"said Dr. Lisa Baumbach-Reardon, an Associate professor of TGEN's Integrated Cancer Genomics Division and the study's senior author.
#Breakthrough in cancer research: Cancer-suppressing proteins The research was conducted in the laboratory of Distinguished Professor Aaron Ciechanover, of the Technion Rappaport Faculty of medicine.
The team was led by research associate Dr. Yelena Kravtsova-Ivantsiv and included additional research students and colleagues,
as well as physicians from the Rambam, Carmel and Hadassah Medical centers, who are studying tumors and their treatment. kpc1 an important and vital pathway in the life of the cell,
-B has been identified as a link between inflammation and cancer. The hypothesis of the connection between inflammatory processes and cancer was suggested first in 1863 by German pathologist Rudolph Virchow,
and has been confirmed over the years in a long series of studies. Ever since the discovery (nearly 30 years ago) of NF?
It is involved in tumors of various organs (prostate, breast, lung, head and neck, large intestine, brain, etc.
which are vital to tumor growth; and increased resistance of cancerous cells to irradiation and chemotherapy.
The current research was conducted on models of human tumors grown in mice as well as on samples of human tumors,
and a strong connection was discovered between the suppression of malignancy and the level of the two proteins,
and/or p50 in the tissue can protect it from cancerous tumors. Professor Ciechanover, who is also the president of the Israel Cancer Society,
notes that many more years are required"to establish the research and gain a solid understanding of the mechanisms behind the suppression of the tumors.
The development of a drug based on this discovery is a possibility, although not a certainty,
#Researchers find protein that may signal more aggressive prostate cancers Biomarkers in the body are analogous to the warning lights in cars that signal something might need repairing.
"In the context of prostate cancer) there's a big interest in trying to find biomarkers to discriminate between aggressive and nonaggressive disease,
Prostate cancer can grow so slowly the carrier dies of natural causes before the cancer spreads,
and could provide a potential new drug target for prostate cancer, "Franceschi said.""It could also be a potential biomarker to discriminate between fast and slow growing tumors."
"The U-M researchers made the discovery in a roundabout way, said Franceschi, whose research lab mainly studies bone formation, not cancer."
"We discovered this regulatory mechanism in bone cells, but subsequently found it was also operative in prostate cancer cells,
"This is the first paper the lab has published on cancer.""The idea is that adding a phosphate group, a process called phosphorylation, to the protein Runx2,
However, in prostate cancer cells, Runx2 triggered genes that fuel tumor growth and metastasis."It's unusual that a protein
whose function is to produce bone has this unusual function in prostate cancer, "Franceschi said.
and found that tumor growth was reduced. Franceschi's lab also collaborated with researchers in Italy to analyze tissue samples from 129 patients with prostate cancer.
They found little or no Runx2 phosphorylation in normal prostate, benign prostate or prostatitis, which suggests that Runx2 phosphorylation is associated closely with the more aggressive forms of prostate cancer.
The next step is to establish an actual cause-effect relationship between Runx2 phosphorylation and prostate cancer.
To do this they will compare prostate cancer formation in normal mice and mice lacking Runx2 in their prostates.
Worldwide, prostate cancer is the second-most common cancer in men, according to the World Cancer Research Fund International.
In the U s.,about 221,000 new cases of prostate cancer will be diagnosed in 2015 resulting in roughly 27,500 deaths s
#Hyper-stretchable elastic-composite energy harvester Scientists have developed a hyper-stretchable elastic-composite energy harvesting device called a nanogenerator.
low-cost molecular tumor diagnosis A device developed by Massachusetts General Hospital investigators may bring rapid,
accurate molecular diagnosis of tumors and other diseases to locations lacking the latest medical technology.
"The global burden of cancer, limited access to prompt pathology services in many regions and emerging cell profiling technologies increase the need for low-cost,
"says Cesar Castro, MD, of the MGH Cancer Center and Center for Systems Biology, co-lead author of the report."
