The scientists are now looking for ways they can use the same approach to develop more effective and less toxic cancer treatments in humans.
and suggest future avenues for developing effective cancer treatments. ost of the drugs we use to fight cancer are designed to kill cancerous cells.
and the side effects can be intense. reatment regimes for advanced colorectal cancer involve combination chemotherapies that are toxic and largely ineffective,
. But his team may have now found a new way to fight the cancer type, by reactivating a gene known as adenomatous polyposis coli (Apc) that turned off in 90 percent of human colorectal tumours.
and six months later there were no signs of the cancer coming back. While scientists have looked previously into turning certain genes on or off in animal models in order to fight cancer,
they've struggled to do so without triggering excess gene activity and causing other problems in normal cells.
Even more impressive was the fact that this approach worked on mice with malignant colorectal cancer tumours that contain Kras
"It is currently impractical to directly restore Apc function in patients with colorectal cancer, and past evidence suggests that completely blocking Wnt signaling would likely be severely toxic to normal intestinal cells,
the team believes that the same approach could be tweaked to suit other cancer types.""If we can define which types of mutations
we will be equipped better to identify the most appropriate treatments for individual cancers, said Lukas Dow, one of the researchers.
"That clinical use involves the carbon spheres being coated with polymer-a polymer that can gradually release drugs into the system to fight cancer and other diseases.
for other kinds of cancers and for other diseases,"says Rohit Bhargava.""You can coat it with different polymers to give it a different optical response.
and paranoia, were triggered by a single pathway in the brain that was separate from the pathway that triggers the drug cancer-killing properties.
called GPC1, was only being carried by exosomes in the blood of the cancer patients. According to Schattner at Forbes
because it's one of the cancers we don't have any reliable screening test for one of the researchers,
Derek Raghavan from the Levine Cancer Institute in the US told Linda Carroll at NBC News."It kills people
which means the team still needs to figure out how to properly differentiate between the different types of cancer it can detect in the final analysis.
But one of the team, Raghu Kalluri from the MD Anderson Cancer Centre in the US, told NBC News that he thinks the blood test could be available in as little as a year.
#Novel method to predict postoperative liver cancer recurrence in transplant patients UCLA transplantation researchers have developed a novel method that more accurately calculates the risk of disease recurrence in liver cancer patients who have undergone a liver transplant,
Chair in Surgery and director of the Pfleger Liver Institute and Dumont-UCLA Transplant and Liver Cancer Centers presented the study during the annual meeting of the Southern Surgical Association.
The predictive calculator also known as a nomogram was developed after the research team analyzed data from UCLA's 30 years of experience with liver transplantation for liver cancer.
The retrospective study included 865 liver cancer patients who had transplants between 1984 and 2013 said study first author Dr. Vatche G. Agopian an assistant professor of surgery in the division
which liver cancer patients might be good candidates for transplant and patients with all sizes and numbers of tumors underwent transplantation often times with early recurrence of disease.
and the existing American Joint Committee on Cancer pathologic TNM staging system giving transplant physicians and oncologists more information to work with in deciding how often to monitor for recurrence and whether or not adjuvant treatment
This novel nomogram includes three important groups of information that proved to be very accurate in predicting recurrence in liver cancer patients better than any other system out there Agopian said.
and have a meaningful discussion with transplant recipients regarding their post-transplant risk of cancer recurrence.
or the number and size of tumors on MRI and CT SCANS three pre-transplant blood biomarkers thought to be predictive for cancer recurrence
or aggressiveness of the tumor and whether the cancer has invaded the liver's blood vessels factors that can't be determined before transplant.
while a patient with a larger tumor might have a very low grade cancer and be at lower risk for recurrence.
and get individualized predicted risks of cancer recurrence Agopian said. The Milan criteria presented a major step in improving the outcomes of liver cancer patients undergoing transplant Agopian said.
However there is now a growing consensus and body of evidence that these criteria are too conservative
About 32000 Americans will be diagnosed with liver cancer this year. Of those 23000 will die of their disease.
Liver cancer is the sixth most common cause of cancer worldwide and the third most common cause of cancer-related death.
In the United states the incidence of liver cancer has doubled nearly over the last two decades.
For most patients who are diagnosed with liver cancer it generally is advanced too to treat with surgery.
In the largest single-institution experience with liver transplant for liver cancer excellent long-term survival was achieved.
A novel clinicopathologic prognostic nomogram accurately predicts liver cancer recurrence after liver transplant and may guide frequency of post-transplant surveillance and adjuvant therapy y
Industry reduced early-stage research favoring medical devices bioengineered drugs and late-stage clinical trials particularly for cancer and rare diseases.
