Cancer treatment revolution potential with new drug

A revolution in cancer treatment could soon be underway following a breakthrough that may lead to a dramatic improvement in cancer survival rates.

A new study at the University of Warwick, published today in the journal Angewandte Chemie International Edition, has developed a new drug that can manipulate the body's natural signalling and energy systems, allowing the body to attack and shut down cancerous cells.

Called ZL105, the drug is a compound based on the precious metal iridium. The study has found ZL105 could potentially replace currently used anticancer drugs, which become less effective over time, cause a wide-range of side-effects and damage healthy cells as well as cancerous.

Commenting on the breakthrough, University of Warwick researcher and study co-author Dr Isolda Romero-Canelon said "The energy-producing machinery in cancer cells works to the limit as it attempts to keep up with quick proliferation and invasion. This makes cancer cells susceptible to minor changes in the cell 'power-house'. Our drug pushes cancer cells over the limit causing them to slow and shut down, whilst normal cells can cope with its effects."

Preliminary data indicate that the novel drug may be ten times more effective in treating ovarian, colon, melanoma, renal, and some breast cancers, according to data obtained by the US National Cancer Institute. The researchers now aim to expand the study to cancers that are inherently resistant to existing drugs and to those which have developed resistance after a first round of chemotherapy treatments.

Study co-author Professor Peter J. Sadler said "Existing cancer treatments often become less effective after the first course, as cancer cells learn how they are being attacked. The drug we have developed is a catalyst and is active at low doses. It can attack cancer cells in multiple ways at the same time, so the cancer is less able to adapt to the treatment. This means the new drugs could be much more effective than existing treatments."

"Platinum-based drugs are used in nearly 50% of all chemotherapeutic regimens, exert their activity by damaging DNA and cannot select between cancerous and non-cancerous cells, leading to a wide-range of side-effects from renal failure to neurotoxicity, ototoxicity, nausea and vomiting.

"In contrast, the new iridium-based drug is specifically designed not to attack DNA, but to have a novel mechanism of action, meaning that it could not only dramatically slow down and halt cancer growth, but also significantly reduce the side effects suffered by patients" argues Professor Sadler.

This research could also lead to substantial improvements in cancer survival rates. "Current statistics indicate that one in every three people will develop some kind of cancer during their life time, moreover approximately one woman dies of ovarian cancer every two hours in the UK according to Cancer Research UK .It is clear that a new generation of drugs is necessary to save more lives and our research points to a highly effective way of defeating cancerous cells" said Dr Romero-Canelon.

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Twenty-five percent of breast cancer survivors report financial decline due to treatment

Four years after being treated for breast cancer, a quarter of survivors say they are worse off financially, at least partly because of their treatment, according to a new study led by University of Michigan Comprehensive Cancer Center researchers. In addition, 12 percent reported that they still have medical debt from their treatment.

Financial decline varied significantly by race, with Spanish-speaking Latinas most likely to be impacted. Debt was reported more frequently in English-speaking Latinas and Blacks, the study found. Results appear in the Journal of Clinical Oncology.

"As oncologists, we are proud of the advances in our ability to cure an increasing proportion of patients diagnosed with breast cancer. But as treatments improve, we must ensure that we do not leave these patients in financial ruin because of our efforts," says study author Reshma Jagsi, M.D., D.Phil., associate professor of radiation oncology at the University of Michigan Medical School.

The researchers surveyed women in Detroit and Los Angeles who had been diagnosed with early stage breast cancer, based on data obtained from the National Cancer Institute's Surveillance, Epidemiology and End Results population-based registry. Women were surveyed about nine months after diagnosis and again about four years later, with 1,502 women responding to both surveys.

The surveys asked about patients' perceptions of whether they were worse off financially since their diagnosis, and whether that has caused long-term challenges. For example, patients were asked if they had altered their medical care because of financial concerns, by skipping medication or by missing a doctor's appointment or a mammogram. Other questions looked at broader hardships, such as going without health insurance, having utilities turned off or moving out of their home.

Blacks and English-speaking Latinas were more likely than Whites to have experienced one of these issues. Other factors that made a woman more likely to experience these hardships include age under 65, household income under $50,000, part-time work at diagnosis, reduced work hours after diagnosis, lack of substantial prescription drug coverage, breast cancer recurrence, and undergoing chemotherapy.

"These patients are particularly vulnerable to financial distress," Jagsi says. "We need to ensure appropriate communication between patients and their doctors regarding the financial implications of a cancer diagnosis and treatment decisions to help reduce this long-term burden."