"The emerging genomic and biological data for various cancers, which can be essential to choosing the most appropriate therapy,
and the results rapidly returned to the point of Care for molecular analysis of tumors, a sample of blood or tissue is labeled with microbeads that bind to known cancer-related molecules
and are loaded into the D3 imaging module. After the image is recorded and data transmitted to the server,
A pilot test of the system with cancer cell lines detected the presence of tumor proteins with an accuracy matching that of the current gold standard for molecular profiling,
along with those used for clinical diagnosis--using microbeads tagged with antibodies against three published markers of cervical cancer.
and depth of cancer screening in a way that is feasible and sustainable for resource limited-settings, "says Ralph Weissleder, MD, Phd, director of the MGH Center for Systems Biology (CSB) and co-senior author of the paper."
the discovery opens new lines of inquiry about the Ash1l gene's potential role in cancers known to involve other members of the same gene family,
like leukemia, or those where Ash1l might be expressed highly or mutated.""It's vital to understand how the basic,
"Leukemia is a cancer of the body's blood-forming tissues, so it's an obvious place that we plan to look at next.
Dysfunction of blood-forming stem cells is well known in illnesses like leukemia and bone marrow failure disorders.
and radiation used to treat cancer. The replacement of these cells through bone marrow transplantation is the only widely established therapy involving stem cells in human patients.
The Ash1l (Absent, small or homeotic 1-like) gene is part of a family of genes that includes MLL1 (Mixed Lineage Leukemia 1),
a gene that is frequently mutated in patients who develop leukemia. The research found that both genes contribute to blood renewal;
including those whose blood stem cells are killed off by cancer treatments. But work continues in the laboratory setting."
#New biomarker for uterine cancer discovered Researchers at Uppsala University have, together with researchers from Turku and Bergen, discovered a new biomarker
which makes it possible to identify women with uterine cancer who have a high risk of recurrence.
Endometrial cancer of the uterus is the most common form of gynecologic cancer in Europe and North america.
The current study looks at the amount of protein ASRGL1 present in the tumour cells in uterine cancer.
Turku and Bergen and is collected based on samples from 500 women who were diagnosed with uterine cancer between the years 1981 and 2007.
or partially lost ASRGL1 in the tumour cells had a much higher risk of the cancer recurring
'I view the results as a first step towards personal treatment of uterine cancer. Today, 10-15 per cent of the patients suffer recurrences,
It was within The Human Protein Atlas project that the expression of the ASRGL1 protein was mapped first in the human body's normal tissues and in different forms of cancer.
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,
and relapse or not from a malignant melanoma.""It is a new and interesting marker that no one has thought of before.
Even though we currently see considerable progress and success from novel treatment strategies for patients with metastatic melanoma,
and cancer Scientists have discovered a protein that plays a central role in promoting immunity to viruses
and cancer, opening the door to new therapies. Experiments in mice and human cells have shown that the protein promotes the proliferation of cytotoxic T cells,
but when faced with serious infections or advanced cancer, they are often unable to proliferate in large enough quantities to fight the disease.
and were more resistant to cancer. They also produced more of a second type of T cells,
Genetically engineering T cells to augment their ability to fight cancer has been a goal for some time and techniques for modifying them already Exist by introducing an active version of the LEM gene into the T cells of cancer patients,
we hope we can provide a robust treatment for patients. ext we will test the therapy in mice,
and unlocked an unexpected way of enhancing the ability of our immune system to fight viruses or cancers.
This discovery has immediate consequences for the delivery of innovative therapeutic approaches to cancer. Its ramifications,
he discovery of a protein that could boost the immune response to not only cancer, but also to viruses, is a fascinating one.
#Immunotherapy combination promising for untreated patients with advanced melanoma The combination of two immunotherapies for first-line treatment of advanced melanoma induces better responses
Further, the combination was effective in the portion of melanoma patients--the majority--who currently have few effective treatment options. hase 2 clinical trial led by Ludwig Harvard's Stephen Hodi
and Ludwig Memorial Sloan Kettering (MSK)' s Jedd Wolchok has found that the combination of two immunotherapies for first-line treatment of advanced melanoma induces better responses
the combination was effective in the portion of melanoma patients--the majority--who currently have few effective treatment options.
and nivolumab against ipilimumab alone in previously untreated patients, were presented today at the 2015 Annual Meeting of the American Association for Cancer Research
who is also director of the Melanoma Center at the Dana-Farber Cancer Institute.""It's very encouraging to see that pattern reflected in this trial with previously untreated patients."
and is also the Chief of the Melanoma and Immunotherapeutics Service at MSK, found that the same concurrent combination of therapies generated notably positive responses in previously treated patients."
