The boy named Minghao had developed a malignant tumor on his spinal cord and some of his bones needed to be removed.
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.
or promoted by inflammation These include mesothelioma, a type of lung cancer caused by inflammation following chronic exposure to asbestos,
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.
These include mesothelioma, a type of lung cancer caused by inflammation following chronic exposure to asbestos,
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
an international collaboration has aided a 54-year-old patient diagnosed with a chest wall sarcoma.
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.
which is an integration of early diagnosis and treatment of melanoma. Zharov is director of the Arkansas Nanomedicine Center at the UAMS Winthrop P. Rockefeller Cancer Institute and a professor in the UAMS College of Medicine Department of Otolarynology-Head and Neck Surgery.
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
we will focus on the most aggressive form of melanoma, which metastasizes at an early disease stage making treatment extremely difficult,
Because not all melanoma cells highly express melanin especially in early disease stages, the researchers proposed genetic,
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.
Zharov said. t will help to better distinguish melanoma-associated small changes in photoacoustic signals at early disease stages.
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,
and melanoma could be the first cancer with metastatic spread that could be treatable by well-timed therapy,
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.
The nanoparticles deliver genes for an enzyme that converts a prodrug called ganciclovir into a glioma cell killer.
There is no reliable treatment for glioma which has a 5-year survival rate of 12 percent.
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
It is almost always found in people with a specific type of NSCLC called adenocarcinoma.
Magnetic resonance imaging and other scanning technologies can indicate the size of a tumor, while the most detailed information about how well a treatment is working comes from pathologistsexaminations of tissue taken in biopsies.
Yet these methods offer only snapshots of tumor response and the invasive nature of biopsies makes them a risky procedure that clinicians try to minimize.
while reducing patientsexposure to serious side effects. e wanted to make a device that would give us a chemical signal about what happening in the tumor,
if the tumor is shrinking, you could get an early read to see if youe moving in the right direction.
on-demand data concerning two biomarkers linked to a tumor response to treatment: ph and dissolved oxygen.
you can see the response chemically before you see a tumor actually shrink, Cima says.
and the inflammation will make the tumor appear to be growing, even while the therapy is effective.
since tumors thrive in low-oxygen (hypoxic) conditions. t turns out that the more hypoxic the tumor is,
could let you see how hypoxia was changing in the tumor, so you could adjust the radiation accordingly.
so we can use them to monitor tumor response, Cima says. e did a little bit of that in these experiments,
#Minimally Invasive Robotic Surgical Tool Feels For Tumors, Study Tumors often look identical to healthy nearby tissue,
but they tend to feel different. Surgeons often use their fingers to feel the size and shape of
The development of a new method to grow three-dimensional organoid cultures of pancreatic tumors directly from patients'surgical tissue offers a promising opportunity for testing targeted therapies
'mini tumors'in a culture dish,"explains the study's corresponding author Senthil Muthuswamy, Phd, Director of the Cell biology Program in the Cancer Research Institute at Beth Israel Deaconess Medical center
or traits that are seen in the patient tumor from which they came and, therefore, can serve as an innovative platform for both cancer research and for cancer treatment."
"We have developed now a new methodology to grow human pancreatic tumor cells from surgical tissues
and have demonstrated that these tumor organoids recreate both morphology and biology of the cancer tissue in the patient,
These new pancreatic progenitor organoids and tumor organoids can be used to model pancreatic cancer and for drug screening to identify precision therapy strategies
The latest incredible feat involves a 54 year old Spanish man suffering from a chest wall sarcoma a type of cancerous tumour.
Immune cells with the PD1 biomarker have already been identified as a target for drugs to treat stage-four melanoma
and works on the synthesis of substances that can inhibit tumor cell growth. The US research group under Professor Anthony J. Arduengo III is interested particularly in developing industrially applicable methods for using materials derived from wood biomass for the sustainable manufacture of a broad array of basic chemicals such as, for example,
as its ever-churning genome spawns new groups and subgroups of tumor cells in a single patient.
This type of information is critical as the treatment of CLL is geared increasingly to the unique genetic features of each patient's tumor.
however, were limited by the relatively small number of tumor tissue samples analyzed, and by the fact that those samples were taken at different stages of the treatment process,
"The growing sample size allows us to start engaging deeply with the complex interplay between different mutations found in any individual tumor,
"Wu and her team collected tumor and normal tissue samples from 538 patients with CLL, 278 of
and analyze large cohorts of tumor tissue samples with defined clinical status, "remarked Gad Getz, Phd, of the Broad Institute and Massachusetts General Hospital, co-senior author of the paper."
