#Researchers identify a target to stop the spread of ovarian cancer UNSW researchers have discovered a method for disrupting the spread of ovarian cancer, by blocking receptors present on the surface of cancer cells.
and stops the cancer will soon be developed. The findings are published in the journal Oncotarget. With no early detection test and a lack of obvious symptoms in the early stages of ovarian cancer,
women are diagnosed usually late after the cancer has spread to other organs in the body.
Survival rates for ovarian cancer remain at around 40%%with the disease killing 150,000 women worldwide every year.
Very little is known about how and why ovarian cancer spreads and researchers say this is due, in part, to a lack of understanding of the key genes and molecules that initiate and control the progression and growth of ovarian cancer.
That is slowly changing thanks to pioneering work by researchers at UNSW Lowy Cancer Research Centre and their international partners.
In their latest study, the UNSW team found tissue sections taken from ovarian cancer patients had a significantly higher expression of the receptor molecule, Ror2
than tissue sections taken from benign samples. It has previously been shown that its ister receptor Ror1,
is expressed also abnormally in ovarian cancer patients and associated with poor survival. The team also established that concurrently silencing both receptors had a strong inhibitory effect on the proliferation, migration and invasion of the cancer cells.
because the receptor molecules identified seem to be expressed universally in all epithelial ovarian cancer patients,
not just those with hereditary ovarian cancer. ome drugs are showing promise as a treatment for patients with hereditary ovarian cancer,
however this group makes up only 15%of all ovarian cancer patients, said Dr Ford from UNSW Lowy Cancer Research Centre. or the majority of patients with ovarian cancer,
treatment options have made little progress over the past 30 years and there are currently no targeted therapies available. ersonalised medicine is about targeting treatment to an individual particular genetic profile,
and unlike other cancer types such as breast, this is still very much in its infancy in ovarian cancer treatment.
Researchers believe the Ror amilyof receptor molecules are attractive drug targets for three reasons. First, the receptors are not usually present in normal adult tissues
and other members of this specific class of receptors have been targeted successfully for cancer therapies. The cancer drugs Herceptin, Gleevec and Iressa all target receptors of this class.
Separate research has also found that the Ror2 receptor is associated with unfavourable prognosis and tumour progression in cervical cancer.
and others suggests that in all gynaecological cancers both Ror1 and Ror2 may be expressed over and is important for disease progression.
and spread of ovarian cancer. nce we better understand the roles of these receptors we will be in a position to develop a drug to target these receptors and hopefully halt ovarian cancer in its tracks,
The UNSW study focused on epithelial ovarian cancer which is the most common type making up about 90%of tumours of the ovary.
Rarer types of ovarian cancer include germ cell tumours (cancer of the egg making cells of the ovary) and sarcomas t
and potentially treating human diseases such as cancer, cardiovascular disease, neurodegenerative conditions and diabetes, which can be driven by mutations in control regions of the genome.
Widely used today to treat cancer, the technique requires doctors to mark unwanted cells with a chemical that makes them sensitive to low-level red light.
yet large enough to carry the chemical payload needed to do the job. n our cancer work,
which is already in clinical trials as a cancer therapeutic; and a more precise next-generation antisense oligonucleotide (ASO) drug developed in collaboration with Isis pharmaceuticals,
and now he believes his team has discovered a revolutionary strategy to treat cancer. he focus of my work has always been to define the signature molecules that are on
and previously unknown, characteristic of cancerous tumors arising from a variety of organs. e discovered membrane proteins that among the normal tissues,
These egg-specific proteins are also found in cancers that arise in a wide range of organs,
For some reason, when many cancers dysregulate, or begin to grow on their own, they revert back and take on features of a developing egg.
