#Possible new treatment for bladder cancer using a mycobacterium Universitat Autònoma de Barcelona researchers have found a mycobacterium that is more effective in treating superficial bladder cancer
Mycobacteria are the only bacteria used in cancer treatment. The administration of the bacterium Mycobacterium bovis (BCG), is the current treatment for superficial bladder cancer.
It is inserted directly into the bladder through a catheter. BCG prevents new tumours from appearing,
Preclinical studies using mouse models of bladder cancer have demonstrated the efficacy of the mycobacterium M. brumae in the treatment of this disease.
which is given significant that in the last few years BCG production problems have led to supply issues for certain bladder cancer patients."
"Our results suggest that Micobacterium brumae is an ideal candidate to replace the current BCG treatment for superficial bladder cancer,
#Groundbreaking computer program diagnoses cancer in two days In by far the majority of cancer cases, the doctor can quickly identify the source of the disease, for example cancer of the liver, lungs, etc.
However, in about one in 20 cases, the doctor can confirm that the patient has cancer
and attempts to locate the origin of the cancer before starting any treatment. Now, researchers at DTU Systems Biology have combined genetics with computer science
Each year, about 35,000 people are diagnosed with cancer in Denmark, and many of them face the prospect of a long wait until the cancer has been diagnosed and its source located.
However, even after very extensive tests, there will still be 2-3 per cent of patients where it has not been possible to find the origin of the cancer.
In such cases, the patient will be treated with a cocktail of chemotherapy instead of a more appropriately targeted treatment
are based on analyses of DNA mutations in cancer tissue samples from patients with metastasized cancer,
i e. cancer which has spread. The pattern of mutations is analysed in a computer program which has been trained to find possible primary tumour localizations.
whether an individual cancer patient will benefit from a specific type of medicine. This is a very effective method,
and it is becoming increasingly common to conduct such sequencing for cancer patients. Associate professor Aron Eklund from DTU Systems Biology explains:"
"We are pleased very that we can now use the same sequencing data together with our new algorithms to provide a much faster diagnosis for cancer cases that are difficult to diagnose,
and thus also as an effective and easy way of monitoring people who are at risk of developing cancer.
Tumor tracer A diagnostic method for determining the primary site of the cancer. The method combines genetics and computer science,
and on this basis provide a number of possible scenarios for where the cancer may have developed
'Complex array of mutations found in rare, aggressive leukemia Sezary syndrome (SS), an aggressive leukemia of mature T cells, is complicated more at a molecular level than ever suspected, according to investigators from the Perelman School of medicine at the University of Pennsylvania.
With a poor prognosis and limited options for targeted therapies, fighting SS needs new treatment approaches.
The team's results uncover a previously unknown, complex genomic landscape of this cancer, which can be used to design new personalized drug regimens for SS patients based on their unique genetic makeup.
complementary gene sequencing approaches to look for mutations in tumor cells from SS patients: whole-genome sequencing in six subjects,
drugs that are approved currently for treatment of other hematologic cancers such as polycythemia vera and myelofibrosis."
#Scientists pave way for diamonds to trace early cancers Physicists from the University of Sydney have devised a way to use diamonds to identify cancerous tumours before they become life threatening.
synthetic version of the precious gem can light up early-stage cancers in nontoxic, noninvasive Magnetic resonance imaging (MRI) scans.
Targeting cancers with tailored chemicals is not new but scientists struggle to detect where these chemicals go since,
if a treatment has been taken up by a cancer. Led by Professor David Reilly from the School of Physics
researchers from the University investigated how nanoscale diamonds could help identify cancers in their earliest stages."
"By attaching hyperpolarised diamonds to molecules targeting cancers the technique can allow tracking of the molecules'movement in the body,
and target cancers long before they become life-threatening, "says Professor Reilly. The next stage of the team's work involves working with medical researchers to test the new technology on animals.
#3d image of cancer protein aids quest for new treatments Scientists at the Walter and Eliza Hall Institute have created the first three-dimensional image of a key protein known to be involved in the development of blood and other cancers.
