which promote the growth of blood vessels that feed tumors. By blocking these in lung endothelial cells,
the researchers were able to slow lung tumor growth in mice and also reduce the spread of metastatic tumors.
#Chemotherapy timing is key to success MIT researchers have devised a novel cancer treatment that destroys tumor cells by first disarming their defenses,
dramatically shrinks lung and breast tumors. The MIT team, led by Michael Yaffe, the David H. Koch Professor in Science,
and targeting it to having smart nanoparticles that deliver drug combinations in the way that you need to really attack the tumor.
which shuts down one of the pathways that promote uncontrolled tumor growth. These pretreated tumor cells were much more susceptible to treatment with a DNA-damaging drug called doxorubicin than cells given the two drugs simultaneously. t like rewiring a circuit,
says Yaffe, who is also a member of the Koch Institute. hen you give the first drug,
found on tumor cell surfaces, has been approved by the Food and Drug Administration to treat pancreatic cancer and some types of lung cancer.
and ovarian tumors. Staggering these drugs proved particularly powerful against a type of breast cancer cell known as triple-negative,
Triple-negative tumors, which account for about 16 percent of breast cancer cases, are much more aggressive than other types
folate, helps direct the particles to tumor cells, which express high quantities of folate receptors.
Once the particles reach a tumor and are taken up by cells, the particles start to break down.
The researchers tested the particles in mice implanted with two types of human tumors: triple-negative breast tumors and non-small-cell lung tumors.
Both types shrank significantly. Furthermore, packaging the two drugs in liposome nanoparticles made them much more effective than the traditional forms of the drugs,
but also for delivering the drugs more directly to the tumor tissue itself, says Rune Linding,
As a next step before possible clinical trials in human patients, the researchers are now testing the particles in mice that are programmed genetically to develop tumors on their own,
instead of having human tumor cells implanted in them. The researchers believe that time-staggered delivery could also improve other types of chemotherapy.
Inhibitors could be targeted to tumors to make them more susceptible to chemotherapy, while enhancers could help protect people who have been exposed accidentally to DNA-damaging agents,
Tumors in low-oxygen environments tend to be more resistant to therapy and spread more aggressively to other parts of the body.
Measuring tumors oxygen levels could help doctors make decisions about treatments but there s currently no reliable noninvasive way to make such measurements.
Doctors often use MRI to diagnose tumors but currently MRI can only reveal the size and location of a tumor.
With the new MIT sensor doctors could track the state of the tumor and predict how it might respond to radiation treatment according to the researchers.
Radiation kills tumors by initiating DNA damage but oxygen is required to help finish the job.
An accurate reading of how much oxygen is present would help doctors calculate how much radiation might be necessary.
Measuring oxygen levels could also reveal the metastatic potential of a tumor: Those with lower oxygen levels tend to spread more aggressively.
What s happening in a tumor This type of sensor could also be useful for monitoring blood flow in diabetic patients who often experience restricted circulation in their extremities
The researchers also anticipate that it could help scientists learn more about tumor biology. As opposed to just studying the genetic profile of tumor cells this could also reveal how they re interacting with the stroma that surrounds the tumor.
Oxygen tension as simple as it sounds is a good measure of what s happening in a tumor Cima says.
The researchers are now working on sensors that could be used to monitor other biological properties such as ph. We hope this is the first of many types of solid-state contrast agents where the material responds to its chemical environment in such a way that we can detect it by MRI Cima says.
#How tumors escape About 90 percent of cancer deaths are caused by tumors that have spread from their original locations.
but not less aggressive tumors, and found that four of those proteins are critical to metastasis. The findings could lead to new tests that predict which tumors are most likely to metastasize,
and may also help to identify new therapeutic targets for metastatic tumors, which are extremely difficult to treat. he problem is,
all the current drugs are targeted to primary tumors. Once a metastasis appears, in many cases, there nothing you can do about it,
Patients whose tumors have a greater abundance of extracellular matrix proteins have a poorer prognosis, but until now, scientists did not know why. he matrix has really been understudied,
Researchers in Hyneslab previously developed a method for identifying extracellular matrix proteins by enriching them from tumors
To compare the extracellular matrix proteins found in different tumor types, the researchers implanted metastatic and nonmetastatic human breast cancer cells into mice.