Herr and his team are bringing awareness to an aspect of cancer that is fundamental to the disease:
At the same time, theye creating an entirely new field of study into cancer-oocyte neoantigens. athologists have appreciated long that cancer cells may de-differentiate
What we have confirmed now is that cancers from many organs de-differentiate to take on features of the oocyte, the original mother cell from
With this discovery, Herr started his first cancer research company, Neoantigenics. Like Ovastasis, Neoantigenics is focused on creating a targeted drug that will affect only those cells identified by the correct cell surface biomarkers.
Their goal is to create a cancer treatment that will track and kill cells that carry the SAS1B protein,
the biomarker that is found only on growing eggs and tumor cells. The monoclonal antibodies to SAS1B can be thought of as a homing mechanism to guide a miniscule warhead selectively to the surface of cancer cells.
and then after binding on the tumor cell surface, the antibody-drug burrows inside them to release a toxic payload. ou add an antibody with a drug on it
The same biomarkers that will help limit the area of impact for Ovastasis birth control will also help Neoantigenics confine the toxic effects of cancer treatment to growing egg and tumor cells.
This unique medication could mean a dramatic reduction of the difficult side-effects of traditional cancer treatments like hair loss, nausea, anemia and neuropathy.
but for female cancer patients especially, a treatment that doesn touch their body healthy tissues is a huge breakthrough. e think we have a way
but a way that could become a frontline treatment for women who have cancers of many types
After the cancer treatment is complete those primordial eggs can begin the cycle of normal egg growth and ovulation again.
and the company will work with U. Va. labs as it begins testing the cancer medication first in model organisms,
Future applications of such a DNA walker might include a cancer detector that could roam the human body searching for cancerous cells
constantly computing whether a cancer is present. ore immediate practical applications may include deploying the DNA walker in the body
Although it may be a long march from diagnosing cancer to curing it, ll breakthroughs begin with baby steps.
and smuggle cancer signals their neighbors New research in The FASEB Journal suggests that an in vitro co-culture system robustly quantifies the transfer of fluorescent proteins between cells
Not only does this cast an important light on how cancer metastasizes and recruits cellular material from healthy cells,
especially the mouse model, will be used by academics to isolate healthy cells modified by tumors, and by the pharmaceutical industry in the quest for novel anticancer drugs that block tumor-organ communication,
said Anne Burtey, Ph d.,study author from the Department of Biomedicine, at the University of Bergen in Bergen,
with increased abilities to diffuse within tumors and even reach the healthy cells involved in tumor progression.
To make this discovery, Burtey and colleagues studied the exchange of molecules between cells, by color-coding them with red or blue cellular fluorescent yesor ags.
suggesting that this protein is a key regulator of cell-cell communication in cancer. Live cell imaging confirmed that the transfer is contact-dependent.
#New treatment targets cancers with particular genetic signature Oxford university researchers have found the Achilles heel of certain cancer cells mutations in a gene called SETD2.
Their findings will be presented to the National Cancer Research Institute conference in Liverpool 2nd november, 2015. It is well known that mutations drive cancer cell growth and resistance to treatment.
The Oxford team found that that was the case for cancer cells with mutations in a key cancer gene called SETD2.
utations in SETD2 are frequently found in kidney cancer and some childhood brain tumours, so we were excited
Importantly, the research team, funded by Cancer Research UK and the Medical Research Council, have developed also a biomarker test to identify SETD2 mutated tumours,
something that can be used immediately in cancer diagnosis. Professor Tim Maughan, Clinical Director of the Cancer Research UK/Medical Research Council Oxford Institute for Radiation Oncology, said:
his novel and exciting finding provides a new scientific basis for precision targeting of some cancers
which are currently very difficult to treat, and we are now taking these findings into clinical trials.
the hope is that these findings will help to target other cancers with similar weak points
and provide a step towards personalized cancer therapy i
#Google Project Loon Set to Enmesh the Globe with Internet Balloons by 2016 Project Loon is yet another highly ambitious project of the tech-giant Google,
For the first time, scientists have identified a protein inside blood vessels found at the invasive edge of brain tumours highlighting the area from where cancer is most likely to spread.