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State-of-the-state on genetic-based testing, treatment for breast cancer revealed

Dartmouth researchers at its Norris Cotton Cancer Center have compiled a review of the role that information gathered through genetic testing plays in the diagnosis and treatment of breast cancer. The paper entitled "Personalized Therapy for Breast Cancer" was accepted on March 17, 2014, for publication in Clinical Genetics. The paper discusses targeted therapies, new biomarkers, and the quality of commercially available testing methods.

Genomic testing is changing the way breast cancer is diagnosed and treated. By examining a woman's genes to look for specific mutations or biomarkers, treatment can be personalized to the tumor cell's biology and a woman's genetics.

"A personalized approach increases the precision and success of breast cancer treatment," said Gregory Tsongalis, PhD, director of Molecular Pathology at Norris Cotton Cancer Center and lead author of the paper. "Molecular profiling exposes a tumor's Achilles' heel. We can see what messages the tumor cells are receiving and sending. It is a biological intelligence gathering mission in an attempt to interrupt the disease.

According to Tsongalis large scale genetic testing of breast cancer is not yet part of routine clinical care as it is with lung and colon cancers, even though he and his team run a genetics laboratory for routine cancer care. Genetic testing according to Tsongalis is a powerful weapon in the diagnosis and treatment of breast cancer.

With results from the genetic testing of a tumor cell's biology, clinicians categorize breast cancer in ways that allow them to select the most effective treatments. Based on genetic biomarkers, there are three categories of breast cancer:

1. ER-positive breast cancer needs hormones, such as estrogen to grow. Estrogen fuels cancer cell growth, stops cancer cells from dying, and helps the cells lay down roots to maintain blood supply for tumors. ER-positive cancers are less aggressive and often treated with drugs that are selective estrogen receptor modulators (SERM), such as Tamoxifen, Raloxifene, Toremifene and aromatese inhibitors (AIs) such as Letrozole, Anastrozole and Exemestane. SERM drugs block estrogen from telling cancer cells to divide and grow; they have been shown successful in treating as well as preventing ER positive breast cancer. AIs block intake of estrogen in the system and reduce estrogen levels in serum, tissue, and tumor cells. AIs are commonly used in post-menopausal women.
2. HER2 -positive breast cancer cells contain large amounts of protein that help them grow and multiply. Medications turn off the production of protein to stop tumor growth and kill cancer cells. HER2 treatments include Trastuzumab, Laptinib, Pertuzumab, and Trastuzumab Emtansine.
3. Triple negative (ER-negative/PR-negative/HER2-negative) breast cancer is the most aggressive type and has the poorest clinical outcome. There is no approved personalized therapy for triple negative, but research has identified six subtypes of tumors. This is the first step in identifying biomarkers that can lead to the development of personalized treatments.

"Genomic testing of breast cancer has expanded our understanding of the disease process and has proven more effective than traditional laboratory tests," said Tsongalis. "At NCCC all of our breast cancer patients are tested for abnormal copies of the HER2 gene using specially designed DNA probes. New biomarkers and the reclassification of cancers based on these biomarkers has led to the development of new, effective treatments that can be personalized to an individual breast cancer patient."

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Genomic study identifies subgroups of breast cancer with varying sensitivities to treatment

Jan. 17, 2014 — Research led by the Translational Genomics Group at Vall d'Hebron Institute of Oncology (VHIO) in Barcelona has not only shown that HER2+ breast cancer can be classified into four different subtypes, but also unmasked a subtype showing both a greater response to and increased benefit from chemotherapy and anti-HER2 therapy. Such newly, refined classification of different tumor subtypes will ultimately facilitate more effective treatment tailored to a specific tumor as well as advance targeted therapy against HER2+ breast cancer.

The study led by Aleix Prat, Principal Investigator of VHIO’s Translational Genomics Group, in collaboration with Jose Baselga, Physician-in-Chief of the Memorial Sloan Kettering Cancer Center, New York (USA), has today been published in the journal Clinical Cancer Research. The research centers on the fact that not all HER2+ tumors respond in the same way to anti-HER2 targeted therapy. Although tumors disappear in many patients, others show no response or become resistant to anti-HER2 therapy in combination with chemotherapy. This observation led to this present retrospective study of patients treated in the phase III NOAH clinical trial, with the objective of establishing the genomic differences of both the treatment-sensitive and the treatment-resistant tumors.