The discovery showed the protein, called Trib1, plays a vital role in controlling how and when other proteins are degraded,
The finding could be used to develop new drugs to treat cancers such as leukaemia, caused by malfunctioning of the Trib1 protein.
causing a type of blood cancer called acute myeloid leukemia (AML). Institute researchers Dr James Murphy and Dr Isabelle Lucet, in collaboration with Dr Peter Mace from the University of Otago, New zealand, characterised the human Tribbles protein Trib1.
and can lead to diseases such as cancer.""Using the Australian Synchrotron, Dr Mace, Dr Murphy and colleagues were able to obtain detailed three-dimensional images of Trib1."
which will provide critical clues for developing drugs that target Trib1 to treat cancers.""Lead investigator Dr Mace said Trib1 acted as a scaffold to bring many proteins together,
which causes a loss of proteins that would normally inhibit cancer. Understanding the structure of Trib1 provides critical clues about how we could block Tribbles for the treatment of AML."
"In one of many successful tests, the lab designed molecules to detect mutation sequences in historic biopsy samples preserved in wax from cancer patients.
One of the researchers'goals is to design noninvasive cancer diagnostics that detect DNA biomarkers in blood samples for early screening and early recurrence detection.
and apply it to cancer detection n
#New approach toward a broad spectrum malaria vaccine Malaria affects millions of people worldwide. Plasmodium falciparum enolase participates in parasite invasion of host red blood cells and mosquito midgut epithelium.
Strangely shaped cells often indicate cancer. While this old, simple technique may seem a quaint throwback in the age of high-technology health care tools like genetic sequencing
ENT surgeons commonly use endoscopic approaches to remove brain tumors through the nose by making a window through the blood-brain barrier to access the brain.
#New computational strategy finds brain tumor-shrinking molecules Patients with glioblastoma, a type of malignant brain tumor,
In mouse models of human glioblastoma, one molecule they found shrank the average tumor size by half.
whose binding is essential for the tumor's survival and growth. This study is the first to demonstrate successful inhibition of this type of protein,
Phd, research scientist at UC San diego Moores Cancer Center, as well as the San diego Supercomputer Center and Department of Neurosciences at UC San diego."
leading to quick-growing tumors. In order to work, transcription factors must buddy up, with two binding to each other and to DNA at same time.
They then tested the molecules for their ability to kill glioblastoma tumors in the Moores Cancer Center lab of the study's senior author
The most effective of these candidate drug molecules, called SKOG102, shrank human glioblastoma tumors grown in mouse models by an average of 50 percent."
#World first lab-in-a-briefcase Academics at Loughborough University hope to boost early detection rates of cancer in developing countries with their portable lab-in-a-briefcase that can operate even at high temperatures.
Believed to be the first kit of its kind dedicated to the portable measurement of cancer biomarkers,
The number of people dying from cancer in developing countries is on the increase, partly due to steadily ageing populations
Cancer is a leading cause of death worldwide, accounting for over 8 million deaths per year,
and 70%of the world's cancer deaths occur in Africa, Asia and Central and South america.
The number of new cancer cases is expected to rise by 70%over the next two decades 1. With the help of his Research Associate Ana Isabel Barbosa,
A new affordable and disposable microfluidic test strip--comprising of tiny tubes about the size of a human hair--is used specifically for the quick measurement of different types of cancer biomarkers in a whole blood sample.
has already been used successfully by Dr Reis in a separate study that detected prostate cancer with the help of a smartphone camera.
and this is what makes it a truly life-changing concept for the screening and monitoring of different types of cancer."
boosting levels of cancer detection in developing countries where ordinarily people would not have such easy access to early diagnostics.
Although the study focused on rapid detection for prostate cancer, Dr Reis said the microfluidic test strip is versatile enough to measure several cancer biomarkers simultaneously from one whole blood sample. 1 World health organization World Cancer Report 201 1
#Detecting diabetes in a saliva sample with a smart phone With the participation of Mexican and international experts,
and at least one relative, is believed also to play a role in cell division and cancer. Arrayin collaboration with Dutch colleagues, the authors now show how important VRAC is, particularly in cancer.