Mapping this inflammation gives scientists a more complete picture of the cancer. The scientists have developed a special dye that recognises
and Cancer Research UK scientist at The University of Oxford, said: f we can map the edge of the tumour,
Professor Charlie Swanton, NCRI chair and Cancer Research UK scientist at the Francis Crick Institute, said:
Harpal Kumar, Cancer Research UK chief executive, said: rain cancers continue to have very poor survival rates,
which is why research into how to treat them is a top priority for Cancer Research UK.
Being able to delineate the edges of brain tumours is an exciting step towards better surgery and radiotherapy for patients.
such as applying anticancer medications to melanomas or applying growth factors and antibiotics for wound healing, said Jin Di,
#Tadpole endoscope offers new hope for gastrointestinal cancer detection Hong kong researchers have devised a swimming housing for a capsule endoscopy camera which can be steered around to provide better images inside the stomach
Cancers in this system the oesophagus, stomach, intestines and rectum are major causes of death and difficult to investigate,
and clinicians in their quests to find cures for cancer, lupus and other diseases. The team used a preexisting next-generation sequencing toolkit,
The American Cancer Society uses cloud-based office and collaboration technology to improve organisational efficiencies.
and monitor cancer patients as well as other diseases. By engaging with pregnant women and monitoring their health via this mobile application,
whose cancers came back even after stem cell transplants. Their cancers were so aggressive they had no treatment options left said the study's senior author Stephan Grupp MD Phd a professor of Pediatrics in Penn's Perelman School of medicine and director of Translational Research in the Center
for Childhood Cancer Research at the Children's Hospital of Philadelphia. The durable responses we have observed with CTL019 therapy are unprecedented.
Shannon Maude MD Phd an assistant professor of Pediatrics and a pediatric oncologist at CHOP and Noelle Frey MD MSCE an assistant professor of Medicine and an oncologist at Penn's Abramson's Cancer Center
are co-first authors of the new study. The research team is led by Carl June MD the Richard W. Vague Professor in Immunotherapy in the department of Pathology and Laboratory Medicine and director of Translational Research in the Abramson Cancer Center
along with David Porter MD the Jodi Fisher Horowitz Professor in Leukemia Care Excellence and director of Blood and Marrow Transplantation in the Abramson Cancer Center.
CTL019 manufacturing begins with a patient's own T cells which are collected via an apheresis process similar to blood donation then reprogrammed in Penn's Clinical Cell
and kill tumor cells. The engineered cells contain an antibody-like protein known as a chimeric antigen receptor (CAR)
which is designed to bind to a protein called CD19 found on the surface of B cells including the cancerous B cells that characterize several types of leukemia.
A signaling domain built into the CAR promotes rapid multiplication of the hunter cells building an army of tumor-killing cells that tests reveal can grow to more than 10000 new cells for each single engineered cell patients receive.
whose cancers returned as CD19-negative leukemia that would not have been targeted by the modified cells.
All patients who received the CTL019 hunter cells experienced a cytokine release syndrome (CRS) within a few days after receiving their infusions--a key indicator that the engineered cells have begun proliferating and killing tumor cells in the body.
which also express the CD19 protein had been eliminated along with their tumors. The researchers note that persistent absence of normal B cells following CTL019 treatment indicates continued activity of the gene-modified T cells
which are thought to provide long-term vaccine-like activity preventing tumor recurrence. Since B cells play a role in helping fight infection patients typically receive immunoglobulin replacement to maintain healthy immune function.
and cells offer new solutions for cancer diagnosis and therapy. Understanding the interdependency of physiochemical properties of nanomedicines in correlation to their biological responses
and functions is crucial for their further development of as cancer-fighters. To develop next generation nanomedicines with superior anticancer attributes we must understand the correlation between their physicochemical properties--specifically particle size
or smaller--exhibited enhanced performance in vivo such as greater tissue penetration and enhanced tumor inhibition. Over the last 2-3 decades consensus has been reached that particle size plays a pivotal role in determining their biodistribution tumor penetration cellular internalization clearance from blood plasma and tissues as well as excretion from the body--all of
which impact the overall therapeutic efficacy against cancers stated Li Tang first author of this PNAS article.