Determining the molecular subtype of any breast cancer is fundamental. Until recently, breast cancer had been classified into three groups according to the presence or absence of hormone receptors and the HER2 receptor: hormone-sensitive, HER2+ and triple-negative (when not included in either of these first two groups). Over recent years however, largely thanks to the stunning advancements in genomic technologies, this classification has been finely-tuned and subsequently shown that there are at least four major breast cancer subtypes (Luminal A, Luminal B, HER2-enriched and Basal-Like). Last year, this very group of researchers refined the classification of hormone-sensitive tumors by genomics.

In this study, the group focuses on HER2+ disease. HER2+ breast cancer affects 20% of women with breast cancer and is characterized by the presence of a large number of HER2 receptors and increased proliferative activity of the respective tumor cells -- all of which translates in a highly aggressive tumor and the consequent increased risk of relapse and cancer-related death. The development of HER2-targeted therapies, such as Trastuzumab or Lapatinib, has greatly improved the prospects and treatment options for patients suffering from this particular type of cancer. However, HER2+ breast cancer is still considered as a single subgroup and receives a similar kind of treatment overall, despite the fact that not all HER2+ breast cancer patients respond equally to such therapy.

This new study evaluated the response of the different molecular subtypes upon treatment with anti-HER2 therapy. The study reveals that the four genomic subtypes in breast cancer (Luminal A, Luminal B, HER2-enriched and Basal-like) are also found in HER2+ breast cancer, and they affect treatment response. "Specifically, we have found that HER2+ tumors in the HER2-enriched subtype have a highly activated HER2 signaling pathway, thereby making them especially sensitive to anti-HER2 targeted therapies such as Trastuzumab. Therefore, among the four defined subtypes, HER2-enriched benefits most from specific anti-HER2 therapy" explains Aleix Prat.

Establishing the genomic and clinical particularities between each of the subtypes may firstly drive more individually tailored treatment strategies, leading in turn to more robust treatment for those who stand to benefit from it. Second, more effectively targeted treatments may also be facilitated for those patients who may benefit from this strategy and thus ultimately receive a more personalized, precise therapy, resulting in better and longer survival. The PAMELA study led by Prat through the support of a Susan G. Komen Foundation grant, involving various Spanish sites coordinated by the SOLTI cooperative research group, will aim to address the latter. The PAMELA study's primary objective is to identify those patients with HER2-positive tumors who can be cured with anti-HER2 biological therapies without the need for chemotherapy.

Cancer genomics: research translated to the clinic

"There is no doubt that gene expression in breast cancer provides us with essential biological information to better determine the diagnosis, treatment, relapse risk and possibilities of survival" says Aleix Prat, "From this moment on, treatment strategies should be based on prior molecular characterization of the tumor, and we must therefore make every effort to ensure accuracy. Genomic tests provide such accuracy and are increasingly being used in daily practice. There really is no other option if we are to continue to combat cancer," he concludes.

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Experimental Treatment for Rare Soft-Tissue Cancer Shows Promise in Mice

Study looked at method for blocking key growth protein in malignant nerve sheath tumors

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When experience fewer side effects from breast cancer patients with anti-cancer drugs receive acupuncture treatment

University of Maryland greenebaum cancer new analysis by researchers from the Center for real and fake acupuncture treatment was found to reduce the side effects of the medications commonly used to treat breast cancer. In published early online cancer peer review journal of the American Cancer Society may help to improve clinical cancer patient care. The results also have beneficial effects such as real acupuncture, do raise the question of Sham acupuncture is truly inert.

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Points better than the new model of drug resistance in breast cancer treatment

In model of human breast cancer tumors metastatic carcinoma transplanted in mice, from the Washington University School of medicine Alvin j. Siteman Cancer Center (home) and provides insights into how to attack breast cancer unresponsive to medications used to treat them in the St. Louis and San Antonio Breast Cancer Symposium according to survey released 12/12.

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Researchers find potential new treatment approach for pancreatic cancer

Dec. 20, 2013 — Scientists from The University of Manchester -- part of Manchester Cancer Research Centre believe they have discovered a new way to make chemotherapy treatment more effective for pancreatic cancer patients.

Pancreatic cancer is an aggressive cancer with poor prognosis and limited treatment options and is highly resistant to chemotherapy and radiotherapy.

But researchers believe they have found an effective strategy for selectively killing pancreatic cancer while sparing healthy cells which could make treatment more effective.