They identified 118 extracellular matrix proteins that were found in both types of tumors. However, there were also several dozen proteins that were abundant in either metastatic or nonmetastatic tumors,
but not both. Manipulating the environment It appears that metastatic tumors as well as the supportive cells that surround them, secrete certain proteins into the extracellular matrix to make it easier for them to escape
Many of the proteins overexpressed in the more aggressive tumors are activated by the same cellular signaling pathways,
the researchers analyzed five of the proteins that are elevated in highly aggressive tumors and found that four of them are necessary for metastasis to occur.
tumors failed to spread. his elegant study sheds new light into the extracellular matrix proteins involved in various steps of the metastatic cascade,
a professor of radiation oncology at Harvard Medical school and Massachusetts General Hospital. ur knowledge about the abundance of extracellular matrix proteins in tumors has been limited.
The researchers also compared their results with human tumor samples and found that when the proteins they had identified in mice were overexpressed in human tumors,
the patients had lower survival rates. It would be impractical to do this kind of large-scale protein screen in patients,
who are now developing such antibodies. hat could become part of a kit that doctors would use to distinguish a patient who has a tumor that going to metastasize,
so they would follow the patient differently from a patient with a tumor they know won metastasize,
which escaped tumor cells often metastasize such as the bone, liver, and lungs make them more receptive to invading cancer cells.
and Howard Hughes Medical Institute investigator Sangeeta Bhatia relies on nanoparticles that interact with tumor proteins called proteases each
and colleagues introduced the concept of a synthetic biomarker technology to amplify signals from tumor proteins that would be hard to detect on their own.
These particles congregate at tumor sites where MMPS cleave hundreds of peptides which accumulate in the kidneys
In tests in mice the researchers were able to accurately identify colon tumors as well as blood clots.
The team is also working to identify signatures of MMPS that could be exploited as biomarkers for other types of cancer as well as for tumors that have metastasized.
and for stimulating the body immune system to attack tumors, says Irvine, who is also a member of MIT Koch Institute for Integrative Cancer Research.
to determine the extent of cancer metastasis after removing a tumor. The dye used for this imaging binds tightly to albumin,
or tumor peptide. e knew we were on the right track because we saw you could get immune responses that were just tremendous,
and the cervical cancer vaccine shrank tumors. t certainly is an interesting approach, and the results are very convincing,
and the consequential suppression of tumor growth are results that would suggest further development and clinical testing.
which allows tumors to survive and continue growing even after chemotherapy severely damages their DNA.
A new study from MIT biologists has found that tumor cells with mutated p53 can be made much more vulnerable to chemotherapy by blocking another gene called MK2.
In a study of mice tumors lacking both p53 and MK2 shrank dramatically when treated with the drug cisplatin while tumors with functional MK2 kept growing after treatment.
The findings suggest that giving cancer patients a combination of a DNA-damaging drug and an MK2 inhibitor could be very effective says Michael Yaffe the David H. Koch Professor in Science
or apoptosis. Tumors that lack p53 can avoid this fate. Usually p53 is the main driver of cell death
if you block the MK2 pathway tumor cells wouldn t recognize that they had DNA damage
if this would hold true in tumors in living animals as well as cells grown in a lab dish.
To do that they used a strain of mice that are programmed genetically to develop non-small-cell lung tumors.
or off allowing them to study tumors with and without MK2 in the same animal.
This new approach allows them for the first time to compare different types of tumors in the same mice where all genetic factors are identical except for MK2 expression.
Using these mice the researchers found that before treatment tumors lacking both MK2 and p53 grow faster than tumors that have MK2.
This suggests that treating tumors with an MK2 inhibitor alone would actually do more harm than good possibly increasing the tumor s growth rate by taking the brake off the cell cycle.
However when these tumors are treated with cisplatin the tumors lacking MK2 shrink dramatically while those with MK2 continue growing.
A nonobvious combination The potential combination of cisplatin and MK2 inhibitors is unlike other chemotherapy combinations that have been approved by the Food
While this study focused on non-small-cell lung tumors the researchers have gotten similar results in cancer cells grown in the lab from bone cervical and ovarian tumors.
The drug kills cells very effectively by damaging nuclear DNA but if tumors become resistant to cisplatin they often grow back.
which contains the metal platinum was approved to treat ovarian and testicular tumors in 1978 and is used now for many other cancers including lung and bladder.
and identify the boundaries of tumors.""This nanoparticle may open the door for new'hypermodal'imaging systems that allow a lot of new information to be obtained using just one contrast agent,
This would enable doctors to better see where tumors begin and end, Lovell says. Explore further:
PTT uses the nanoparticles to focus light-induced heat energy only within the tumor harming no adjacent normal cells.
That means the photo-thermal effect of iron-oxide nanoparticles may show in the next decade a strong promise in human cancer therapy likely with localized tumors.