Our studies show clear evidence that there is an optimal particle size for anticancer nanomedicines resulting in the highest tumor retention.
Among the three nanoconjugates investigated the 50 nm particle size provided the optimal combination of deep tumor tissue penetration efficient cancer cell internalization as well as slow tumor clearance exhibits the highest efficacy against both
primary and metastatic tumors in vivo. To further develop insight into the size dependency of nanomedicines in tumor accumulation
and retention the researchers developed a mathematical model of the spatiotemporal distribution of nanoparticles within a spherically symmetric tumor.
The results are extremely important to guide the future research in designing new nanomedicines for cancer treatment Cheng noted
In addition a new nanomedicine developed by the Illinois researchers--with precisely engineered size at the optimal size range--effectively inhibited a human breast cancer
and prevented metastasis in animals showing promise for the treatment of a variety of cancers in humans.
Seitz Materials Research Laboratory and University of Illinois Cancer Center. Tang who obtained his Phd degree from the University of Illinois with Jianjun Cheng is currently a CRI Irvington postdoctoral fellow at the Massachusetts institute of technology.
Errors in copying DNA are found in certain cancers and this work could one day help develop new treatment methods that stall
#Prostate cancers penchant for copper may be a fatal flaw Like discriminating thieves prostate cancer tumors scavenge
This proclivity for copper uptake is something we have known could be an Achilles'heel in prostate cancer tumors as well as other cancers said Donald Mcdonnell Ph d. chairman of the Duke Department of Pharmacology and Cancer Biology and senior author
of a study published Oct 15 2014 in Cancer Research a journal of the American Association of Cancer Research.
Our first efforts were to starve the tumors of copper but that was unsuccessful. We couldn't deplete copper enough to be said effective Mcdonnell.
and then use a drug that requires copper to be effective to attack the tumors.
Disulfiram had at one time been a candidate for treating prostate cancer--it homes in on the additional copper in prostate cancer tumors
along with the disulfiram the combination resulted in dramatic reductions in prostate tumor growth among animal models with advanced disease.
Androgens the male hormones that fuel prostate cancer increase the copper accumulation in the cancer cells.
or similar compounds and copper especially beneficial for men who have been on hormone therapies that have failed to slow tumor growth.
Unfortunately hormone therapies do not cure prostate cancer and most patients experience relapse of their disease to a hormone-refractory
Although tremendous progress has been made in treating prostate cancer there is clearly a need for different approaches
Andrew Armstrong M d. associate professor of medicine was involved with a recent study at Duke testing disulfiram in men with advanced prostate cancer.
While we did not observe significant clinical activity with disulfiram in men with recurrent prostate cancer in our recent clinical trial this new data suggests a potential way forward
or similar compounds in men with progressive prostate cancer particularly in settings where the androgen receptor is active.
Flip could affect electrical grid cancer ratesthe discovery comes as new evidence indicates that the intensity of Earth's magnetic field is decreasing 10 times faster than normal leading some geophysicists to predict a reversal within a few
or temporary loss of the field before a permanent reversal could increase cancer rates. The danger to life would be even greater
#Immune cells in liver drive fatty liver disease, liver cancer Fatty liver disease--alongside fatty liver due to massive alcohol consumption--is caused mainly by excessive consumption of fat
These liver diseases (NAFLD and NASH) along with chronic viral infections are the most common causes of liver cancer or hepatocellular carcinoma (HCC.