Dr Jason Bruce, from the Physiological Systems and Disease Research Group, who led the research, said: "Pancreatic cancer is one of the most aggressive and deadly cancers. Most patients develop symptoms after the tumour has spread to other organs. To make things worse, pancreatic cancer is highly resistant to chemotherapy and radiotherapy. Clearly a radical new approach to treatment is urgently required. We wanted to understand how the switch in energy supply in cancer cells might help them survive."

The research, published in The Journal of Biological Chemistry this month, found pancreatic cancer cells may have their own specialised energy supply that maintains calcium levels and keeps cancer cells alive.

Maintaining a low concentration of calcium within cells is vital to their survival and this is achieved by calcium pumps on the plasma membrane.

This calcium pump, known as PMCA, is fuelled using ATP -- the key energy currency for many cellular processes.

All cells generate energy from nutrients using two major biochemical energy "factories," mitochondria and glycolysis. Mitochondria generate approximately 90% of the cells' energy in normal healthy cells. However, in pancreatic cancer cells there is a shift towards glycolysis as the major energy source. It is thought that the calcium pump may have its own supply of glycolytic ATP, and it is this fuel supply that gives cancer cells a survival advantage over normal cells.

Scientists used cells taken from human tumours and looked at the effect of blocking each of these two energy sources in turn.

Their study, funded by the Biotechnology and Biological Sciences Research Council (BBSRC), National Institute of Health Research (NIHR) Biomedical Research Centre and AstraZeneca, shows that blocking mitochondrial metabolism had no effect. However, when they blocked glycolysis, they saw a reduced supply of ATP which inhibited the calcium pump, resulting in a toxic calcium overload and ultimately cell death.

Dr Bruce added: "It looks like glycolysis is the key process in providing ATP fuel for the calcium pump in pancreatic cancer cells. Although an important strategy for cell survival, it may also be their major weakness.

"Designing drugs to cut off this supply to the calcium pumps might be an effective strategy for selectively killing cancer cells while sparing normal cells within the pancreas."

Maggie Blanks, CEO of the national charity, the Pancreatic Cancer Research Fund said: "These findings will certainly of great interest to the pancreatic cancer research community and we'd be keen to see how this approach progresses. Finding weaknesses that can be exploited in this highly aggressive cancer is paramount, so we want to congratulate the Manchester team for their discovery."

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B cells can provide a potential treatment of RNA has changed a bit.

California College San Diego medical Moores Comprehensive Cancer Center (home) of researchers successfully different kinds of white blood cells, and designed to provide a bit of a non-coding RNA or microRNA (miRNA)-it plays a central role in the immune response of the body – is targeting the T lymphocytes. Achieved in the mouse study published in this week National Science Academy Journal online early Edition are probably used for genetic recombination miRNA therapeutic purposes, the first step of the prominent vaccine and cancer treatment.

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Translate the new findings to enhance treatment of patients with malignant melanoma cancer researchers.

From translational researchers at UCLA's Jonsson Comprehensive Cancer Center (number of days), published results of a study provide insightful journal Cancer found BRAF inhibitor resistance two key areas critical to tumor how two back-to-back: focus and use to learn how to be resistant to melanoma tumor cells inhibitor with cell signal transduction pathway BRAF-mutant, evolve and limited development cell BRAF inhibitor drug resistance is how black keys.

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Cyclin D1 is the dominating microRNAs in breast cancer treatment.

Cells to replicate through the help push, cyclin D1 protein cell cycle is also brokering process mature microRNA (miRNA), Thomas Jefferson University's Kimmel Cancer generation published according to a new study from the Center for natural communication 11/29. Research is protein is strongly involved in human cancer protein coding dominated non-genome also suggests. Different species make up most of the formerly called junk DNA is unlike the genome the human genome coding and non-coding genome.

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Admit intestinal microorganisms based on NIH mouse determines the results of cancer treatment.

National cancer are in the population of microorganisms that live in symbiotic Gut microflora, intestinal as required according to the mouse study by scientists at the Institute (NCI) ideal response to cancer treatment.

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Working towards personalized cancer treatment

Nov. 12, 2013 — Cancerous tumors are different. Large variations in mutation can be found among individual cancerous cells. In addition, cancer cells' reaction to treatment varies: sometimes the treatment works, while at other times it only makes things worse.