With this technology a low-power laser beam is directed at the tumor where a small amount of magnetic iron-oxide nanoparticles are present either by injecting the particles directly into the tumor
Sufficient heat is generated then locally by the laser light raising the tumor temperature rapidly to above 43 degrees Celsius
but only generates local heat within the tumor therefore posing much less side effects than the traditional chemo or radiation therapies.
because the tumors are usually stage three or four before they can be detected. He stated With nanomaterial technology we can detect the tumor early
and kill it on sight at the same time. Each tumor has a corresponding protein that is cancer specific called a tumor specific ligand
or an antibody antigen reaction that only has expression for that specific cancer such as breast or prostate cancer.
Scientists identify this certain bio-marker that is specific to a certain tumor then conjugates this bio-marker on the surface of the nanocarrier that only has the expression for that specific kind of cancer cell.
and biodegradable and can potentially stay in the tumor cells until its job is finished then dissolve
So far in vivo testing in mice has shown that this approach produces significant accumulation of drugs in tumor sites instead of healthy organs.
the combination of carrier and drug also dramatically reduced tumor growth compared with the drug alone.
A key challenge in chemotherapy is ensuring that the drugs are delivered only to the tumor
and filtered out of the body by the immune system before it reaches the tumor. Micellar nanocomplexes of less than 100 nanometers in dimension are formed from the OEGCG core
and renal clearance while providing for tumor targeting. The research team conducted animal studies to evaluate the performance of IBN's green tea-based protein delivery system.
The study revealed that IBN's green tea nanocomplex loaded with Herceptin reduced tumor growth much more effectively
Using the new nanocarrier twice as much drug accumulated in the cancer cells indicating an improved tumor targeting ability.
A nanosheet with a heat-sensitive polymer could burn surrounding tumors to destroy them functioning as a kind of super-specific chemotherapy.
#'Stealth'nanoparticles could improve cancer vaccines Cancer vaccines have emerged recently as a promising approach for killing tumor cells before they spread.
Now scientists have developed a new way to deliver vaccines that successfully stifled tumor growth when tested in laboratory mice.
Hiroshi Shiku Naozumi Harada and colleagues explain that most cancer vaccine candidates are designed to flag down immune cells called macrophages and dendritic cells that signal killer T cells to attack tumors.
When molecules for signaling killer T cells were put inside the nanoparticles they hindered tumor growth far better than existing vaccines.
The nanogel-based vaccine significantly inhibited in vivo tumor growth in the prophylactic and therapeutic settings compared to another vaccine formulation using a conventional delivery system incomplete Freund's adjuvant.
In a newly published article in the journal ACS Advanced Materials & Interfaces, researchers Ravi Saraf and Chieu Van Nguyen describe a thin-film sensor that can detect tumors too small and deep
the researchers ued the film to successfully detect tumors as small as 5 millimeters, hidden up to 20 millimeters deep.
when tumors are diagnosed at less than 10 millimeters. Saraf said the thin-film tool would have at least three advantages to a manual breast exam performed by a physician:
or none get left behind to form new tumors. The method reported in the journal ACS Nano could someday vastly improve the outlook for patients.
and go specifically to tumor cells and not to normal brain cells. Using a handheld Raman scanner in a mouse model that mimics human GBM the researchers successfully identified
Here we evaluated the ability of a hand-held Raman scanner guided by surface-enhanced Raman scattering (SERS) nanoparticles to identify the microscopic tumor extent in a genetically engineered RCAS/tv-a glioblastoma mouse model.
and correlation with histology showed that SERS nanoparticles accurately outlined the extent of the tumors.
So, they can be used to enhance contrast of optical imaging of tumors along with that of MRI I
when the tumor is composed already of millions of cancer cells and the disease is starting to advance into a more mature phase.
In 2010 they successfully obtained funding for the project called SPEDOC (Surface Plasmon Early Detection of Circulating Heat shock proteins and Tumor Cells) under the 7th Framework Program (FP7) of the European commission.
Tumors appeared accelerate the tissue aging process by 36 years and healthy breast tissue near breast tumors were an average of 12 years older than tissue elsewhere in the body.
In contrast transforming adult human cells into#pluripotent stem cells which reprograms them to act like embryonic stem cells effectively resets the cells'clock to zero Horvath says.#
The early detection of circulating tumor cells, or CTCS, in the bloodstream can speed up diagnosis and lifesaving treatment.
Now, a precise mechanism by which chronic inflammation can lead to cancer has been uncovered by researchers at MIT a development that could lead to improved targets for preventing future tumors.