"It was apparent following that trial that the combination should be tested as a first line therapy for metastatic melanoma,
"Rationally combined immunotherapies hold great promise for cancer treatment as long as their side effects can be managed.""Ipilimumab interferes with a process by
PD-1 is engaged often aberrantly by tumor cells themselves to thwart T cell attack. Both drugs have been approved by the US Food and Drug Administration.
The Phase 2, double-blind trial enrolled 142 patients with advanced melanoma who had received not prior therapy.
The tumors of 109 of these patients had the normal form of the gene BRAF
which is mutated frequently in melanoma. This is significant because while melanoma patients with the mutant BRAF gene can be treated with a targeted therapy, the majority
whose tumors encode a normal BRAF have few effective treatment options. In this group of patients, 72 received ipilimumab plus nivolumab, followed by nivolumab alone,
while 37 got ipilimumab plus placebo. Patients whose tumors had a normal BRAF gene showed an overall objective response rate of 61%.
%This included a 22%complete response rate. Those with a normal BRAF who received only ipilimumab had a response rate of 11%,with no complete responses.
which primarily affects boys, causes bleeding, severe and recurrent infections, severe eczema and in some patients autoimmune reactions and the development of cancer.
Research from Rutgers Cancer Institute of New jersey shows genomic profiling identifies genomic mutations in a gene associated with a rare subset of breast cancer--mutations that cannot otherwise be identified with standard clinical analysis of cells and tissue.
being presented as part of a poster presentation at the Annual Meeting of the American Association for Cancer Research (AACR) being held in Philadelphia,
Invasive lobular carcinoma is a cancer that starts in the lobules, an area of the breast where milk is produced.
Pleomorphic invasive lobular carcinoma is a unique subset of lobular breast cancer that has abnormally aggressive tumor cells and results in poorer outcomes than the classic lobular breast cancer.
As part of the precision medicine initiative at the Cancer Institute of New jersey, investigators--which include colleagues from Rutgers Robert Wood Johnson Medical school and RUCDR Infinite Biologics, the world's largest university-based biorepository,
With genomic sequencing detecting ERBB2 alterations in this form of cancer, we have an opportunity to identify anticancer therapies that would specifically target that abnormality
standard of care laboratory testing for breast cancer,"says lead author Kim M. Hirshfield, MD, Phd, breast medical oncologist at the Cancer Institute and assistant professor of medicine at Rutgers
Utilizing the invasive breast cancer data set of 962 cases in The Cancer Genome Atlas all breast cancers with alterations in the CDH1 gene (that gives instructions to make a protein that causes cancer cells to stick to one another
Tumors were evaluated by a pathologist at the microscopic level to classify them as either classic or pleomorphic lobular breast cancer.
An additional 16 cases from the Cancer Institute were evaluated using an advanced form of tumor DNA sequencing at RUCDR.
Of 116 eligible breast cancers from The Cancer Genome Atlas 86 were invasive lobular breast cancer. Of that number, 21 cases were found to be the pleomorphic type.
There were no significant differences in the frequency of the other gene alterations examined between the two types of cancer.
Data from the additional 16 cases from the Cancer Institute validate the findings observed on breast cancers from The Cancer Genome Atlas."
"In identifying a specific abnormality in a patient's cancer instead of the overall organ where it first presented,
the opportunity exists to provide tailored therapies for patients,"notes Lorna Rodriguez, MD, Phd, director of the precision medicine initiative at the Cancer Institute and professor of obstetrics, gynecology and reproductive sciences
It is our aim at Rutgers Cancer Institute of New jersey to build upon this work,"notes senior author of the work, Shridar Ganesan, MD, Phd, associate director for translational science at the Cancer Institute
"Prof Shirley Hodgson, Professor of Cancer Genetics, St george's University of London, said:""I think that this is a significant departure from currently accepted research practice.
could allow biomedical engineers to identify appropriate binding sites for drugs used to treat cancer and other diseases.