Cancer and HIV/AIDS were funded well above the predicted levels based on U s. disability alone with cancer accounting for 16 percent of total NIH funding and 25 percent of all
#Mechanism leading to drug resistance metastasis in melanoma patients discovered Moffitt Cancer Center researchers have discovered a mechanism that leads to resistance to targeted therapy in melanoma patients
and improve outcomes for many cancer patients, when compared to the adverse effects of standard chemotherapeutic drugs.
B-Raf is a protein that is frequently mutated in human cancers leading to increased tumor cell growth, survival and migration.
The study was published in the online edition of Cancer Discovery on Dec 26 2014 0
#Toward quantum chips: Packing single-photon detectors on an optical chip is crucial for quantum-computational circuits Single-photon detectors are notoriously temperamental:
#Researchers uncover key cancer-promoting gene One of the mysteries in cancer biology is how one protein,
TGF-beta, can both stop cancer from forming and encourage its aggressive growth. Now, researchers at the University of Michigan Comprehensive Cancer Center have uncovered a key gene that may explain this paradox
and provide a potential target for treatment. TGF-beta is known as a tumor suppressor, meaning it necessary to keep cells in check
and it becomes a tumor promoter, fostering aggressive growth and spread of cancer. The researchers identified Bub1 as a key gene involved in regulating TGF-beta receptor.
Researchers also have known that Bub1 is expressed highly in many different types of cancer. Because Bub1 is found in many types of cancer
developing a drug to target it could potentially impact multiple cancers. A compound to target Bub1 has been developed
but is not ready for testing in patients. Initial lab testing suggests that a Bub1 inhibitor can very specifically target Bub1 without causing damage to other parts of the cell. hen you look at gene expression in cancer,
Bub1 is in the top five. In addition, Bub1 expression levels correlate with outcome in patients with lung and breast cancer.
#Blood test for prostate cancer investigated Mitchell believes the technique will be transformative in providing improved cancer diagnostics that can both predict treatment outcomes and monitor patient responses to therapy.
In a large retrospective study of blood samples the researchers showed that the method called a liquid biopsy could accurately distinguish prostate cancer from normal controls without prior knowledge of the genetic signature of the tumors and with over three times the sensitivity of current prostate specific-antigen
Based on the reported data and work in progress I believe the'liquid biopsy'will revolutionize cancer diagnostics
The study collected serum from more than 200 patients with prostate cancer and more than 200 controls.
The researchers reported that the technique distinguished prostate cancer from normal controls with 84-percent accuracy and cancer from benign hyperplasia and prostatitis with an accuracy of 91 percent.
Because the method quantifies the inherent chromosomal instability of cancer and can be followed as a function of time without having to do an invasive tissue biopsy it is called a liquid biopsy.
and quantify cancer-specific DNA from normal controls by the identification and chromosomal location of billions of specific DNA fragments present in blood as cell-free DNA.
The prostate cancer study identified 20 hotspots of greatest chromosomal instability as additions or deletions in less than 0. 5 percent of the total DNA present in human chromosomes.
Since the entire genome was surveyed the researchers were able to identify a non-coding region of the genome as a hotspot which may be generating previously unrecognized chromosomal control elements in prostate cancer.
and cell control processes that are highly relevant to cancer. Since cell-free DNA has a relatively short half-life in the circulation sequencing of cell-free DNA soon after therapy may be used to detect minimal residual disease in solid tumors Mitchell said.
Their computational approach could be especially useful for forecasting drug resistance mutations in other diseases such as cancer HIV
which will be available commercially later this year so the Feinstein Institute can start investigating how to engineer other kinds of tissue like bone or 3d print custom-made shields for cancer and radiation treatment.
Developed by the National Cancer Institute and the National Surgical Adjuvant Breast and Bowel Project, BCRAT is currently the most commonly used model for predicting breast cancer risk in women with BBD.
whereas predictions derived from the new model were calibrated appropriately to observed cancers (P. 247).""Since women with benign breast disease are at higher risk for breast cancer,
Ultimately it will help researchers achieve breakthroughs in a wide variety of areas in the life sciences such as neuroscience diabetes and cancer.
#How cancer turns good cells to the dark side A new computational study by researchers at the Rice-based Center for Theoretical Biological Physics shows how cancer cells take advantage of the system by
and Jos Onuchic the researchers decode how cancer uses a cell-cell interaction mechanism known as notch signaling to promote metastasis. This mechanism plays a crucial role in embryonic development
which the researchers mapped the flow of information through genetic circuits involved in cancer metastasis. At the heart of our new understanding is that the primary agents of metastasis are clusters of hybrid epithelial (nonmobile)
These and not the fully mesenchymal cells are the'bad actors'of cancer progression that pose the highest risk.