These discoveries will form the basis for precision medicine of CLL and other tumor types
BRAF-mutant melanoma A team of Massachusetts General Hospital (MGH) investigators has discovered a new combination of drugs that may be effective against one of the deadliest cancers, malignant melanoma.
even with the increasing number of drugs targeting specific molecular abnormalities that drive tumor growth,
often because their tumors have become resistant, and some tumors never respond to the targeted drugs.
While combining anticancer drugs appears a promising strategy, the sheer volume of drugs currently in use or in development-more than 500,
This study utilized 36 well-characterized melanoma cell lines assembled by the MGH Center for Molecular Therapeutics to test all possible combinations of more than 100 oncology drugs,
looking for effects on the number and viability of tumor cells. While several combinations showed synergistic effects-with some drugs sensitizing the cells against several other drugs-most combinations increased the response of only one or two cell lines
implying that the vulnerability of an individual patient's tumor to these combinations depends on its unique genetic signature.
and found significant synergistic effects against both tumor models.""We need to confirm this synergistic activity of vemurafenib
and cediranib across a broader range of melanoma models, investigate why the particular combination is effective,
and find biomarkers that predict which patients with BRAF-mutant melanoma should receive this combination,
and identify patients whose tumors might respond.""He adds, "This study was actually a pilot project for a much larger effort within the Center for Molecular Therapeutics to map responses against drug combinations across hundreds of cancer cell lines, not just melanoma,
and look for novel combinations that will benefit subsets of patients regardless of the particular type of tumor they have.
Since our collection of cell lines is annotated completely genetically -which means that mutations and expression changes in each line's genes have been documented-we should be able to identify in advance patients who will benefit from specific combinations.
and quickly develop tumors. The new work, published the week of November 2, 2015 in PNAS, suggests that Epha2 could be a new target for a subset of lung cancer,
"Sometimes there are hundreds of mutations in the genes of a patient's tumors, but you don't know
"Two gene mutations in particular are known to spur the growth of human tumors: KRAS and p53. Though both genes have been studied heavily,
and efficiently test the effect of these thousands of genes on tumor development. In animal models, the Salk team found that 16 of these cell-signaling genes produced molecules that had a significant effect on KRAS-and p53-related tumors.
Of these 16 molecules one especially stood out: the Epha2 enzyme, originally discovered in the lab of another Salk scientist, Tony Hunter.
but the team discovered that its absence let KRAS-associated tumors grow much more aggressively."
"With a mutation in KRAS, a tumor forms in 300 days. But without Epha2, the KRAS mutation leads to tumors in half the time, 120 to 150 days,"says Verma,
who is also an American Cancer Society Professor of Molecular biology.""This molecule Epha2 is having a huge effect on restraining cancer growth
we believe that the enzyme might serve as a potential drug target in KRAS-dependent lung adenocarcinoma,
though the role of these mutations has not been understood well in lung cancer (especially adenocarcinoma, which makes up almost a quarter of all lung cancers).
From the Cancer Genome Atlas data, the Salk team found that genetic alterations of Epha2 were detected in 54 out of 230 patients with adenocarcinoma.
The team also found, surprisingly, that the loss of Epha2 activated a pathway commonly associated with cancer (dubbed Hedgehog) that promotes tumor growth."
So, in some instances, Epha2 is not suppressing tumors and may be context-dependent. Therefore, we need to carefully evaluate the molecule's function
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, Norway."
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'dyes'or'tags.'
#A newly discovered tumor suppressor gene affects melanoma survival Of the hundreds of genes that can be mutated in a single case of melanoma,
a Weizmann Institute of Science team has revealed now one of the drivers of a particularly deadly subset of melanomas-one that is still seeing a rise in new cases.
This gene is identified a newly member of a group of genes called tumor suppressor genes.
It is mutated in some 5. 4%of melanomas. Furthermore its expression was found to be lost in over 30%of human melanomas;
and this loss, according to the finding, was associated with reduced patient survival. This discovery might open new doors to understanding how this cancer grows and spreads,
Yardena Samuels and her team in the Institute's Molecular Cell biology Department were specifically searching for tumor suppressor genes in their database,
which consists of more than 500 melanoma genomes and exomes-protein-building sequences-making it the largest melanoma dataset to date.
