival to prostate cancer patients.
The drug-like compounds can be modified and developed into medicines that target a protein in the human body that is responsible for chemotherapy resistance in cancers,
said biochemist Pia D. Vogel, lead author on the scientific paper reporting the discovery. So far there's no approved drug on the market that reverses cancer chemotherapy resistance caused by P-glycoprotein
or P-gp for short, said Vogel, a biochemistry professor at SMU. One potential drug, Tariquidar, is currently in clinical trials,
"The problem when a person has cancer is that the treatment itself is composed of cellular toxins--the chemotherapeutics that prevent the cells from dividing.
Usually upon the first chemo treatment the cancer responds well, and initially goes away. Ideally it doesn't come back,
"Sometimes, however, the cancer returns,"she said.""The reason often is that some of the cancer cells"learn,"after the first rounds of chemotherapy,
"As a result, P-gp causes resistance of the diseased cells to a majority of drugs currently available for the treatment of cancer,
commonly used to treat prostate cancer patients. Also, each was tested on a companion cell line already multi-drug resistant,
they were able to push back the sensitivity of the resistant cancer line to the level of the non-resistant one."
just as if the cancer was seeing the chemotherapy for the first time, "Vogel said. About 14 percent of men will be diagnosed over their lifetime with prostate cancer, according to the National Cancer Institute.
Survival is diagnosed highest if early before it has spread, the institute reports s
#Nano-dunes with the ion beam Many semiconductor devices in modern technology--from integrated circuits to solar cells and LEDS--are based on nanostructures.
which then increases the risk of infection and cancer. These immune processes are therefore very important and contribute to the outlook where only five out of ten patients will survive for at least five years."
#New leukemia gene stops blood cells'growing up'Scientists have identified a gene--FOXC1--that, if switched on, causes more aggressive cancer in a fifth of acute myeloid leukemia (AML) patients,
according to a Cancer Research UK study published in the journal Cancer cell, today. The FOXC1 gene is switched normally on during embryonic development
and is needed to turn cells into specialised tissues, like the eyes, kidney, brain and bone.
But this new research found that in certain patients with AML--a type of blood cancer that affects white blood cells
This triggers the cancer to be more aggressive, as young cells are able to replicate more than mature cells--causing cancer cells to grow faster
Of these, around 20 per cent would have had the FOXC1 gene wrongly switched on in their cancer.
Dr Tim Somervaille, lead author from the Cancer Research UK Manchester Institute at The University of Manchester,
which makes the cancer grow more rapidly.""There are certain situations where this gene is necessary,
it causes more aggressive forms of leukemia.""Nell Barrie, senior science communication manager at Cancer Research UK, said:"
"It's essential that we continue to research basic biology to further understand how cells become cancerous.
The better we understand the nuts and bolts of each cancer, the sooner we can find new ways to stop it
#Research breakthrough in fight against muscle wasting diseases It is estimated that half of all cancer patients suffer from a muscle wasting syndrome called cachexia.
Cancer cachexia impairs quality of life and response to therapy, which increases morbidity and mortality of cancer patients.
Currently, there is no approved treatment for muscle wasting but a new study from the Research Institute of the Mcgill University Health Centre (RI-MUHC) and University of Alberta could be a game changer for patients, improving both quality of life and longevity.
Recent studies show that muscle wasting is much more common in cancer than we think."
In addition, they looked at USP19 levels in human muscle samples from the most common cancers that cause muscle wasting:
and from 60 to 80 per cent in advanced cancer. In all of these chronic conditions, muscle wasting predicts earlier death."
"Cancer patients often present with muscle wasting even prior to their initial cancer diagnosis, ''says Dr. Antonio Vigano, director of the cancer rehabilitation program and cachexia clinic at the MUHC."
"In cancer, cachexia also increases your risk of developing toxicity from chemotherapy and other oncological treatments, such as surgery and radiotherapy.
At the Mcgill Nutrition and Performance Laboratory we specialize in cachexia and sarcopenia. By treating these two pathologic conditions through inhibiting the USP19 gene, at an early,
rather than late, stage of the cancer trajectory, not only can we potentially improve the quality of life of patients,
The new study shows that this crosstalk is important not only for launching immune responses against tumors,
"This finding could be helpful for developing strategies to target cancer and inflammatory diseases,"said TSRI Assistant professor of Immunology Young Jun Kang,
Their research suggests that RIPK3 regulates the activation of natural killer T cells (NKTS), the immune cells that play dual roles in the development of autoimmune diseases and the destruction of cancers.
scientists may be able to develop ways to better control NKTS to attack tumors. The new study also suggests there may be a way to intervene in the pathway to block inflammation.
either hone the pathway's cancer-killing role or reduce its role in inflammation. In addition to Kang and Lerner, authors of the study,"Regulation of NKT cell-mediated immune responses to tumours and liver inflammation by mitochondrial PGAM5-Drp1 signaling,"were Bo-Ram Bang, Kyung Ho Han
or tissue which are telltale signs of DNA mutation or the presence of cellular malfunctions such as cancer.