"We all have a unique composition of hereditary variants of genes that affects how both our body and the tumor react to cancer treatment," Ola Myklebost tells us. He is Professor of Molecular Biology in the Department of Biosciences at the University of Oslo, and also holds a post at the Institute for Cancer Research at Oslo University Hospital. Professor Myklebost has now received a grant of NOK 75 million from the Research Council of Norway to develop the idea for next generation cancer treatment -- personalized cancer therapy, directed specifically towards the various mutation faults in cancerous tumors. This is a national research project for personalized cancer medicine called the Norwegian cancer genomics consortium

"Today's treatment most often utilizes broad-spectrum chemotherapy against all tumors. Targeted treatment that is specially selected for the individual tumor can be effective against a very specific mechanism."

Myklebost is now in particular investigating the mutations in tumors from patients with extremely rare types of cancer.

"Our dream is to provide more precise treatment. When only a few patients suffer from a disease there is often little commercial interest in developing medicines. We want to expand the use of targeted treatment against several types of cancer. This means that more patients can be treated for high-risk types of cancer for which the current treatment option is inadequate. For example we hope that intestinal cancer medicine can also be used against other forms of cancer, but due to complex regulatory mechanisms in various types of cells we're not sure it will work.," Myklebost says to the research magazine Apollon.

Helping those with soft tissue sarcomas

Examples of types of cancer with poor odds are lung cancer, pancreatic cancer and sarcomas. Sarcomas are soft tissue cancer, a type of cancer that affects at least 200 Norwegians a year -- children more often than adults.

"We hope to find the same mutations in patients with sarcomas as we do in those with other types of cancer for which treatment is available today. Sarcoma patients can then perhaps be given the same treatment."

To find this out, Myklebost's research group will use DNA sequencing on tumors from as many sarcoma patients as possible. They will examine patients from the whole of Norway. So far they have collected DNA samples from both cancerous and healthy tissue from several hundred patients.

"We have to know which gene variants are normal in order to find the mutations that are only relevant for tumors."

Provided that the sequencing machine is in function 24 hours a day, the work of DNA sequencing a thousand samples will take a year.

The researchers will define a thousand genes that may be related to cancer diseases. They will make no progress if they only compare the DNA of healthy and cancerous tissue from one patient: they must analyze the DNA connection between all the patients to find out which mutations can lead to cancer.

Only a fraction of the genome is genes. In the approximately 20,000 genes we all have there is everything from a few to several tens of thousands of mutations in the cancer cells. The question is which mutations are to be treated. During their work the researchers have found large mutation differences among the cells in the same tumor.

"We can point to mutations that are only found in a quarter of the cells. If you select treatment that only hits three-quarters of the cells, the remaining quarter will be able to grow and become resistant. Then the patient will have a relapse," Professor Myklebost tells us, and continues, "If we find mutations for a certain form of treatment, we contact the doctors in charge to give them the information, but we have no funds for structured clinical trials."

All Norwegian cancer patients

In the next phase, Myklebost wants the health service to analyze the DNA of the tumors of all the 26,000 Norwegians who are diagnosed with cancer each year.

"This will give us opportunities that are unique on a global basis."

The collection of the DNA samples requires comprehensive logistics at the hospitals. Pathologists send in tumor samples either frozen or paraffin-embedded.

"The best thing would be samples from surgical interventions. The problem is that if the patients has already been treated with chemotherapy then the cells are often dead. And we'll do far more than the pathologists: while they only examine a few genes today, we want to analyze at least a thousand."

Ola Myklebost is now part of a national consortium and is working on spreading the sequencing technology to all the health regions.

Enormous calculations

Gene interpretation demands enormous statistical analyzes on computers that have a huge capacity for calculation. The limitation today is precisely the lack of access to such high-performance computing, as well as the storage of large amounts of data.

Bearing in mind that our genome has 20,000 genes and that a cancerous tumor is due to not only one mutation but to the combination of many, the researchers must gather enormous amounts of data to enable them to produce statistical information that is sufficiently accurate. Such analyzes demand massive calculations.

Gene therapy is expensive

Precision treatment is of course more expensive than traditional cancer treatment.

"The advantage is less wasted treatment. If we avoid half of the current wrong treatment, it won't be dearer in total even though precision treatment is twice as expensive. So it's not certain that our method will lead to more expensive treatment. And even if our analyzes were to cost some tens of thousands of Norwegian kroner, it isn't more than MRI scans. And it's far cheaper that unsuccessful treatment," is Professor Myklebost's opinion.