They investigated cell lines to determine the role played by VRAC and its subunits in the transport of cisplatin and carboplatin into the cell.
From the researchers'point of view, this goes some way into explaining why some people are resistant to some forms of cancer therapy.
Researchers led by Sven Rottenberg of the Cancer Research Centre in Amsterdam also identified LRRC8D as a relevant gene in a genome-wide screen for cellular cytostatic resistance.
They studied the genetic data of ovarian cancer patients, who had been treated with cisplatin or carboplatin, with regard to their survival time.
#DNA in blood can track cancer development, response in real time Scientists have shown for the first time that tumour DNA shed into the bloodstream can be used to track cancers in real time as they evolve
and respond to treatment, according to a new Cancer Research UK study published in the journal Nature Communications.
Over three years, researchers at the University of Cambridge took surgical tumour samples (biopsies) and blood samples from a patient with breast cancer that had already spread to other parts of her body.
and timing of genetic changes appearing as the cancer developed and responded to treatment. The results provide the first proof-of-principle that analysing tumour DNA in the blood can accurately monitor cancer within the body.
Study author Professor Carlos Caldas, senior group leader at the Cancer Research UK Cambridge Institute, said:"
"This definitively shows that we can use blood-based DNA tests to track the progress of cancer in real time.
The findings could change the way we monitor patients, and may be especially important for people with cancers that are difficult to reach,
as taking a biopsy can sometimes be quite an invasive procedure.""The patient in the study had had breast cancer that already spread to a number of other organs.
and Nitzan Rozenfeld laboratories at the Cancer Research UK Cambridge Institute--were even able to distinguish between the different secondary cancers
We now need to see if this works in more patients and other cancer types,
"Dr Kat Arney, science information manager at Cancer Research UK, said:""Spotting tumour DNA in the bloodstream is a really promising area of research,
and monitoring cancers. But this work gives us a window into the future, where we'll use less invasive techniques to track the disease in real time
to successfully detect cell stiffness changes associated with certain cancers and other diseases. Brian Patchett, a research assistant and instructor within the Department of physics at Utah Valley University, will describe the group's method,
and how they change during the process of cancer and disease development.""The stiffness of the cell is the primary change detected with our high-frequency ultrasound;
The group's method can also help distinguish between different types of cancer--such as aggressive breast cancer vs. less aggressive forms."
"This method can be used to explore the aspect of cells that changes during Alzheimer's disease, the metastasis of cancer,
and characterize cancer or other diseases.""Our method identifies aggressive types of breast cancer, for example, while in the operating room,"Patchett noted."
"We're collaborating with the Huntsman Cancer Institute--part of the University of Utah healthcare system--to explore various types of breast tissues under levitation to refine our pathology detection methods,
personalized medical treatments based on our ability to quickly and effectively detect cancers and diseases in patients
This same type of approach potentially also could be used to make other currently plant-based medicines for fighting cancer
such as a free mobile app where users help find data patterns in cancer research by playing games.
Colorectal cancer commonly referred to as colon cancer is one of the three most common cancers worldwide and the most common in Singapore.
Almost 95 per cent of colorectal cancers are from malignant tumours. The research team found that Imatinib,
Professor of Metabolic Disease at NTU Lee Kong Chian School of medicine and senior principal investigator with the National Cancer Centre Singapore. ur work has important clinical implications,
and cancer progression in patients predisposed to develop colorectal cancer, said Prof Pettersson, who is also a Professor of Host-Microbe Interactions at Karolinska Institutet.
#Unusual Chance to Study Patient's Residual Tumor Leads to New Finding Capitalizing on a rare opportunity to thoroughly analyze a tumor from a lung cancer patient who had developed resistance to targeted drug treatment,
the researchers were able to durably wipe out cancer cells in mice implanted with cells from the drug-resistant tumor. ven in cancers that are responding to targeted therapy by conventional criteria,
the senior author of the new study, Trever Bivona, MD, Phd, assistant professor of medicine and member of the UCSF Helen Diller Family Comprehensive Cancer Center (HDFCCC).
which drug-resistant cells that survive treatment form residual, often lethal, tumors. Understanding the biological basis of acquired resistance has proved difficult,
leaving scientists with few drug-resistant tumors to use in research. But as described in the online edition of Cell Reports on Thursday, April 2, 2015,
a team of UCSF researchers recently had unusual access to a surgically resected tumor from an EGFR-mutant lung cancer patient who had experienced a substantial,
and Evangelos Pazarentzos, Phd, a postdoctoral fellow, the research group analyzed cells from this tumor using next-generation genome sequencing in an effort to understand how the cells sidestepped erlotinib treatment.
