including cancer. The human body has a nifty way of turning its proteins on and off to alter their function and activity in cells:
Trouble in the phosphorylation process can be a hallmark of disease, such as cancer, inflammation and Alzheimer disease.
the researchers produced a human kinase that is involved in tumor cell proliferation and showed that it was functional and active.
impacting normal growth as well as cancer and disease. Dysregulation of histone methylation patterns is observed in a variety of human cancers, inflammation,
and neurodegenerative diseases, validating histone methyltransferases (HMTS) as an important class of drug targets among biomedical researchers.
#New Leukemia Gene Stops Blood cells rowing Upuniversity of Manchester scientists have identified a gene FOXC1 that,
if switched on, causes more aggressive cancer in a fifth of acute myeloid leukemia (AML) patients, according to a Cancer Research UK study published in the journal Cancer cell.
The FOXC1 gene is switched normally on during embryonic development and is needed to turn cells into specialised tissues,
But this new research found that in certain patients with AML a type of blood cancer that affects white blood cells
This triggers the cancer to be more aggressive, as young cells are able to replicate more than mature cells causing cancer cells to grow faster
Of these, around 20 percent would have had the FOXC1 gene wrongly switched on in their cancer.
Dr. Tim Somervaille, lead author from the Cancer Research UK Manchester Institute at The University of Manchester,
which makes the cancer grow more rapidly. here are certain situations where this gene is necessary,
Nell Barrie, senior science communication manager at Cancer Research UK said: t essential that we continue to research basic biology to further understand how cells become cancerous.
The better we understand the nuts and bolts of each cancer, the sooner we can find new ways to stop it.
This study was funded by Cancer Research UK with additional funding from the charity Bloodwise which recently changed its name from Leukaemia & Lymphoma Research a
Researchers from Dana-Farber/Boston Children Cancer and Blood disorders Center have found that changes to a small stretch of DNA may circumvent the genetic defect behind sickle cell disease.
a leader of Dana-Farber/Boston Children who serves as chairman of pediatric oncology at the Dana-Farber Cancer Institute
Lead author Nicolas Bertrand, a former professor at MIT Koch Institute for Integrative Cancer Research, told Laboutlook that he
stopped brain cancer in rats by delivering gene therapy through nanoparticles. 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.
As in cystic fibrosis, a current delivery method of gene therapy relies on using a virus, which can pose significant safety risks.
however, drugs could be encapsulated in protein cages that accumulate inside of a tumor and dissolve once heated.
a common brain cancer whose ability to grow, migrate and hack into the brain blood supply appears to rely on a pattern of gene activity similar to that now identified in these neural stem cells. he cerebral cortex is so different in humans than in mice,
and the Damon Runyon Cancer Research Foundation e
#Gene Test Finds Which Breast cancer Patients Can Skip Chemo Many women with early-stage breast cancer can skip chemotherapy without hurting their odds of beating the disease-good news from a major study that shows
whose cancers are so likely to respond to hormone-blocking drugs that adding chemo would do little
In the study, women who skipped chemo based on the test had less than a 1 percent chance of cancer recurring far away
"said the study leader, Dr. Joseph Sparano of Montefiore Medical center in New york. An independent expert, Dr. Clifford Hudis of New york's Memorial Sloan Kettering Cancer Center, agreed."
The study was sponsored by the National Cancer Institute. Results were published online Monday by the New england Journal of Medicine
and discussed at the European Cancer Congress in Vienna. The study involved the most common type of breast cancer-early stage, without spread to lymph nodes;
hormone-positive, meaning the tumor's growth is fueled by estrogen or progesterone; and not the type that the drug Herceptin targets.
and could seed a new cancer later. Doctors know that most of these women don't need chemo
About 94 percent were free of any invasive cancer, including new cancers at other sites or in the opposite breast."
"These patients who had low risk scores by Oncotype did extraordinarily well at five years,
#Pseudo-platelet Drug Delivery System Targets Cancer Researchers are using patients own platelet membranes to coat drugs and use as nanovehicles for anticancer treatments.