The absence of light sources that cover enough of the infrared spectrum with sufficient brilliance to detect minute concentrations originating from onco-metaboloids has been the main challenge in cancer detection.
Jens Biegert and his colleagues at ICFO are currently investigating molecular sensitivity for the identification of cancer biomarkers on the single cell level using all optical techniques in the mid-wave infrared wavelength range g
and destroy cancers, Swartz said. For Swartz and his principal collaborator, Yuan Lu, now a pharmacology researcher at the University of Tokyo, the result is a vindication.
"But I believe we can use this smart particle to deliver cancer-fighting immunotherapies that will have minimal side effects."
while treating cancer. Looking for a model in nature, many researchers focused on viruses, which target specific cells,
Swartz said the next step is to attach cancer tags to the outside of this smart particle,
to use it to train the immune system to recognize certain cancers. Those experiments would likely occur in mice.
however, drugs could be encapsulated in protein cages that accumulate inside of a tumor and dissolve once heated.
a two-drug combination discovered by UF Health researchers that inhibits tumors and kills cancer cells in mouse models.
For the first time, researchers have shown that a certain protein becomes overabundant in pancreatic neuroendocrine tumors, allowing them to thrive.
The findings were published recently in the Journal of the National Cancer Institute by a group that includes Rony A. François, an M d./Ph d. student working with Maria Zajac-Kaye, Ph d.
because less than 5 percent of patients with pancreatic neuroendocrine tumors respond to everolimus, the most commonly used pharmaceutical,
Neuroendocrine tumors, which form in the hormone-making islet cells, account for 3 percent to 5 percent of pancreatic malignancies
and have a five-year survival rate of about 42 percent, according to the National Cancer Institute.
Pancreatic neuroendocrine tumors are increasingly common, which medical experts and researches have attributed to better diagnostic imaging,
an aging population and heightened awareness of the disease stemming from the 2011 death of Apple Inc. cofounder Steve jobs. Zajac-Kaye's group discovered that a single protein is behind the process that allows pancreatic neuroendocrine tumors to thrive.
But when islet cells begin turning into tumors, the FAK protein gets overproduced, researchers found.
This overabundance of the protein allows tumors to resist chemotherapy and evade efforts to kill them off.
After identifying FAK's role in tumor development François started looking for ways to get it in check.
Daily doses of the compound reduced tumor volume by about 50 percent after 25 days, they found.
While everolimus can extend some patients'lives by holding tumors in check, it does little to make them regress
The findings also have potential uses for most other types of solid tumors, including those affecting the lungs and ovaries,
one cancerous cell breaks off from a tumor, slips into the bloodstream and quickly lodges elsewhere in the body.
These colonizers may bloom into deadly metastatic cancer right away or lie dormant for years, only to trigger a recurrence decades after the primary tumor is removed.
Metastases cause the vast majority of cancer deaths, but their tiny seeds are so difficult to track that few researchers have managed to study them.
Now, scientists from UC San francisco describe capturing and studying individual metastatic cells from human breast cancer tumors implanted into mice as the cells escaped into the blood stream
and began to form tumors elsewhere in the body. The researchers discovered that genetic programs expressed in these cells were quite distinct from the primary tumors in
which they originated and included genes typically expressed in mammary stem cells. The findings, published online Sept. 23,2015 in Nature, could change the way researchers think about how cancer spreads
and suggest new drugs to track down and disable its deadly seeds. For the most part, modern cancer drugs ignore differences between primary
and metastatic tumors, said Zena Werb, Phd, professor and vice-chair of anatomy at UCSF, and a senior author on the new study."
"We test drugs for their ability to make primary tumors shrink, but most just don't work on metastases,
"Patients have their original tumor treated or removed, but then the cancer comes back 20,30, 40 years later because there were just a few metastatic cells sitting around."
"Catching metastatic cancer cells in the act No one really knows how dormant metastatic cells can survive incognito for decades,
"It's a big black box in the cancer field--mostly because it's very difficult to study,
only about 7 percent of all breast cancer funding goes to studying metastatic cancer, despite the fact that it causes virtually all breast cancer deaths.