In the United states HCC is the fastest-growing form of cancer at the moment. No efficient causal therapy exists for HCC patients of which approximately 800000 die every year.
and also show how it can develop into liver cancer. Inflammatory events offer starting point for prevention
#Discovery of cellular snooze button advances cancer, biofuel research The discovery of a cellular snooze button has allowed a team of Michigan State university scientists to potentially improve biofuel production and offer insight on the early stages
of cancer. The discovery that the protein CHT7 is a likely repressor of cellular quiescence
and oil production also wields control of cellular growth--and tumor growth--in humans. Christoph Benning MSU professor of biochemistry and molecular biology and his colleagues unearthed the protein's potential
Its application in cancer research however was a surprise finding that is leading Benning's lab in a new direction.
In terms of human medicine this discovery gives scientists a promising new model to study tumor suppression and growth.
For cancer research it's a new paradigm Benning said. The switch that tells an organism to grow
That is the first step of tumor growth. Story Source The above story is provided based on materials by Michigan State university.
#Research leads to brain cancer clinical trial Researchers at the University of Calgary's Hotchkiss Brain Institute (HBI)
and Southern Alberta Cancer Research Institute (SACRI) have made a discovery that could prolong the life of people living with glioblastoma--the most aggressive type of brain cancer.
Samuel Weiss Phd Professor and Director of the HBI and Research Assistant professor Artee Luchman Phd and colleagues published their work today in Clinical Cancer Research
and therapies that can be tested in the clinic provides the greatest hope for brain cancer patients
Glioblastoma is the most common and deadly form of brain cancer among adults. The progression and complexity of the tumours are often difficult to treat.
and Dr. Greg Cairncross--director of SACRI and leader of the Terry Fox Research Institute (TFRI'Therapeutic Targeting of Glioblastoma research program at the university--are now working with cancer researchers Dr. Warren Mason (Princess
Margaret Cancer Centre in Toronto) and Dr. Lesley Seymour (Director of the NCIC Clinical Trials Group's Investigational New Drug Program) and drug manufacturer Astrazeneca to plan a clinical trial testing a similar but newer drug
This is an important initiative--to test new drugs being developed for other types of cancers in the laboratory to identify which are most promising for testing in patients with glioblastoma.
which will be funded by a grant from the TFRI as well as grants from Canadian Cancer Society Research Institute to NCIC CTG says Seymour r
These mutations cause more than 200 diseases and contribute to others such as diabetes cancer Parkinson's disease and Alzheimer's disease.
CRISPR with Suntag Already Is Shedding Light on Cancer and Normal Developmentcrispr--an acronym for clustered regularly interspaced short palindromic repeats--is a natural system that bacteria use to defend themselves against viruses. The basis for CRISPR applications in the lab is a protein from this system called Cas9
CRISPR activation and interference can be used to understand how specific genes work in cancer regenerative medicine or neurodegenerative disease according to Weissman.
The Weissman team used CRISPR activation to identify a number of tumor suppressor genes that inhibit the growth of cancer cells.
In a paper published today in the journal Cancer cell the researchers report how the drug known as DTP3 kills myeloma cells in laboratory tests in human cells
Multiple myeloma is an incurable cancer of the bone marrow which accounts for nearly two per cent of all cancer deaths.
Professor Guido Franzoso from the Department of Medicine at Imperial College London who led the research said:
and potentially several other types of cancer but we will need to confirm this in our clinical trials the first
and the immune and stress response systems was discovered to be overactive in many types of cancer and responsible for switching off the normal cellular mechanisms that naturally lead to cell death.
The Imperial researchers took a different approach looking for target genes downstream of NF-kb that might be responsible for its role in cancer specifically.
-B pathway with our DTP3 peptide therapeutic selectively kills myeloma cells could offer a completely new approach to treating patients with certain cancers such as multiple myeloma Professor Franzoso said.