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.
A team from Oxford university's Department of Physiology, Anatomy and Genetics led by Dr. Deborah Goberdhan worked with cancer doctor and researcher, Professor Adrian Harris,
and acquire nutrients is critical for a cancer to grow. Dr. Goberdhan's and Prof Harris's groups collaborated to develop an antibody that could be used to highlight PAT4 in human tissue samples.
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,
'The research, funded by Cancer Research UK, the Wellcome Trust and the Biotechnology and Biological sciences Research Council will be published in the science journal Oncogene on 5 october 2015.
It continues and may eventually provide a way of increasing survival from cancer r
#Scientists Grow Old Brain cells from Patientsskin Cells Researchers from the Salk Institute for Biological Studies have found a way to create aged brain cells from patientsskin samples for the first time.
#Radiotherapeutic Bandage Could Treat Skin cancer Research behind a new radiotherapeutic bandage that could potentially treat squamous cell carcinoma (SCC) cancer was presented Wednesday, at the American Association of Pharmaceutical Scientists (AAPS) Annual Meeting and Expo in Orlando.
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,
This procedure could eventually also be extended to men who have lost their penises from penile cancer or as a last-resort treatment for severe erectile dysfunction due to medication side effects.
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:
57.1 percent and 68.8 percent, respectively. 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;
DOR). ) Alectinib demonstrated a safety profile consistent with that observed in previous studies. The most common adverse events (Grade 3 or higher occurring in at least 2 percent of people) were an increase in muscle enzymes (increased blood levels of creatine phosphokinase), increased liver enzymes
and these studies suggest that alectinib can shrink tumors in people with this difficult-to-treat disease,
and the NP28761 study will be presented by Dr. Leena Gandhi, assistant professor of medicine, Dana-Farber Cancer Institute, Boston (Abstract#8019, Monday, June 1, 8: 00-11:30 A m. CDT).
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.
About Lung cancer According to the American Cancer Society, it is estimated that more than 221,000 Americans will be diagnosed with lung cancer in 2015,
A team at Barts Cancer Institute, Queen Mary University of London, has shown that the three-protein'signature'can both identify the most common form of pancreatic cancer
-and distinguish between this cancer and the inflammatory condition chronic pancreatitis, which can be hard to tell apart.
03 august in the journal Clinical Cancer Research, was funded by the UK charity, the Pancreatic cancer Research Fund.
while patients suffering from chronic pancreatitis had significantly lower levels than cancer patients. When combined, the three proteins formed a robust panel that can detect patients with stages I-II pancreatic cancer with over 90 per cent accuracy.
when the cancer has already spread. This means they are not eligible for surgery to remove the tumour-currently the only potentially curative treatment.
The five-year survival rate for pancreatic cancer in the UK is the lowest of any common cancer
if the 3-biomarker signature is present during the latency period-the time between the genetic changes that will cause the cancer to develop and the clinical presentation."
"For a cancer with no early stage symptoms, it's a huge challenge to diagnose pancreatic cancer sooner,
"says co-author and Director of Barts Cancer Institute, Professor Nick Lemoine.""With pancreatic cancer, patients are diagnosed usually
when the cancer is already at a terminal stage, but if diagnosed at stage 2,
Early diagnosis is an important part of our overall efforts against this aggressive cancer, alongside developing new treatments to tackle the disease once diagnosis is made.
#Real-time Data For Cancer Therapy, MIT Study Biochemical sensor implanted at initial biopsy could allow doctors to better monitor
and adjust cancer treatments. In the battle against cancer, which kills nearly 8 million people worldwide each year,
doctors have in their arsenal many powerful weapons, including various forms of chemotherapy and radiation.
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.
Now, researchers at MIT Koch Institute for Integrative Cancer Research are closing that information gap by developing a tiny biochemical sensor that can be implanted in cancerous tissue during the initial biopsy.