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Common genetic pathway can be a conduit to the Pediatric Oncology treatment

Johns Hopkins and Kimmel Cancer Center investigators provide new target for the treatment of these cancers may, discovered the genetic pathway is known in many difficult to treat pediatric brain tumor called a low-grade glioma. The pathway is called the mammalian target of rapamycin in laboratory studies researchers found (mTOR) Pediatric low-grade glioma tumors are very active and, using an experimental drug may block mTOR activity these decreased growth.

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FDA clears UCB's Cimzia for psoriatic arthritis treatment

BRUSSELS (Reuters) - U.S. regulators have cleared UCB's Cimzia for the treatments of adult patients with active psoriatic arthritis, the Belgian group said on Monday.

Psoriatic arthritis is an inflammatory disease that affects joints and tendons, and usually occurs in combination with psoriasis.

In the United States, Cimzia is already approved for the treatment of moderate to severe rheumatoid arthritis and for reducing the signs and symptoms of Crohn's disease, UCB said.

(Reporting by Robert-Jan Bartunek)

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Targeted radiation therapy safe, effective treatment for elderly with pancreatic cancer

Sep. 24, 2013 — A highly targeted cancer radiation therapy may offer a safe and effective treatment option for elderly pancreatic cancer patients unable to undergo surgery or combined chemotherapy and radiation therapy, according to researchers at Henry Ford Hospital in Detroit.

Called stereotactic body radiotherapy (SBRT), the study finds patients lived, on average, six to seven months longer following treatment with minimal side-effects even when they had other severe comorbidities such as chronic obstructive pulmonary disease (COPD), heart disease and diabetes.

Two of the patients in the study lived nearly two years.

“Elderly individuals, those ages 75 and older, account for approximately 40 percent of patients diagnosed with pancreatic cancer,” says study lead author Raphael Yechieli, M.D., with the Department of Radiation Oncology at Henry Ford Hospital.

“These patients are too ill to receive any other treatment, but with stereotactic body radiotherapy we’re able to deliver a safe and effective treatment in two weeks that can provide them with a substantial quality of life with minimal side effects.”

The study was presented at the 55nd annual American Society for Radiation Oncology (ASTRO) meeting in Atlanta.

In 2013, there will be an estimated 45,220 new cases of pancreatic cancer, and approximately 38,460 will die from the disease, according to the National Cancer Institute. Risk factors for pancreatic cancer include smoking, diabetes, obesity, family history of the disease and pancreatitis. Most people diagnosed with the disease are older than 65.

Surgery is the only known cure for resectable pancreatic cancer, where the cancer is localized to the pancreas and hasn't spread. It is estimated that only 20 percent of pancreatic cancer patients have their tumors present with localized disease amendable to surgical removal.

A select number of those patients, however, are not candidates for surgery due to having other co-morbidities such as COPD, heart disease and diabetes. This leaves only chemotherapy and radiation, or a combination of the two, available for treatment.

But for a large portion of elderly patients with localized pancreatic cancer even chemotherapy and radiation therapy are not options.
The Henry Ford study looked to determine if SBRT – a method of giving radiation that can be highly targeted to the tumor, sparing the normal tissue around it – was a viable option for this group of patients. SBRT provides a higher dose of radiation, meaning patients have fewer treatments. In this case, treatment averaged two weeks.

The study included 20 patients with a median age of 83, all of whom were medically unable to tolerate surgery or combined chemo-radiation therapy. The majority of patients in the study (90 percent) received SBRT treatment at the time of diagnosis.

Seven patients reported side-effects from treatment: nausea, vomiting and fatigue.

Among the patients: 13 had a recurrence of cancer; nine had cancer spread from the original tumor to distant organs or distant lymph nodes.

Median overall survival was 6.7 months, and median recurrence-free survival was 8.1 months. At six months post-treatment, 61 percent of patients were alive; two patients in the study survived nearly two years.

“National trends tell us that very few patients over the age of 75 are getting any treatment at all for pancreatic cancer due to comorbidity risks,” notes Dr. Yechieli. “So we want to push the envelope to give them a treatment option that, while not a cure, is short, effective and safe, and has the potential to give them a good quality of life.”

The next step in this research, Dr. Yechieli says, is to closely follow patients after SBRT and get their direct feedback to measure post-treatment quality of life.

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Proton therapy is cost effective for patients with pediatric brain tumor treatment.