The significant progress made by Professor Franzoso in multiple myeloma is one of the many cancers we believe his signal transduction research could be applied to.
and releases the drugs very quickly once inside the cancer cellgu says. n addition because we used self-assembling DNA techniques it is relatively easy to manufacturesays Wujin Sun lead author of the paper
and think it holds promise for delivering a variety of drugs targeting cancer and other diseases. he paper ocoon-Like Self-Degradable DNA-Nanoclew for Anticancer Drug Deliverywas published online Oct 13 in the Journal
at The Ohio State university Comprehensive Cancer Center--Arthur G. James Cancer Hospital and Richard J. Solove Research Institute.
Dr. Julia White of Ohio State's Comprehensive Cancer Center--James Cancer Hospital and Solove Research Institute has helped develop a modified treatment board that allows patients to lie comfortably on their stomachs
while the breast tissue falls away from the chest wall allowing the radiation to target the cancer.
Researchers characterize new tumor syndrome Scientists at the Luxembourg Centre for Systems Biomedicine (LCSB) of the University of Luxembourg have published their findings that mutations in a gene known as ARMC5 promote the growth of benign tumors in the adrenal glands
ARMC5 appears to belong to the group of so-called tumor suppressor genes. It is the first time in years that scientists have characterized such a gene.
The ARMC5 gene was discovered by independent workgroups studying benign tumors--so-called adrenal adenomas--in connection with Cushing's syndrome.
Now for the first time a mutation of ARMC5 has been characterized as the cause behind the growth of meningeal tumors.
The results on this tumor syndrome obtained by the group of Dr. Patrick May and PD.
In search of the causes of Cushing's syndrome scientists recently encountered certain genetic causes of benign tumors of the adrenal cortex.
Growth of these adrenal cortex adenomas is based on a combination of hereditary and spontaneous mutations: It affects people in
However because the tumor cells multiply faster than other body cells and the number of cells in the tumor increases the blood cortisol level rises in the course of the disease says Dr Schneider.
Then the cortisol level in the body rises and ultimately results in the onset of Cushing's syndrome.
When other scientific workgroups discovered that further benign tumors--in this case meningeal tumors--occur more often in ARMC5-Cushing families the group of Patrick May
We demonstrated for the first time in a patient with an adrenal cortex tumor and simultaneously a meningeal tumor that somatic that is nonhereditary ARMC5 mutations are present in both tumors.
This observation suggests that ARMC5 is a true tumor-suppressor gene. It must now be explored Schneider continues to what extent patients with adrenal cortex tumors ought to be screened for simultaneous presence of meningioma and in
which other types of tumor ARMC5 mutations are responsible for tumor growth: Building upon that we can learn
whether the gene and the metabolic pathways it influences offer new approaches for treating the tumor syndrome.
Story Source: The above story is provided based on materials by Université du Luxembourg. Note: Materials may be edited for content and length.
Journal Reference e
#Ultra-fast charging batteries that can be recharged 70 in just two minutes Scientists from Nanyang Technological University (NTU Singapore) have developed a new battery that can be recharged up to 70 per cent in only
When one of these wrong genes is turned on by mistake the result can be rampant cell growth--cancer.
I think epigenetics is a new frontier of cancer research says Brian Strahl Ph d. a professor of biochemistry and biophysics in the UNC School of medicine.
and what we're finding is that many cancers have mutations in the epigenetic machinery.
We're not just finding this in cancer cell lines in the lab but in cancer patients.
The director's cutstrahl who's a member of the UNC Lineberger Comprehensive Cancer Center said major questions surround how histones wrap up the DNA into chromatin--a structure that allows
and in turn contribute to cancers and other diseases. Adding a twist to this idea however is the fact that not every histone is the same.
Some studies indicated that Bre1 had a role as a tumor suppressor Strahl said. Other studies showed that it's a cancer promoter.
So there's been conflicting evidence about all of this. Now we know. If there's too little Bre1 the gene won't turn on.
This could turn off the genes that protect the cell from cancer. If there's too much Strahl said.
This could also trigger cancer development. When you think about it Bre1 could be a really good target for a cancer drug Strahl said.
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