The device is intended for use in remote laboratory settings to diagnose various types of cancers and nervous system disorders
#Uncovering new functions of a gene implicated in cancer growth opens new therapeutic possibilities Two decades ago,
was also present in cancer patients and contributing to tumor progression. The present study reveals another way that Id1 works, hijacking a normal pathway in immune cell development and interfering with the entire immune system, starting in the bone marrow.
Without competent immune cells, the body can't fight off tumors, and instead, cancer is allowed to grow,
spread and thrive.""Targeting Id1 offers the potential to restore overall immune function, "said senior author Dr. David Lyden, the Stavros S. Niarchos Professor in Pediatric Cardiology and a professor of pediatrics in the Department of Pediatrics at Weill Cornell Medical College."
"When the immune system is functioning, treatment options are more plentiful. Given the increased incidence and death rates tied to advanced stage metastatic cancers,
there is also an increased urgency to understand how pro-metastatic, immunosuppressive mechanisms, like those driven by Id1,
"The investigators discovered that a tumor-secreted protein called transforming growth factor beta (TGF? promotes the activation of Id1.
and allowing cancer to grow and spread unabated.""Normally, the bone marrow produces, among other immune cell types, dendritic cells,
and growth of tumors,"said first author Dr. Marianna Papaspyridonos, who was a Fulbright Cancer Research Fellow at Cornell University in Dr. Lyden's lab."But when TGF?
is released by the tumor and Id1 is upregulated, the normal generation of dendritic cells is interrupted,
and instead another subset of immune cells, which suppresses the immune system, is formed.""Those immune cells, called myeloid-derived suppressor cells,
allow cancer to more readily grow and spread. The researchers validated this finding in advanced melanoma patients,
who have increased TGF? plasma levels and higher levels of Id1 in myeloid peripheral blood cells. Targeting Id1 might provide a three-pronged therapeutic approach,
which would first reduce the metastatic potential of the tumor itself, then reduce the tumor's ability to form new blood vessels, a process called vasculogenesis,
and finally restore the patient's systemic immune function.""With this approach, immune cells will recognize a tumor as foreign and attack it,
"said Dr. Lyden, who also has appointments in the Sandra and Edward Meyer Cancer Center and the Gale and Ira Drukier Institute for Children's Health at Weill Cornell Medical College."
"This will improve vaccine development, lead to better treatment outcomes and ultimately benefit cancer patients
#Can photosynthesis be measured over large areas? Scientists find a way"Plant photosynthesis is a fundamental process that drives all ecosystem functions.
"SIRT1 is known to be expressed abnormally in a variety of cancers and might be a good target for therapy.
Ubiquitin-proteasome inhibitors have already been used successfully in cancer therapy and clinical trials. Therefore, this research might provide molecular bases
and insights for developing additional therapeutic strategies in the future,"explained Ed Seto, Ph d.,senior member of the Cancer Biology and Evolution Program at Moffitt t
The new work also reveals more about certain cancers that arise when these processes go astray, for example,
"Both the Wnt and Activin signaling processes operate differently in cancer, compared to stem cells.
The aberrant behavior of the Activin process, meanwhile, is tied to the metastasis of many cancers."
because these would have strong anticancer activity for many tumor types, "says Estar#s ."Because the environment of stem cells and cancer cells are quite distinct,
and regulation that we have defined in stem cells operates in the cells of a tumor. u
NONO helps to mend the damage The study appeared as advanced online publication on Oncogene, a journal in cancer research from the Nature Publishing Group.
a multifunctional protein involved in melanoma development and progression, in the cellular response to UV radiations.
or transmitted to daughter cells during mitosis. Luigi Alfano, Phd of the National Cancer Institute of Naples-Pascale Foundation-CROM-Cancer Research center of Mercogliano,
"Considering that many studies are identifying NONO alterations in cancer, our findings will likely help to shed light on the molecular mechanisms of tumorigenesis, especially in tumour types like melanoma, in which exposure to UV radiations plays such a prominent part.