They found that the tumor cells retained the EGFR mutation targeted by erlotinib and had acquired not additional cancer-driving mutations,
or any other mutations known to confer drug resistance. These results suggested that the cells were still potentially susceptible to erlotinib,
when cells from the tumor were implanted in mice that were treated then with erlotinib. The drug effectively inhibited EGFR activity,
and they discovered that this increase is mediated by a previously unknown biochemical complex formed within the tumor cells.
a growing body of work has tied the NF-KAPPA-B pathway to various forms of cancer. An experimental drug known as PBS-1086 directly targets the NF-KAPPA-B pathway,
the implanted tumors shrank significantly, suggesting that combining a compound like PBS-1086 with erlotinib at the outset of therapy may help to prevent acquired drug resistance in EGFR-mutant NSCLC.
Combined drug regimens designed to overcome drug resistance at the outset of therapy are now the norm in treating certain forms of melanoma,
we see tumors shrink. In lung cancer patients treated with these drugs, and that a substantial number of patients, this could be a very powerful companion therapy to minimize
Isaac Hilton, postdoctoral fellow in the Gersbach Lab and first author of the study. ut many diseases, like cancer,
#Biologists identify brain tumor weakness Biologists at MIT and the Whitehead Institute have discovered a vulnerability of brain cancer cells that could be exploited to develop more-effective drugs against brain tumors.
The study, led by researchers from the Whitehead Institute and MIT Koch Institute for Integrative Cancer Research, found that a subset of glioblastoma tumor cells is dependent on a particular enzyme that breaks down the amino acid glycine.
Without this enzyme, toxic metabolic byproducts build up inside the tumor cells, and they die. GLDC caught the researchersattention as they investigated diseases known as nborn errors of metabolism
which occur when cells are missing certain metabolic enzymes. Many of these disorders specifically affect brain development;
the most common and most aggressive type of brain tumor found in humans. The researchers found that GLDC,
These regions are often found at the center of tumors, which are inaccessible to blood vessels.
which makes them better suited to survive in the ischemic tumor microenvironment, Kim says. However, this highly active SHMT2 also produces a glut of glycine,
#Wearable Device Slows Deadly Brain tumors, Clinical Trial Finds A wearable device that emits low-level electrical fields can slow the progression of glioblastoma, the deadliest form of brain cancer,
and extend patientslifespans, a major clinical trial at the University of Virginia School of medicine and more than 80 other institutions has found.
noting that glioblastoma is notoriously difficult to treat. his is a tumor type that it been very hard to make real progress against.
Because this trial clearly shows an improvement both in time until the tumor starts growing but more importantly in overall survival.
#New Way to Fight Cancer Targeted cancer therapies work by blocking a single oncogenic pathway to halt tumor growth.
But because cancerous tumors have the unique ability to activate alternative pathways, they are often able to evade these therapies and regrow.
Moreover, tumors contain a small portion of cancer stem cells that are believed to be responsible for tumor initiation, metastasis and drug resistance.
Thus, eradicating cancer stem cells may be critical for achieving long-lasting remission, but there are no drugs available that specifically attack cancer stem cells.
A Surprising Discovery Now a research team led by investigators at Harvard Medical school and the Cancer Center at Beth Israel Deaconess Medical center
has identified an inhibitor of the Pin1 enzyme that can address both these challenges in acute promyelocytic leukemia (APL) and triple-negative breast cancer.
Their surprising discovery demonstrates that the Vitamin a derivative ATRA (all-trans retinoic acid), a treatment for APL that is considered to be the first example of modern targeted cancer therapy,
can block multiple cancer-driving pathways and, at the same time, eliminate cancer stem cells by degrading the Pin1 enzyme.