The multifaceted mechanism by which notch-delta-jagged signaling promotes cancer progression has been a mystery until now Ben-Jacob said
Cancer takes advantage of jagged proteins'influence to form what are essentially migrating units of hybrid cancer stem cells Ben-Jacob said.
Notch-jagged signaling also helps cells develop resistance to chemotherapy and radiotherapy and facilitates metastasis formation by promoting communications between cancer
and stromal (connective tissue) cells at the new locations he said. Recent findings showed stromal cells in the tumor environment secrete jagged ligands.
and prompt them to boost their production of the ligand reinforcing the cancer's chances of survival.
The researchers suggested cells'internal expression of jagged may also increase the production and maintenance of therapy-resistant cancer stem cells.
The finding that MBI substantially increases detection rates of invasive cancers in dense breasts without an unacceptably high increase in false positive findings has important implications for breast cancer screening decisions particularly as 20 states now require mammography facilities
and encourage discussion of supplemental screening options says Dr. Rhodes. These findings suggest that MBI has a more favorable balance of additional invasive cancers detected
Recent studies have reported supplemental cancer detection rates of 1. 9 per 1000 women screened with automated whole breast ultrasound
so our finding of an additional 8. 8 cancers per 1000 women makes MBI a very compelling option for women who elect supplemental screening says Dr. Rhodes. Michael O'connor Ph d. a Mayo Clinic scientist
This opens up new possibilities for future cancer treatments. Patients who visit the doctor because of malignant skin cancer often go too late--the aggressive cancer has formed already numerous metastases in their bodies.
This rapid malignant metastatic formation of melanoma, was previously put down to the high mutation rate that is characteristic of melanoma,
Joining forces with dermatologists and oncologists from the University Hospital in Zurich and backed by the University Research Priority Program"Translational Cancer Research,
In their study, the researcher exploited this central position of EZH2 to combat the cancer:
As a result, the researchers were able to prevent the growth and malignant spread of the cancer in the animal model and human melanoma cells."
Epigenetic factors like EZH2 therefore appear to be highly promising targets for future cancer treatments,
some of the genes are implicated in cancer and mental illness. In October 2014, the NIH invested nearly $32 million in its Big data Initiative,
#New cancer-fighting strategy would harden cells to prevent metastasis Existing cancer therapies are geared toward massacring tumor cells
This is a novel approach to cancer therapy that we believe could fight the disease with less potential for side effects
Since changes in cell shape figure into conditions from cancer to chronic obstructive pulmonary disease to degenerative nerve diseases compounds that affect cells shape could turn out to stall disease progress.
#Scientists invent system to improve effectiveness of cancer surgery With the goal of making it easier for surgeons to detect malignant tissue during surgery
and hopefully reduce the rate of cancer recurrence, scientists have invented a new imaging system that causes tumors to ight upwhen a hand-held laser is directed at them. surgeon goal during cancer surgery is to remove the tumor,
as well as enough surrounding tissue to ensure that malignant cells are not left behind, said Aaron Mohs, Ph d,
Current technology allows cancer surgeons to scan tumors prior to surgery with magnetic resonance imaging and other systems.
#New antibodies for cancer treatment A research team at Aarhus University i Denmark has developed ten new antibodies that can possibly be used in the battle against cancer.
The antibodies we've found prevent a cancer tumour from growing. They appear to work perfectly in the laboratory
A cancer tumour deprived of oxygen and nutrients becomes dormant and is made thereby harmless. If it receives a supply from the bloodstream
They are among the world's leading specialists in developing artificial antibodies for cancer treatment
To date they have identified actually ten that appear to be able to impede the development of cancer.
The demand for therapeutic antibodies for cancer treatment is steadily increasing. In 2013 alone worldwide sales amounted to more than DKK 340 billion.
New method improves single-cell genomics analyses Single-cell RNA-sequencing is a relatively new technology that helps scientists understand how genes are expressed in different types of healthy tissue and in cancers.
The authors also found a possible link to cancer. In mice prone to develop benign skin tumors-papillomas-the activation of Fra-2 reduced skin tumor burden.
therefore cause a variety of diseases such as cancer. However, the molecular functions of lncrnas remain to be elucidated fully.
These results are published in a Molecular Cancer article titled""Long noncoding RNA, CCDC26, controls myeloid leukemia cell growth through regulation of KIT expression.""
including diabetes, heart disease, and cancer. According to Carrie Partch a professor of chemistry and biochemistry at UC Santa cruz and corresponding author of the paper, the connection between clock disruption and cancer is still unclear."