Research affecting mainly children when healthy organs and tissues, spare the Proton line treatment cost effectiveness, external beam radiation therapy were compared with spinal cord and a standard photon radiation therapy, providing accurate tumor dose Proton, announced that the fast-growing brain tumor treatments in the 55 annual general meeting of the American Society of radiation therapy (Astro Boy) by researchers from the Mount Auburn hospital, according to Harvard Medical School (Dana Farber Cancer Institute component) of is a teaching hospital.

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Kids' race may play a role in ER treatment for pain

By Genevra Pittman

NEW YORK (Reuters Health) - Black children who are brought to the emergency room for stomach pain and cramps are less likely than white children to be given painkillers, a new study suggests.

Using records from more than 2,000 ER visits, researchers found that white children and teenagers more often received painkillers available over the counter, such as ibuprofen and acetaminophen (Tylenol), or more powerful opioids, including oxycodone. The difference remained after the severity of children's conditions and various hospital-related factors were taken into account.

Dr. Robert Fortuna, a health services researcher from the University of Rochester Medical Center in New York, said it was "especially concerning" to see that pattern show up among kids.

Fortuna's own work and other studies have found similar racial disparities in painkiller prescribing with adult patients (see Reuters Health story of July 5, 2013 here: http://reut.rs/12r77jH).

"Moving forward, we need to better understand why these disparities exist and work to correct them," he told Reuters Health, noting that blaming the differences on doctors' racial biases would be an "oversimplified response."

"I don't believe the vast majority of physicians knowingly or consciously treat patients differently," he said. But, "The bottom line is that minority children in this study were less likely to receive pain medications, and that's concerning."

Oxycodone and other powerful painkillers have been in the spotlight recently as deaths from overdoses rise and more drugs end up in the hands of people taking them for non-medical purposes.

Dr. Tiffani Johnson from Children's Hospital of Philadelphia and her colleagues said the stressful environment of an ER and lack of an established doctor-patient relationship, combined with the subjective nature of stomach pain, may lead doctors to use mental shortcuts including racial stereotypes when making treatment decisions.

The researchers used data from a national study that surveys hospitals about their ambulatory care and scales up the results to reflect the general U.S. population. Their report included information on 2,298 patients age 21 and under who visited an ER in 2006 to 2009 with stomach pain, cramps or spasms, representing 8.1 million such visits across the country.

Among children in severe pain - defined as a rating of seven or higher on a 10-point scale - 27 percent of white kids were given some type of painkiller, compared to 16 percent of black children and 19 percent of Hispanic children.

Across the board, black children were 39 percent less likely than white children to receive any painkillers and 62 percent less likely to be given a narcotic in particular. Differences between white and Hispanic youth were small enough that they could have been due to chance, according to findings published Monday in Pediatrics.

There were no racial or ethnic disparities in the number of diagnostic tests doctors ordered or in how many children were admitted to the hospital, the researchers found.

However, both black and Hispanic youth were 60 to 70 percent more likely to spend over six hours in the ER, compared to their white counterparts.

For the most part, the researchers could not distinguish between different underlying diagnoses that contributed to stomach pain and may have influenced the results.

Emergency departments are stressful settings, Johnson and her colleagues point out, and research on adults has found that when doctors are under pressure and have little information about a patient, they are "more likely to be influenced by stereotypes and bias."

Parents' preferences regarding medication could be playing a role as well, though the study did not examine that question.

Future research should also look into "system-level factors," including the availability of primary care doctors, specialists, interpreters and pediatric formulations of painkillers in hospitals serving different populations, the authors write.

Johnson's team said their findings can be used to develop and test interventions to target treatment differences. Until then, doctors should be aware of these disparities and "make efforts to address pain control that may be suboptimal among minority children."

Parents know their children best, Fortuna said, and need to be their advocates. He encouraged all parents to have a conversation with the doctor about their child's treatment in the ER.

"Until we can better understand where the system is breaking down, the best way to fight against this bias is to have open and honest communication," he said.

SOURCE: http://bit.ly/cxXOG Pediatrics, online September 23, 2013.

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Washington U researchers have developed a new model of drug resistance in breast cancer treatment tips for better.

May be researchers in medicine, Washington University in St. Louis were transplanted into human breast cancer tumors are a valuable tool in search models of metastatic carcinoma of superior and better treatments are shown.

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New protein knowledge offers hope for better cancer treatment

Sep. 19, 2013 — When the pharmaceutical industry develops new medicines -- for example for cancer treatment -- it is important to have detailed knowledge of the body's molecular response to the medicine.

