and MIT's 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. Blocking this enzyme in glioblastoma cells could offer a new way to combat such tumors,
says Dohoon Kim, a postdoc at the Whitehead Institute and lead author of the study,
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,
thus blocking Hur function as a tumor-promoting protein, "said Liang Xu, associate professor of molecular biosciences and corresponding author of the paper.
a critical tumor suppressor, shuts off growth signals Today, scientists at Cold Spring Harbor Laboratory (CSHL) publish new evidence explaining precisely how the protein encoded by PTEN (called PTEN) works--specifically,
And in view of PTEN's critical role as a tumor suppressor, it's also important that the process we uncovered is controlled a one,
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,
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,
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,
"It could also be a potential biomarker to discriminate between fast and slow growing tumors."
However, in prostate cancer cells, Runx2 triggered genes that fuel tumor growth and metastasis."It's unusual that a protein
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.
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.
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
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,
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 tumors of 109 of these patients had the normal form of the gene BRAF
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,
Patients whose tumors had a normal BRAF gene showed an overall objective response rate of 61%.
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.
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.
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,
"The investigators discovered that a tumor-secreted protein called transforming growth factor beta (TGF? promotes the activation of Id1.
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,
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."
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
#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."
"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."
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.
even those present in relatively few cells or in tumor samples that include normal cells along with tumor cells,
"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,
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,
"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,
"We work closely together with two clinics to study tumors, "Eggl says.""One of our plans is to image breast tissue samples
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
or a living biobank, has been derived from patient tumors, "says senior study author Mathew Garnett, a geneticist at the Wellcome Trust Sanger Institute."
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 the new study, the researchers grew 22 organoids derived from tumor tissue from 20 patients with colorectal cancer
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
Moving forward, the researchers plan to expand the panel of existing colon organoids as well as develop an organoid biobank for other tumor types."
#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,
But in diseases such as breast cancer, the breakdown of this order has been associated with the rapid growth and spread of tumors."
or structural changes in mammary glands can lead to the breakdown of tissue architecture associated with tumors that metastasize,
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."
#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,
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."
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,
which respond to therapies differently than other tumor subtypes, so we are interested very in seeing
"Overall, the findings suggest that treatment decisions should be based on both a patient's stroma and tumor subtype.
The new study shows that this crosstalk is important not only for launching immune responses against tumors,
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.
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.
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
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.
only to trigger a recurrence decades after the primary tumor is removed. Metastases cause the vast majority of cancer deaths,
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
"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."
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
by the time you've detected the tumor, that horse is either already out of the barn
Tumor tracer A diagnostic method for determining the primary site of the cancer. The method combines genetics and computer science,
complementary gene sequencing approaches to look for mutations in tumor cells from SS patients: whole-genome sequencing in six subjects,
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,
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."
#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,
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,
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.
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.
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
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
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,
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.
and as a result can control over 50 oncogenes and tumor suppressors, many of which are known to also control cancer stem cells.
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,
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.
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,
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,
The researchers found that targeting specific innate immune cells within the tumor did not reverse the negative effects of PI3K activation.
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.
he said. he more we can define how the tumor is evading the immune system, the more specific we can make the treatment.
#Molecular spies to fight cancer Tracking the tumor: PNA-antibodies detect initially the diseased cells (red)
and accumulate at the tumor site. Afterwards the radioactively labeled probes (blue) selectively bind to them by specific base pairing.
thus to visualize the tumor. Scientists at the Helmholtz-Zentrum Dresden-Rossendorf (HZDR), in cooperation with colleagues at the University of Zurich and the Ruhr-Universität Bochum, have tested for the first time successfully a new tumor diagnosis method under near-real conditions.
The new method first sends out an antibody as a pyto detect the diseased cells and then binds to them.
The scientists could then clearly visualize the tumor by utilizing a tomographic method. This procedure could improve cancer treatment in the future by using internal radiation.
however, be produced in a laboratory to precisely bind to tumor cells. They are used in cancer research to detect
It also makes the exact localization of the tumor in the body more difficult because the resulting images are less sharp. ogether with colleagues at the University of Zurich and the Ruhr-Universität Bochum,
to scout out the enemy the tumor cells. The piesthen share their position with their troops,
In various types of tumors, there is an increase in this molecule formation or it might be found in a mutated form,
the scientists first injected the PNA-EGFR antibody into tumor-bearing mice and gave this pytime to accumulate at the tumor site.
They then administered the PNA counterpart, labeled with the radioactive substance technetium-99m. mages we took using single photon emission computed tomography show that both the antibody
The tumor could thus be visualized clearly within a short period of time. urthermore, the radioactively labeled probes had disappeared already from the bloodstream after sixty minutes,
and their matching PNA counterparts can be used in diagnosing tumors in humans. ur results however show that the PNAS we tested are suitable candidates for further preclinical studies, Stephan sums up.
it could also be used to transport therapeutically effective radioactive substances to the tumor in order to irradiate it from within
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