Our work also provides the preclinical framework supporting the development of new agents targeting NONO that could be used to sensitize cancer cells to a variety of drugs that cause DNA damage,
such as common chemotherapy agents,"states Francesca Pentimalli Phd from the National Cancer Institute of Naples co-corresponding of the study with Antonio Giordano,
Director of the Sbarro Institute for Cancer Research and Molecular Medicine, at Temple University, Philadelphia a
#Scientists dramatically improve method for finding common genetic alterations in tumors St jude Children's Research Hospital scientists have developed a significantly better computer tool for finding genetic alterations that play an important role in many cancers
The comparison involved the normal and tumor genomes from 43 children and adults with brain tumors, leukemia, melanoma and the pediatric eye tumor retinoblastoma."
whole-genome sequencing to better understand the genetic landscape of cancer genomes and lay the foundation for the next era of cancer therapy,
"said corresponding author Jinghui Zhang, Ph d.,a member of the St jude Department of Computational biology.""In this study of the tumor and normal genomes of 43 patients, CONSERTING identified copy number alterations in children with 100 times greater precision and 10 times greater precision in adults."
"First author Xiang Chen, Ph d.,a St jude senior research scientist, added:""CONSERTING helped us identify alterations that other algorithms missed,
and copy number alterations present in a small percentage of tumor cells.""Using CONSERTING, researchers discovered genetic alterations driving pediatric leukemia, the pediatric brain tumor low-grade glioma, the adult brain tumor glioblastoma and retinoblastoma.
The algorithm also helped identify genetic changes that are present in a small percentage of a tumor's cells.
The alterations may be the key to understanding why tumors sometimes return after treatment. In addition, Zhang said CONSERTING should make it easier to track the evolution of tumors with complex genetic rearrangements,
sometimes involving multiple chromosomes that swap pieces when they break and reassemble. St jude has made CONSERTING available for free to researchers worldwide.
The software user manual and related data can be downloaded from http://www. stjuderesearch. org/site/lab/zhang.
scientists can upload data for analysis. Work on CONSERTING began in 2010 shortly after the St jude Children's Research Hospital--Washington University Pediatric Cancer Genome Project was launched.
The Pediatric Cancer Genome Project used next-generation, whole-genome sequencing to study some of the most aggressive and least understood childhood cancers.
and provide insight into the origins of a patient's cancer. CONSERTING has now been used to analyze next-generation,
whole-genome sequencing data for the Pediatric Cancer Genome Project. The project includes the normal and cancer genomes of 700 pediatric cancer patients with 21 different cancer subtypes.
CONSERTING combines a method of data analysis called regression tree, which is a machine learning algorithm, with next-generation,
even those present in relatively few cells or in tumor samples that include normal cells along with tumor cells,
Diseases like cancer and AIDS propagate throughout the body by hijacking exosomes.""Exosomes are engineered by nature to be the perfect delivery vehicles for proteins and genetic material,
"We could completely inhibit tumor growth after just one dose of the cancer vaccine in the animal model,
. Ph d."This is the most amazing result we have seen ever in a tumor treatment study.""The success of the treatment, Shen and his team learned, appears to be the porous silicon microparticles (PSMS) themselves.
In vivo and in vitro studies confirmed the microparticles stimulated a strong, sustained innate immune response at local sites of tumor activity and growth--with or without any antigen loaded."
"We have shown for the first time that a microparticle can serve as a carrier for sustained release and processing of tumor antigens,
"Cancer vaccines are designed to turn a patient's own immune system more strongly against cancer cells, and have been an area of recent and intense interest among oncologists.
Since 2010, the FDA has approved vaccines and other immunotherapy drugs for melanoma, prostate cancer, and lung cancer.
There are currently dozens of active clinical trials evaluating vaccines for cancer therapy. Approximately 235,000 new diagnoses of breast cancer were made last year,
a cell surface hormone receptor that is overexpressed in the tumor cells of 15 to 30 percent of breast cancer patients.