DNA sequencing of a developing gastrointestinal tumor revealed two types of mutation: cytosine (C) bases changing to thymine (T) bases,
or patterns of DNA mutations, associated with cancerous tumors. e believe that in the context of inflammation-induced damage of DNA,
including tumor metastasis and drug/toxin sensitivity.""This is important as pharmaceutical companies and regulatory agencies look for new,
an"oncoprotein"that binds to RNA and promotes tumor growth. The findings, which could lead to a new class of cancer drugs,
thus blocking Hur function as a tumor-promoting protein, "said Liang Xu, associate professor of molecular biosciences and corresponding author of the paper.
Now, a precise mechanism by which chronic inflammation can lead to cancer has been uncovered by researchers at MIT a development that could lead to improved targets for preventing future tumors.
DNA sequencing of a developing gastrointestinal tumor revealed two types of mutation: cytosine (C) bases changing to thymine (T) bases,
or patterns of DNA mutations, associated with cancerous tumors. e believe that in the context of inflammation-induced damage of DNA,
and a tumor,"said Ali Salanti from University of Copenhagen.""The placenta is an organ,
In a manner of speaking, tumors do much the same, they grow aggressively in a relatively foreign environment."
because the protein appears to only attach itself to a carbohydrate that is only found in the placenta and in cancer tumors in humans."
remove a tumor from a 60-year-old woman kidney and to help repair a 28-year-old woman atlantoaxial dislocation condition.
and feels just like their patient kidney tumor. This technology has the potential to reinvent the way we teach
First, Anatomics produced a 3d reconstruction of the patient chest wall and tumor with high-resolution CT SCANS, with
the presence of an unseen tumor or show whether an infection has developed around a surgical implant."
"Dr. Mindy George-Weinstein, Professor of Biomedical sciences at the Cooper Medical school of Rowan University, stated,"Myo/Nog cells have also been found in a variety of tumors,
where we predict they contribute to tumor growth. This targeted 3dna immunodepletion strategy may be useful as an adjuvant therapy to reduce tumor expansion and recurrence."
"Dr. Robert Getts, Chief Science Officer of Genisphere, said, "Since the antibody has broad utility
#Packaging Cancer drug into Nanoparticles Double Tumor Destroying Efficacy Researchers have packaged a widely used cancer drug into nanoparticles,
more than doubling its effectiveness at destroying tumors. The drug paclitaxel has been used for decades to fight breast, ovarian, lung and other cancers.
reducing its accumulation in tumors. Many molecular packaging systems have been developed to deliver the drug while counteracting these effects, with a protein-bound version of the drug called Abraxane currently the leading therapy.
the Duke team doubled tumor exposure to the drug compared to Abraxane while simultaneously reducing its effects on healthy tissue.
This kept mice with tumors alive significantly longer and, in some cases, completely eradicated the tumors.
and accumulate in tumors where they take advantage of a tumor's acidic environment.""The chemical bonds holding the polypeptide cage together are stable in blood,
but dissolve in a tumor's lower ph levels,"said Jayanta Bhattacharyya, senior researcher in Chilkoti's lab and first author on the paper."
"This delivers the drug directly to the tumor and helps prevent it from randomly absorbing into healthy tissue, reducing side effects."
A second group of mice had human prostate tumors growing under their skin. Similarly, while they did not survive past 60 days
the Duke technology showed a higher concentration of paclitaxel in the tumors with more staying power than Abraxane,
#Translational Grant for Interaction Study of Laser radiation with Circulating Tumor Cells and Melanin Nanoparticles University of Arkansas for Medical sciences (UAMS) researcher Vladimir Zharov, Ph d.,D. Sc.
Zharov has pioneered the development of identifying tumor cellscirculation in the blood stream of melanoma patients by looking directly through the patient veins using a technology called photoacoustic flow cytometry.
and superficial veins and can heat the natural melanin nanoparticles in melanoma circulating tumor cells (CTCS).
This can improve the detection of CTCS by 1000-fold. he goal of this translational research grant is for patients to benefit from the knowledge obtained during our study of the interaction of laser radiation with circulating tumor cells and nanoparticles
The researchers also discovered that many standard medical procedures especially vigorous manipulation of the tumor, certain types of biopsies and surgery can trigger the release of cancer cells from a primary tumor into circulation, increasing CTC counts.
So while some treatments can provide temporary positive effects, in the long term CTCS released during a medical procedure may cause the cancer to metastasize.
A metastatic tumor or hypothetically even a single tumor cell, while undetectable with existing diagnostic techniques, can release specific markers in blood that can be detected with this technique. his is a completely new concept of early cancer diagnosis,
For example, chemotherapeutic agents used in the treatment of cancer are linked often chemically to antibodies that recognize antigens found only on the surface of the target tumor.