Making cancer treatments more targeted and precise would boost their efficacy 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,
says Michael Cima, the David H. Koch (1962) Professor in Engineering in the Department of Materials science and engineering and a Koch Institute investigator who oversaw the sensor development. ather than waiting months to see
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,
While the primary application of these sensors would be cancer care, Cima is also eager to collaborate with researchers in other fields, such as environmental science. or example,
and demonstrate for opioid pain relievers can be adapted to produce many plant-derived compounds to fight cancers, infectious diseases and chronic conditions such as high blood pressure and arthritis.
#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
bring researchers closer to creating an implantable intestine as replacement therapy for a range of devastating disorders-including infections, cancer and trauma-that result in loss or death of gut tissue.
Strangely shaped cells often indicate cancer. While this old, simple technique may seem a quaint throwback in the age of high-technology health care tools like genetic sequencing
and Genistein, the compound found in soybean which has been suggested to play a role in prevention of steroid-hormone related cancers, particularly breast cancer.
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."
"Scientists have been growing cells in 3d culture for decades. These models are used to help understand various biological processes such as tissue development and cancer growth,
and Muthuswamy's laboratory has spent the past 15 years growing normal and cancer-derived cells from human breast tissue as 3d organoids.
This new paper provides an innovative new direction for this technology.""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,
"says Muthuswamy, who conducted this research while at the University of Toronto. The research team also demonstrated that these clonally derived organoids could be used to identify patient-specific sensitivities to novel therapeutic agents."
"From a research point of view, this organoid approach now provides us with a'live'biobank of tissue for discovery
"said Pier Paolo Pandolfi, MD, Phd, Director of the BIDMC Cancer Center.""Patients diagnosed with locally advanced
These new pancreatic progenitor organoids and tumor organoids can be used to model pancreatic cancer and for drug screening to identify precision therapy strategies
#Cancer Patient Receives 3d Printed Titanium Ribs & Sternum 3d printing continues to profoundly affect the modern world.
The latest incredible feat involves a 54 year old Spanish man suffering from a chest wall sarcoma a type of cancerous tumour.
#Scientists brew cannabis chemical THC for better drugs for cancer sufferers An active ingredient typically found in cannabis has been engineered genetically in the lab for the first time.
They believe the breakthrough will lead to more effective and easier-to-manufacture cancer and HIV drugs
It's often used to treat nausea associated with HIV or cancer therapies but this new process could offer a less expensive,
It's often used to treat nausea associated with HIV or cancer therapies, but this new process could offer a less expensive,
'Interestingly, some of these markers have also been shown to be good targets for therapy in some cancers.'
Immune cells with the PD1 biomarker have already been identified as a target for drugs to treat stage-four melanoma
or end stage cancer. Researchers are now considering how to manipulate immune cells with the PD1 marker in their HIV research.
and turnover,"said senior author Jamey Marth, Ph d.,professor in SBP's NCI-designated Cancer Center."
"It has been known that circulating glycosidase enzyme levels are altered in diseases such as sepsis, diabetes, cancer and various inflammatory conditions.
and Genistein, the compound found in soybean which has been suggested to play a role in prevention of steroid-hormone related cancers, particularly breast cancer.
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,
#New finding offers clues for blocking cancer gene A new study suggests a potential new way to block one of the most common cancer-causing genes, without causing severe side effects.
The Notch gene plays a role in many types of cancer. It's the most common cancer-causing gene in T-cell acute lymphoblastic leukemia.
About 60 percent of children and adults with T-cell leukemia harbor a Notch mutation. But drugs designed to block Notch have caused serious side effects such as severe diarrhea or skin cancers.
Now a team from the University of Michigan Comprehensive Cancer Center offers a potential new target to block Notch without the toxic effects.
Researchers found that a protein called Zmiz1 sticks to Notch triggering the gene to turn on its cancer function.
But Zmiz1 does not impact normal healthy Notch functions.""Notch controls the genes that cause cancer,
but it's also important for normal health. The challenge is to knock out the cancer function of Notch
but preserve its normal function,"says Mark Chiang, M d.,Ph d.,assistant professor of internal medicine at the University of Michigan Medical school."