"But these vaccines have mostly not been very potent because of inefficient vaccine delivery, a poor immune response at the site of the tumor,
We have shown that the PSM-mediated vaccine is not only potent enough to trigger tumor cell killing,
but also modifies the tumor microenvironment in a way that favors tumor treatment.""An important aspect of PSM function is stimulating the body's own immune system to fight cancer,
Shen said.""PSMS persistently challenge the antigen-presenting cells to activate the T cells, "he said."
"And the PSMS modify the tumor microenvironment so that the cytotoxic T cells maintain their activity.""Shen said the use of PSMS could work for any variety of cancer antigens and cancers,
and that the PSMS could be loaded with multiple antigens for a single vaccine target, or multiple antigens for several targets, possibly enhancing the approach's effectiveness further."
"This is a technology platform that can be applied by other scientists to develop vaccines for other types of cancers, ultimately helping,
we hope, more types of cancer patients.""Before human clinical trials can begin, Shen said the researchers must evaluate the toxicity of antigen-loaded PSMS s
Implications for Cancer, Materialsthe success of this research, which was done on a CLS prototype, has led to the commissioning of the first commercial device.
and dark-field CT in preclinical studies--an approach that could help visualize cancer.""We work closely together with two clinics to study tumors,
"Eggl says.""One of our plans is to image breast tissue samples and also entire breasts after mastectomy to better understand the clinical picture of breast cancer."
and can reach 11 percent or even higher in bone repairs for gunshot wounds or reconstruction after tumor removal.
when a tumor or accident requires replacement of a large segment of bone. These bone materials can come either from the patient
#3d'organoids'grown from patient tumors could personalize drug screening Three-dimensional cultures (or'organoids')derived from the tumors of cancer patients closely replicate key properties of the original tumors,
reveals a study. These'organoid'cultures are amenable to large-scale drug screens for the detection of genetic changes associated with drug sensitivity
and pave the way for personalized treatment approaches that could optimize clinical outcomes in cancer patients."
"This is the first time that a collection of cancer organoids, or a living biobank, has been derived from patient tumors,
"says senior study author Mathew Garnett, a geneticist at the Wellcome Trust Sanger Institute.""We believe that these organoids are an important new tool in the arsenal of cancer biologists
and may ultimately improve our ability to develop more effective cancer treatments.""To study the causes of cancer
and develop new cancer treatments, many laboratories use experimental model systems such as cells grown from patient tumors.
However, currently available cell lines have been derived under suboptimal conditions and therefore fail to reflect important features of tumor cells.
As a result, it has been challenging to predict the drug sensitivity of individual patients based on their unique spectrum of genetic mutations.
In recent years, scientists have developed organoid cell culture systems as an alternative approach to grow normal and diseased tissue in a dish.
In contrast to cell lines organoids display the hallmarks of the original tissue in terms of its 3d architecture,
whether these cultures could potentially bridge the gap between cancer genetics and patient outcomes. In the new study, the researchers grew 22 organoids derived from tumor tissue from 20 patients with colorectal cancer
and then sequenced genomic DNA isolated from these cultures. The genetic mutations in the organoid cultures closely matched those in the corresponding tumor biopsies and agreed well with previous large-scale analyses of colorectal cancer mutations.
These findings confirm that the cultures faithfully capture the genomic features of the tumors from
which they are derived as well as much of the genomic diversity associated with colorectal cancer. To link drug sensitivity to genetic changes,
the researchers next screened the responses of the organoids to 83 experimental and approved cancer drugs.
indicating that the subset of cancer patients with RNF43 mutations would strongly benefit from a drug that inhibits a protein called porcupine."
"At some point in the future, this approach may be suitable for modeling individual patient response to cancer therapies to inform clinical treatment,
Moving forward, the researchers plan to expand the panel of existing colon organoids as well as develop an organoid biobank for other tumor types."
"Cancer is a diverse and complex disease and having a large collection of organoids is necessary to encompass this diversity to enable scientists
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