One obvious and highly promising application is in the production of so-called antibody-drug conjugates (ADCS) for use in tumor therapy.
As mentioned above, ADCS enable cytotoxic agents to be transported directly to the tumor tissue thus minimizing deleterious side-effects."
In a 2011 study, researchers in his group discovered that breast cancer cells can break free from tumors
in a 2012 study, they found that macrophages a type of white blood cells were key in helping tumor cells break through blood vessels.
In the body, cells break loose from a tumor and migrate through tissue into the blood system,
Then they can escape from inside the vessel to form another tumor. AIM Biotech microfluidics device produces a similar microenvironment:
Tumor cells can be introduced, flowing naturally or getting stuck in the vessels. Kamm said this environment could be useful in testing cancer drugs,
as well as anti-angiogenesis compounds that prevent the development of blood vessels, effectively killing tumors by cutting off their blood supply.
MIT researchers used Kamm's microfluidics technology to screen several drugs that aim to prevent tumors from breaking up
To test the nanoclew CRISPR-Cas delivery system, the researchers treated cancer cell cultures and tumors in mice.
the researchers produced a human kinase that is involved in tumor cell proliferation and showed that it was functional and active.
however, drugs could be encapsulated in protein cages that accumulate inside of a tumor and dissolve once heated.
hormone-positive, meaning the tumor's growth is fueled by estrogen or progesterone; and not the type that the drug Herceptin targets.
not only attack the main tumor site, but are more likely to find and attach themselves to tumor cells circulating in the bloodstream essentially attacking new tumors before they start,
said Quanyin Hu, lead author of the paper and a Ph d. student in the joint biomedical engineering program.
Studies on mice found that using the combination drug delivery system in the form of a pseudo-platelet was significantly more effective against large tumors
and circulating tumor cells than using the drugs in a nanogel delivery system without the platelet membrane. e like to do additional preclinical testing on this technique,
#Identifying Cancer's Food Sensors May Help Halt Tumor Growth Oxford university researchers have identified a protein used by tumors to help them detect food supplies.
This was used then to study anonymous tumor samples taken from patients with colorectal cancer, a common form of the disease.
Those who had higher levels of PAT4 in their tumors did less well than those with lower levels-being more likely to relapse and die.
cancerous tumors grew more slowly. Dr. Goberdhan said:''These findings support each other. Not only do higher levels of PAT4 mean a worse outcome,
After 15 days of monitoring tumor size, three out of 10 mice that wore the radioactive bandage had their tumors completely eliminated.
The seven other mice in that group had significantly smaller tumor volumes, compared to control groups,
which can require large and specialized equipment. hese bandages can be tailored individually for easy application on tumor lesions of all shapes and sizes,
s Alectinib Shrank Tumors in Nearly Half of Patients With Specific Lung cancer Mutation Genentech Investigational Medicine Alectinib Shrank Tumors in Nearly Half of People With Specific Type of Lung cancer--Alectinib showed response rates of up to
its oral investigational anaplastic lymphoma kinase (ALK) inhibitor, shrank tumors (overall response rate; ORR: 50.0 percent and 47.8 percent, respectively) in people with advanced ALK-positive non-small cell lung cancer (NSCLC) whose disease had progressed following treatment with crizotinib.
In addition, alectinib was shown to shrink tumors in people whose cancer had spread to the central nervous system (CNS)( CNS ORR:
People whose tumors shrank in response to alectinib continued to respond for a median of 11.2 and 7. 5 months, respectively (duration of response;
and these studies suggest that alectinib can shrink tumors in people with this difficult-to-treat disease,
whose tumors were characterized as ALK-positive by an investigational companion immunohistochemistry (IHC) test being developed by Roche.
An investigator assessment also showed tumors shrank in 47.8 percent of people who received alectinib.
CNS tumors shrank in response to alectinib in 57.1 percent of people whose disease had spread to the brain or other parts of the CNS.
In addition, the people whose tumors shrank in response to alectinib continued to respond for a median of 11.2 months (DOR
An investigator assessment showed tumors shrank in 46.0 percent of people who received alectinib. CNS tumors shrank in response to alectinib in 68.8 percent of people
whose disease had spread to the brain or other parts of the CNS. In addition the people whose tumors shrank in response to alectinib continued to respond for a median of 7. 5 months (DOR, immature data.
The immature median PFS was 6. 3 months (95 percent confidence interval CI 5. 5ot estimable.
whose tumors are identified as ALK-positive. ALK-positive NSCLC is often found in younger people who have a light
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