"The clock is disrupted not always in cancer cells, but studies have shown that disrupting circadian rhythms in mice causes tumors to grow faster,
It belongs to a group of proteins known as"cancer/testis antigens, "which are expressed normally in the germ line cells that give rise to sperm and eggs,
Cancer researchers have been interested in these proteins as markers for cancer and as potential targets for therapeutic cancer vaccines."
"For very few of these do we understand the roles they might play in driving cancer,
We could potentially find ways to disrupt it in those cancers in which it is expressed."
"Beyond its role in cancer, Partch is interested also in understanding the normal role of PASD1
and we have ongoing studies to explore its role in cancer and other human health problems
Lung cancer is the leading cause of cancer deaths in both men and women in the United states. However,
According to the American Cancer Society, if NSCLC is caught in its earliest stage, the five-year survival rate is 49 percent.
we can detect the cancer earlier with a less expensive, less invasive and more accurate blood test.
"In this study, Huang and his colleagues focused on cancer testis antigens (CTAS), since they are often found in tumor cells that circulate in the blood.
"said Dario C. Altieri, M d.,President and CEO of The Wistar Institute and director of Wistar's Cancer Center."
carboplatin and oxyplatin, have been used to treat cancer for more than 35 years. While they remain among the most prescribed and most potent chemotherapy drugs,
they become less available to treat the cancer, and can also cause toxicity.''In the past few years, Ho and his colleagues were developing cellular nanotags to help detect organ rejection,
His own lab is also using it to look for antibodies that attack a body's own tissue in certain autoimmune diseases that are associated with cancer.
and its Laura and Isaac Perlmutter Cancer Center are reporting a potentially important discovery in the battle against one of the most devastating forms of leukemia that accounts for as many as one in five children with a particularly aggressive form of the disease
The experiments also left white blood cells cancer free for more than 30 weeks in live mice. Further, the research team found that in mice bred to develop T-ALL
Schwab says T-ALL is"a particularly devastating cancer "because there are not many treatment options.
Co-senior study investigator and cancer biologist Iannis Aifantis, Phd, says the study offers the first evidence that"drugs targeting
"Aifantis, the chair of the Department of Pathology at NYU Langone and a member of its Perlmutter Cancer Center,
It's hoped the discovery will inform the development of better treatments for a range of conditions from inflammatory bowel diseases (IBD) to certain cancers.
However, when these cells choose the wrong function this can result in severe inflammation leading to conditions such as inflammatory bowel diseases and even cancer.
an important process that when abnormal can promote diabetes, cancer, and rare genetic diseases. The researchers determined that an enzyme called Protein kinase c (PKC) can regulate
'said senior author Dr. Richard Wang, assistant professor of dermatology and a member of UT Southwestern's Harold C. Simmons Comprehensive Cancer Center.'
'This process is defective in a variety of diseases including diabetes and cancer.''Scientists have known how glucose is transported across cells,
and cancer,'said Wang, whose lab focus includes non-melanoma skin cancer, in which GLUT1 is expressed highly d
blood cancer can result.''In the long run, we anticipate that the ability to drive immune reaction ex vivo at controllable rates grants us the ability to reproduce immunological events with tunable parameters for better mechanistic understanding of B cell development and generation of B cell tumors,
cancer Plants can undergo the same extreme'chromosome shattering'seen in some human cancers and developmental syndromes,
Although plants don't get cancer it might also allow cancer researchers to use the laboratory plant Arabidopsis as a model to study chromosome behavior in cancer.
Chromothripsis involves slicing chromosomes into apparently random pieces, and reassembling it like a broken vase,
#Scientists find genetic variants key to understanding origins of ovarian cancer New research by an international team including Keck Medicine of USC scientists is bringing the origins of ovarian cancer into sharper focus.
It remains a mystery where these cancers come from, 'said Simon Gayther, Ph d.,professor in preventive medicine, Keck School of medicine of USC, corresponding author of the international genome-wide association study (GWAS).'
This study tells us more about the biology of ovarian cancer from the early development stage than most research has.'
'Ovarian cancer is the fourth leading cause of cancer in American women and seventh most common cancer in women throughout the world (World health organization.
In 2015, more than 14,000 American women will die of ovarian cancer, according to the American Cancer Society.
Most ovarian cancers have low survival rates, typically because of the misunderstanding of symptoms and discovery of the cancer in later, less treatable stages.'