Reported online in Nature Medicine, these novel findings suggest a promising new way to fight cancerarticularly cancers that are aggressive
or drug resistant. in1 changes protein shape through proline-directed phosphorylation, which is a major control mechanism for disease,
explained co-senior author Kun Ping Lu, HMS professor of medicine and director of translational therapeutics in the Cancer Research Institute at Beth Israel Deaconess. in1 is a common key regulator in many types of cancer
and as a result can control over 50 oncogenes and tumor suppressors, many of which are known to also control cancer stem cells.
Lu also co-discovered the enzyme in 1996. A Different Approach Until now, agents that inhibit Pin1 have been developed mainly through rational drug design.
Although these inhibitors have proven active against Pin1 in the test tube when they are tested in vitro in a cell model
in order to bind Pin1. hile it has been shown previously that ATRA ability to degrade the leukemia-causing fusion oncogene PML-RAR causes ATRA to stop the leukemia stem cells that drive APL,
when two tumor suppressors fuse together to become an oncogene, added co-author Pier Paolo Pandolfi, the HMS George C. Reisman Professor of Medicine and director of the Cancer Genetics Program at Beth Israel Deaconess,
whose own pioneering work revealed the molecular underpinnings of APL and led to its cure. hese new findings demonstrate that by inhibiting Pin1,
thereby stopping cancer stem cells from replicating. This is a critically important discovery that will impact the treatment of other forms of cancer
since Pin1 inhibition is also affecting other key oncogenes. To that end, the authors also tested ATRA in triple-negative breast cancer, one of the most aggressive types of breast cancer.
They discovered that ATRA-induced Pin1 ablation also potently inhibits triple-negative breast cancer growth in human cells and in animal models by simultaneously turning off many oncogenes and turning on many tumor suppressors.
or more potent and specific Pin1-targeted ATRA variants for cancer treatment. he current ATRA drug has a very short half life of only 45 minutes in humans,
and offers a promising new approach for targeting a Pin1-dependent common oncogenic mechanism in numerous cancer-driving pathways in cancer
and cancer stem cells. This is especially critical for treating aggressive or drug-resistant cancers. a
#Computer-Designed Rocker Protein Worlds First To Biomimic Ion Transport For the first time, scientists recreated the biological function of substrate transportation across the cell membranes by computationally designing a transporter protein.
Says Study Angiogenesis inhibitors widely used class of cancer drugs designed to shrink tumors by preventing them from forming new blood vesselsften work in the short term,
and prevent cancer relapse. Working with laboratory models of pancreatic and breast cancer, the scientists found that myeloid cells,
During anti-angiogenic therapy, said Bergers, the Neill H. and Linda S. Brownstein Endowed Chair in Brain tumor Research and a member of the UCSF Helen Diller Family Comprehensive Cancer Center,
he tumor hijacks the second stage of the natural process we see in wound healing for its own advantage.
which prevents the tumor from forming new blood vessels, thereby shrinking it. The researchers found that during the initial phase of therapy,
VEGF inhibition stimulates myeloid cells within the tumor to release the signaling protein CXCL14, which is angiostatic
and the tumor shrinks. But thenrobably in response to reduced oxygen flow within the tumoryeloid cells switch to their opposite state nd become real bad guys
and tumor growth. nce the PI3K pathway is activated, therapy becomes ineffective, and you have said relapse,
so the cancer just ignores the therapy. The researchers found that targeting specific innate immune cells within the tumor did not reverse the negative effects of PI3K activation.
Eliminating macrophages one type of white blood cell resulted in an increase in neutrophils another type of white blood cell.
This so-called myeloid-cell oscillation maintained the tumor resistance to the therapy. Instead, said Bergers,
and significantly increased survival in a mouse model of pancreatic neuroendocrine tumor. Bergers noted that the discovery potentially gives physicians a way to determine how effective anti-VEGF therapy might be in individual patients
we could test to determine how many myeloid cells in the tumor were activated already, which could tell us to what extent the tumor would still be responsive to anti-VEGF therapy,
she said. In patients undergoing therapy, e could take advantage of the fact that myeloid cells occur not only in the tumor,
but also in the blood, said Bergers. simple blood test would give us a noninvasive biomarker to check on the state of myeloid activation.
whether and how the cancer will spread. At the same time, the discovery also opens new doors for future improved treatment of patients with melanomas.