"With a better knowledge of the many complex processes which are activated in connection with illness and medication, the better the possibility of developing new drugs. We have now moved closer to targeting and treating certain cancers using the so-called PARP inhibitors -- medical inhibitors used in the latest types of cancer treatment. Certain types of tumours rely heavily on PARP proteins in order to self-repair, and PARP inhibitors can be used specifically to kill cancer cells," says Michael Lund Nielsen, Associate Professor at The Novo Nordisk Foundation Center for Protein Research, University of Copenhagen.

The researchers have developed an advanced method for identifying the proteins which are modified with ADP-ribosylation -- a biological modification affecting a cell's ability to repair DNA damage. The research findings have just been published in the scientific journal Molecular Cell.

The forms of cancer causing most deaths among women are lung cancer, breast cancer, colon cancer, pancreatic cancer and ovarian cancer. PARP inhibitors appear to be an effective treatment for hereditary breast and ovarian cancer, but little is known about the treatment details. Our new analysis method can help shed light on precisely how the PARP inhibitor treatment is working because it can offer us more knowledge about the biological function of PARP proteins. In the long term, it will enable us to design better and more precise PARP inhibitors, says Michael Lund Nielsen, Associate Professor at the Novo Nordisk Foundation Center for Protein Research.

DNA repair crucial for cell health

Every day, our DNA is exposed to damage which our healthy cells are capable of repairing and thus keep healthy. But the ability of certain cancer cells to repair their own DNA damage is impaired compared to standard cells and this is exploited using PARP inhibitors which block the repair systems of cancer cells. In principle, PARP inhibitors both damage healthy and cancer cells, but normal cells have different survival mechanisms in comparison to cancer cells. PARP inhibitors therefore appear to offer new and much improved cancer treatment options.

Treatment with PARP inhibitors

PARP treatment is a new and individualised type of cancer treatment. It is a so-called targeted treatment which exploits a weakness inherent in cancer cells. PARP inhibitors have yet to be marketed, but many companies are testing them in clinical (phase 1-3) trials. So far, the PARP inhibitors are only available for experimental purposes.

"Our analysis method makes it possible to map the movement of PARP inhibitors, opening up possibilities for the optimised treatment of breast and ovarian cancers with fewer side effects. It is also being examined whether PARP inhibitors can be used in combination with chemotherapy and/or radiation therapy in connection with other cancers. In particular, radiation therapy produces many unpleasant side effects, but there are indications that optimised treatment could be achieved by combining radiation therapy with PARP inhibitors, as PARP inhibitors make cancer cells more susceptible to radiation therapy," says Michael Lund Nielsen.

Using radiation and chemical compounds, the researchers started by damaging the DNA in cells. They then isolated proteins modified with the ADP-ribosylation and identified them using mass spectrometry, a technique making it possible to determine a protein's identity and the sites where the ADP-ribosylation chemical changes occur.

ADP-ribosylation

ADP-ribosylation is a biological protein modification controlling several key cellular processes, such as the repair of DNA damage. Every day, our DNA suffers damage between one thousand and one million times and it is therefore crucial that the cells can repair their DNA. Certain cancer cells are incapable of self-repair without ADP-ribosylation and this can be exploited for targeted cancer treatment via PARP inhibitors. By inhibiting the PARP proteins that perform ADP-ribosylation, it is thought that these cancer cells are prevented from self-repair and will therefore perish.

PARP and PARP inhibitors

PARP is a group of DNA repair proteins that play an important role in some cancers as certain types of tumours are highly dependent on PARP in order to repair themselves. These tumours are therefore vulnerable to targeted treatment using PARP-inhibiting compounds. PARP inhibitors block the DNA repair system of cancer cells, but few details are known about the molecular aspects surrounding the PARP inhibitors, including which proteins are affected by them. The researchers' new analysis method makes it possible to map the movement of PARP inhibitors, which enables optimised treatment with fewer side effects.

Protein modifications

Proteins are chain-shaped biological macromolecules built up of amino acids. The cells are predominantly controlled by proteins, and many of the characteristics of the protein functions are controlled by, among others, molecular modifications that can be attached to amino acids. Functions that are controlled by protein modifications include: the localisation of proteins at specific locations in the cell, the marking of proteins for degradation and the turning on/off of the biological activity of the protein. Studies of the modifications that proteins contain are therefore important for understanding a wide range of cellular processes.

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