And Zmiz1 seems to be selective in turning on the cancer functions of Notch, "Chiang adds.
We think this would block the Notch cancer pathway without causing toxic side effects, like we see with current Notch inhibitors,
While the majority of kids with T-cell leukemia are cured, about 20 percent will relapse. Those kids face a grim prognosis.
"We need to develop therapies against Notch to help kids with relapsed cancer and to cure kids with fewer toxicities or long-term effects,
the brushes also could someday deliver cancer therapeutics s
#Researchers want to turn acid-loving microbes into safe drug-carriers Usually the microbe S. islandicus is found in hot and acidic volcanic springs,
Together with Professor Jonas A Nilsson at Sahlgrenska Cancer Center at the University of Gothenburg
#Study charts'genomic biography'of form of leukemia A new study by scientists at Dana-Farber Cancer Institute and the Broad Institute of MIT and Harvard offers a glimpse of the wealth of information
that can be gleaned by combing the genome of a large collection of leukemia tissue samples. By analyzing genetic material in chronic lymphocytic leukemia (CLL) and normal tissue from more than 500 patients,
including two that had never before been linked to human cancer. They began to trace how some of these abnormalities affect the course of the disease and its susceptibility to treatment.
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."
"Our work has enabled us to discover novel cancer genes, begin to chart the evolutionary path of CLL,
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.
whether very-large-scale screening across a diverse collection of cancer cell lines and a large number of drugs could yield new combinations for patients with cancer,
"says Adam Friedman, MD, Phd, of the CBRC and the MGH Cancer Center, who led the study."
"By conducting such a screen, we found one specific combination of agents that are already being used clinically that potentially could be used for a specific group of patients-those with BRAF-mutant cancers."
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.
'In recent years, Héctor Peinado, Head of the Microenvironment and Metastasis Group at the Spanish National Cancer Research Centre (CNIO), David Lyden from Weill Cornell Medical College,
and Jaqueline Bromberg from the Memorial Sloan Kettering Cancer Center, have developed a theory that supports Paget's'seed
and pancreas cancer to the liver--metastasis is reduced in these organs. LAYING THE GROUNDWORK The researchers have discovered also the molecular signals that intercede in the reaction of the recipient tissue
inflammation is associated a process with cancer. These results represent the identification of potential new pharmacological targets,
as well as plasma from cancer patients. The latter served for the preliminary study of the predictive power of the integrins identified, that is,
and pancreas cancer seems to predict the organ where the metastasis will occur, "says Peinado."
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,
and is the leading cause of cancer-related deaths worldwide.""Sometimes there are hundreds of mutations in the genes of a patient's tumors,
but you don't know whether they are drivers of the disease or byproducts,"says senior author Inder Verma, professor of genetics and holder of Salk's Irwin and Joan Jacobs Chair in Exemplary Life science."
"We found a new way by which to identify cancer suppressor genes and understand how they could be targeted for therapies."
"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
when KRAS is mutated.""Mutated KRAS is a common culprit in approximately 10 to 20 percent of all cancers, particularly colon cancer and human lung cancer."
"Since activating Epha2 led to the suppression of both cell signaling and cell proliferation, we believe that the enzyme might serve as a potential drug target in KRAS-dependent lung adenocarcinoma,
"says Narayana Yeddula, a Salk research associate and first author of the paper. A 10-year national project called the Cancer Genome Atlas mapped the genomes of hundreds of patients for over 20 different cancers
and uncovered a number of related genetic mutations, 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."
"Oddly, among human lung cancer patients with Epha2 mutations, around 8 percent of patients actually have high Epha2 expression.
So, in some instances, Epha2 is not suppressing tumors and may be context-dependent. Therefore, we need to carefully evaluate the molecule's function
when designing new therapeutics,"adds Yifeng Xia, a Salk staff researcher involved in the work k
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