Today it is not possible to predict spreading from malignant melanomas. Melanoma metastases are furthermore extremely difficult to eliminate as traditional treatment such as chemotherapy
and radiotherapy is mostly ineffective. Only ten per cent of the patients survive once they reach an advanced stage with distant metastases.
The discovery point towards the possibility of identifying aggressive melanomas at an earlier stage than is currently possible,
Pigment Cell & Melanoma Research. May be Possible to Predict Disease Progression It is the first time that the protein megalin,
Even though we currently see considerable progress and success from novel treatment strategies for patients with metastatic melanoma,
researchers studying a range of conditions from West Nile to multiple sclerosis to diabetes to cancer can generate an unprecedented level of detailed data about cells from relatively small samples.
Similarly, in his lab, Hafler applies Cytof to the study of cellular complexities at the root of diseases such as a multiple sclerosis and cancer.
In one current project, his team is investigating specific types of immune cells extracted from brain tumors. ee isolating T cells from brain tumors,
Understanding how multiple molecules function at the same time in a single cell may reveal clues about how brain tumors manage to survive
he said. he more we can define how the tumor is evading the immune system, the more specific we can make the treatment.
and profile whole populations of immune cells for the study of cancer and other complex diseases.
#An end to cancer pain? U of T researcher finds the ain trigger A new study led by University of Toronto researcher Dr. David Lam has discovered the trigger behind the most severe forms of cancer pain.
Released in top journal Pain this month, the study points to TMPRSS2 as the culprit:
a gene that is also responsible for some of the most aggressive forms of androgen-fuelled cancers.
Head of Oral and Maxillofacial Surgery at the Faculty of dentistry, Lam research initially focused on cancers of the head and neck,
Studies have shown that these types of cancers are the most painful, with sufferers experiencing pain that is immediate and localized,
and neck cancer patients are men leading him to investigate a genetic marker with a known correlation to prostate cancer,
TMPRSS2. rostate cancer research already knows that if you have the TMPRSS2 gene marker, the prostate cancer is much more aggressive.
Theye also shown that this is androgen (male hormone) sensitive. In his study, Lam, who is appointed jointly as a Consultant Surgeon at the Princess Margaret Cancer Centre
and a Clinician at the Mount sinai Wasser Pain Management Centre, ascertained that TMPRSS2 was not only present in patients suffering from head
and neck cancers it was also prevalent in much greater quantities than in prostate cancer.
Lam and his fellow researchers followed up this observation by looking at different types of cancers with known pain associations for instance, certain breast and melanoma cell lines.
and neck cancer is the most painful form of cancer, followed by prostate cancer, while melanoma,
or skin cancer, sits at the bottom of the pain scale. But what surprised the researchers was that the presence
and amount of TMPRSS2 in these cancer cell cultures stood in exact correlation with the known level of pain each cancer causes. t was exactly
what we know clinically about pain association, adds Lam. A New Direction for Drug Research The startling discovery of TMPRSS2 role in triggering cancer pain may lead to the creation of targeted cancer pain therapies that effectively shut down the expression of this gene
or its ability to infiltrate pain receptors in the body. Dr. Brian Schmidt, Professor at New york University college of Dentistry, Director of the Bluestone Center for Clinical Research and a co-author of the study states,
he discovery that TMPRSS2 drives cancer pain demonstrates another way that cancers lead to suffering.
Inhibition of its activity in patients might provide a new form of treatment for cancer pain. ny cancer that is painful before initiating drug treatment we can label the cancer cells for TMPRSS2
what role the increased expression of TMPRSS2 plays in the aggressiveness and morbidity rates associated with certain aggressive cancers
Overtext Web Module V3.0 Alpha
Copyright Semantic-Knowledge, 1994-2011