As their name suggests, tumor suppressor genes normally inhibit cell growth, including that of cancer cells.
However, when mutated, they act like defective brakes on cellular proliferation. Thus studying these genes is crucial in cancer biology."
"The identification of targetable alterations in melanoma is need an urgent. An in depth understanding of the functional effects of mutations in these genes is the first step toward revealing the underlying mechanism of melanoma growth,
"says Dr. Nouar Qutob, a postdoctoral fellow in Samuels'lab who participated in this research. Indeed, the melanoma genome sequences contained mutations in known tumor suppressor genes,
but there was also a new gene that stood out in the team's search, named RASA2.
and the most recurrent mutated versions to see their effects on melanoma cells. They found that RASA2 regulates a key protein in the cell, called RAS.
When they restored the production of the protein in melanoma cells that harbored RASA2 mutations,
Patients with dysfunctional RAS pathways tend to have a worse prognosis than those with other types of melanoma,
to find out what proteins it communicates with in healthy cells and melanoma, as well as in the cells'response to targeted therapy,
"Most targeted cancer therapies nowadays work by inhibiting the products of oncogenes that are overactive in melanoma cells.
However, loss or mutations in tumor suppressor genes like RASA2 also contribute to melanoma development;
#CWRU researcher lands grant to build stealthy brain tumor treatment A Case Western Reserve University researcher has received a 5-year,
The researchers expect the chemotherapy will destroy the majority of tumor cells and the inhibitor will eliminate cancer cells that are resistant
and can cause brain tumors to reoccur. Their goal is to develop a treatment that eradicates the cancer with one safe dose."
"Glioblastoma multiforme is the most common and most malignant tumors of glial cells, which provide structure to the brain.
when tumors are present, preventing drugs from crossing from the blood stream into the diseased tissue.
"Brain tumor cells are often invasive and spread throughout the normal brain, and drugs--if they get in--do nothing because of resistance that develops."
"To reach inside tumors, Karathanasis'lab developed a short chain of magnetic nanoparticles made of iron oxide
and attach to the tumors'vascular walls. When nanochains congregate inside a tumor, the researchers place a wire coil,
called a solenoid, outside near the tumor. Electricity passed through the solenoid creates a weak radiofrequency field.
The field causes the magnetic tails of the chain to vibrate bursting the liposome spheres,
releasing their drug cargo into the brain tumors. In testing with mouse models of aggressive brain tumors, the technology took out far more cancer cells, inhibited tumor growth better and extended life longer than traditional chemotherapy delivery.
The targeted delivery system also used far less drug than used in traditional chemotherapy, saving healthy tissue from toxic exposure.
and to form tumors. Normal neural cells do not. In testing with mouse models of the cancer, models injected with an inducible nitric acid synthase inhibitor had fewer and smaller tumors compared to control models.
In addition to the grant money, the researchers will have access to the National Cancer Institute's Alliance for Nanotechnology in Cancer,
steel braces straighten crooked teeth, steel scalpels remove tumors. Most of the goods we consume are delivered by ships
The researchers have proved the anti-tumor effects of the drug on immunodeficient mice. The new compound and its derivatives enabled the researchers to reduce tumor activity by 50 percent after 41 days of treatment with the drug,
administered twice a week, to mice with induced tumors. They have managed also to successfully describe the mechanisms by which the drug acts on the cancer stem cells (CSCS.
This crucial scientific breakthrough has been made by the UGR research groups"Research and development of Pharmaceutical Drugs, "directed by Professor Joaquín Campos Rosa, and"Advanced Therapies:
Moreover, from a pharmaceutical perspective this anti-tumor drug can be produced successfully in large quantities. The researchers were able to obtain the required amount of the synthesis in just five days.
which maintains the biological activity of its predecessor as an effective anti-tumor drug, but which can also be synthesized
In order to be able to test the new drug on mice and gauge its effectiveness on human tumors,
first of all they had to inject human tumor cells into immunodeficient mice (to ensure they did not reject these cancerous cells).
they discovered that some of the compounds effectively inhibited the growth of the tumor cells and the migration ability of these cells to other healthy tissues,
Althoughcscs are only found in small quantities in tumors, from a clinical perspective the ability to target them directly is of fundamental importance,
given that they are responsible for originally causing the tumor, relapses and resistance to anticancer treatments.
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