'Although MOCS are a less common type of ovarian cancer with generally good prognosis when diagnosed in early stages,
'said Andrew Berchuck, M d.,director of gynecologic oncology at Duke university Cancer Institute, and senior author of the study.'
644 women diagnosed with MOC and more than 21,000 women without ovarian cancer. The research was conducted as part of the Collaborative Oncological Gene-environment Study (COGS),
launched in 2009 with the goal of determining risks of breast, ovarian and prostate cancer.'
which was made possible by pooling data contributed by investigators from over 40 international studies of ovarian cancer within the Ovarian Cancer Association Consortium,
D.,associate professor and researcher at the Hollings Cancer Center at the Medical University of South carolina,
we could identify genetic variants that were significantly more common in women with MOC compared to those without ovarian cancer.'
'Co-first author Kate Lawrenson, Ph d. of Keck Medicine of USC believes the research will lead the way to the development of risk prediction strategies followed by clinical interventions with the potential to prevent ovarian cancer altogether,
'The five year survival rates for ovarian cancer have not changed much in the past 30 years and is partly from viewing ovarian cancer as a single disease,
'she said.''Our results shed light on differences in genetic risk factors for the different ovarian cancers such as MOCS.
I'm hanging my hopes on prevention. My bet is that prevention approaches will be better than finding a cure for a disease that is often diagnosed late
Researchers at Lawson Health Research Institute have identified a new stem cell population in the colon linked to cancer growth.
Colon cancer is the second leading cause of cancer death in Canada. It is estimated that in 2015 that 25,100 Canadians will be diagnosed with colon cancer representing 13 percent of all new cancer cases.
Dr. Samuel Asfaha, a clinician-scientist at Lawson and an assistant professor of medicine at the Schulich School of medicine & Dentistry, Western University,
however, makes them the most likely cell of origin for cancer. In this study, the researchers sought to identify
According to Asfaha, the identification of the cellular origin of cancer, specifically colorectal cancer, is critical to the understanding of how cancer arises
'These findings are exciting as we have identified an important new target for cancer therapy. It is also proof that more than one stem cell can give rise to
telling us that our cancer therapy needs to target more than one stem cell pool.''Until now, the only stem cell population linked to colon cancer was radiation sensitive,
and was the first enzyme to be targeted for chemotherapy cancer treatment. Drugs were designed to bind strongly to DHFR to prevent it from working,
#Beating advanced cancers: New epigenomic block for advanced cancer Array"If you think of late-stage cancer as a runaway car,
most of our drugs take a shot at a tire here and there, but sometimes they miss
"We believe we have identified a mechanism that seizes the cancer's biological engine and could potentially stop it in its tracks."
which could help providers identify more aggressive cancers or find the best drug for the individual patient to further personalize medical care."
and efforts are ongoing to expand this to tumors beyond kidney cancer, "says Dr. Ho.
Similarly, cancers often subvert a cell's normal epigenomic mechanisms to become more aggressive e
"From our previous research, we learned that cancer stem cells reside in the hypoxic zones to maintain self-renewal property,
like cancer, may also have figured out the advantage of hiding in the hypoxic area.""To test this hypothesis, Dr. Das and his collaborators at Jawarharlal Nehru Univeristy (JNU), New delhi,
and its application to global health issues including TB, HIV and oral cancer, all critical problems in the area where Kavikrishna Laboratory is located d
'Since reduced AIM2 activity in colorectal cancer patients is associated with poor survival, it might be useful to detect the level of AIM2 expression in polyps taken from colonoscopy and use this as one of the biomarkers for prognosis,
'In people who already have colorectal cancer, therapies that boost the expression of AIM2, such as interferons, might reduce tumor progression.
or a group of'good'bacteria to patients with colorectal cancer at the early stage of disease may prolong survival,
Cancer researchers had known that mutations in AIM2 were frequently found in patients with colorectal cancers.
However, AIM2's established function in the cell was not in the machinery of cancer
'This was how we became interested in AIM2 and colorectal cancer.''In their experiments with mice, the scientists used chemicals to trigger the process mimicking the development of colorectal cancer.
They found that the mice showed drastically reduced AIM2 function, confirming the finding in humans with the cancer.
They also found that mice genetically altered to have reduced AIM2 function, when treated with the chemicals,
because we have found a new role for AIM2 in regulating colorectal cancer, and it does so by inhibiting excessive proliferation of stem cells in the large intestine.'
'What this might suggest is that transfer of some of the'good'microbiota from wild-type mice to replace the'bad'microbiota from mice lacking AIM2 offers increased protection against colorectal cancer,
or decelerate the progression of colorectal cancer in humans, especially in those who have mutations in the AIM2 gene,
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