Previous work by Werb's group had found a subset of cells at the edges of breast cancer tumors that seemed primed to metastasize.
and with proteins in the surrounding tumor microenvironment seemed to turn on genetic programs akin to those of mammary stem cells--the cells that allow breasts to form during puberty
These genes for self-replication could make these cells particularly apt to generate new tumors elsewhere in the body.
which involves transplanting human tumor cells into mice. Against the backdrop of healthy mouse tissue, rogue metastatic cells from the human tumor stick out like flares.
The researchers developed a new method using flow cytometry that let them capture individual human metastatic cancer cells traveling through the mouse's blood
the cancer cells'gene activity looked much like that of the primary tumor that had been transplanted into the mice,
In contrast, early-stage metastases and cancer cells traveling through the blood expressed genes typically active in mammary stem cells and quite distinct from primary tumor cells.
Remarkably, the same signature pattern of gene activity was found in metastatic cells in mice whose tumors came from genetically and clinically diverse human patients.
In other words, the genetic program that makes a cell metastatic did not depend on the genetics of its tumor of origin--suggesting that new techniques might allow researchers to find
Since metastatic cells that were beginning to differentiate into secondary tumors showed high expression of genes cmyc and CDK2, the researchers treated 24 PDX mice with dinaciclib,
Whereas 44 percent of control mice (11 of 25) developed secondary tumors within four weeks, researchers could only find metastatic cells in one drug-treated mouse (4 percent.
was that the drug managed to nearly eliminate metastases without shrinking the primary tumor.""If this drug had only been tested on primary tumors,
we would have said it doesn't work, "she said.""This tells us you actually have to look at metastases
"Preventing metastatic cells from invading other parts of the body has been a priority for cancer researchers for many years,
by the time you've detected the tumor, that horse is either already out of the barn
including in cancer research, "said Levi Garraway, an institute member of the Broad Institute, and the inaugural director of the Joint Center for Cancer Precision Medicine at the Dana-Farber Cancer Institute, Brigham and Women's Hospital,
and the Broad Institute. Garraway was involved not in the research. Zhang, Broad Institute, and MIT plan to share the Cpf1 system widely.
#Cabozantinib improves survival in patients with advanced kidney cancer: Results from the METEOR trial Patients with advanced kidney cancer live for nearly twice as long without their disease progressing
if they are treated with cabozantinib, a drug that inhibits the action of tyrosine kinases--enzymes that function as an"on
"or"off"switch in many cellular processes, including cancer. In the second of two late-breaking presentations of research that is predicted to change the way kidney cancer patients are treated,
Professor Toni Choueiri will tell the presidential session of the 2015 European Cancer Congress 1,
about results from the first 375 patients out of a total of 658 patients recruited to the phase III clinical METEOR trial comparing cabozantinib with everolimus,
Analysis of results in July 2015 showed that the estimated median (average) progression-free survival time for patients with advanced clear cell kidney cancer,
who is Associate professor of Medicine at Harvard Medical school and Clinical Director and Kidney Cancer Center Director at The Lank Center for Genitourinary Oncology, Dana-Farber Cancer Institute,
since the results may change the standard of care in patients with advanced kidney cancer who have received prior standard therapy that targets the vascular endothelial growth factor receptor (VEGFR)."
"Although treatment with VEGFR-targeted drugs has been very effective in the first line of therapy for patients with advanced kidney cancer,
Regaining tumour control after prior targeted therapy may reduce symptoms related to kidney cancer and eventually help patients live longer."
Overall, these results should give new hope to patients diagnosed with advanced kidney cancer as cabozantinib may become a new treatment option."
"Clear cell kidney cancer (or renal cell carcinoma) is one of the commonest kidney cancers--70-80%of kidney cancer patients have this type.
or resistance to standard therapies is critical for improving long-term outcome for our patients with advanced kidney cancer.
Further studies include a randomised phase II study of cabozantinib versus standard of care with sunitinib as a first treatment for advanced renal cell cancer.
and an early stage clinical trial combining cabozantinib with immune checkpoint inhibitors has been initiated in urological cancers,
including patients with kidney cancer.""The trial has stopped recruiting patients and researchers are hoping that cabozantinib may become available to patients with advanced kidney cancer some time in 2016.
In the USA, the Food and Drug Administration (FDA) has designated it as a breakthrough therapy,
"I am excited over the advances in treatment of renal cell carcinoma that we are at present.
who will be reporting results from the Checkmate 025 randomised phase III trial of nivolumab versus everolimus in advanced kidney cancer r
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