This immunotherapy combination shrinks rare, neuroendocrine

According to a new research, there is a significant clinical benefit for patients with high-grade neuroendocrine carcinoma, which is the cancer of the neuroendocrine cells that often form tumours in the lungs and along the digestive tract too.

Even though, this cancer is rare, about 12,000 people in the United States are diagnosed with it, every year. But, do you know that the general prevalence of the disease grew six-fold between 1973 and 2012? Patients with the high-grade, or rapidly growing, form have tend to have only few treatment options.

“We saw a benefit in patients with high-grade carcinoma, which is the population that really needs an effective treatment option,” said a Dr. These early results are really encouraging and intriguing. We found a clear difference in response to treatment between the high-grade and low-grade forms of this cancer type,” said the Dr.”So tumour biology makes a difference. We don`t yet know why, but we`ve opened another treatment arm of the trial to patients with just high-grade neuroendocrine carcinoma to see if we find the same response to the immunotherapy combination,” the Dr. added.

DART features an innovative ‘basket’ design which allows the testing of a single drug or drug combination in a variety of tumour types. DART, currently tests the immunotherapy combination of ipilimumab and nivolumab in patients with 37 types of rare cancers, which together make up almost a quarter of all cancers diagnosed worldwide.

Researchers enrolled 33 patients with neuroendocrine tumours. Of those 33 patients, 19 had high-grade disease. Most patients’ tumours were located in the gastrointestinal tract or the lungs. All patients received doses of ipilimumab every six weeks and doses of nivolumab every two weeks and continue on the treatment for as long as their bodies respond to the drugs. Results showed that 42 per cent of patients with the high-grade form of neuroendocrine carcinomas saw their tumours shrink partially or completely after treatment, while none of the low-grade patients did. For all the patients, 70 per cent saw their cancer spread within six months.

Patients survived a median of at least 11 months after treatment. Some patients are alive more than a year after treatment, and doctors continue to track their progress.”There’s a myth that you can’t successfully complete clinical trials in rare cancers. Researchers think it’s too hard to find patients. But DART shows us that we can run rare cancer trials, and enroll patients quickly and learn if therapies are effective in rare diseases,” he said.”We can also offer investigational drugs to patients’ right in their communities. They don’t necessarily need to travel to a cancer centre to get enrolled in a clinical trial.”

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Cancer treatment: new insight into survival of cancer cells

Researchers have discovered new genetic mutations that may promote the survival of cancer cells, and a clearer understanding of how some cancer cells are able to resist treatment, researchers said. “All cancers are caused by genetic damage, mutations to key genes that control the lives of cells,” said co-author of the study.

“Mutant genes that cancers depend upon for survival are called ‘driver’ mutations.”

For the study, researchers tested genes in 44 cancers that no longer responded to therapy. The tumour types included breast, lung, colorectal, sarcomas, neuroendocrine, gastric and ovarian among others.
The researchers found that these advanced cancers had selected many new possible “driver” mutations never described before, in addition to drivers already known — the cancers had evolved new driver mutations to become resistant.

In some cases, evidence was found that an individual cancer had evolved two or even three drivers in the same gene, a sign that multiple cancer cell clones had evolved in the same tumour that had found different ways of mutating a particularly important gene.

Many of these new genetic mutations are in functional pathways that can be targeted with existing drugs, the researcher said.

“These findings imply that genomic testing should be performed as early as possible to optimise therapy, before cancers evolve new mutations, and that recurrent cancers should be tested again, because their driver mutation may be different from those that existed at diagnosis,” the author noted.
 

THIS IS ONLY FOR INFORMATION, ALWAYS CONSULT YOU PHYSICIAN BEFORE HAVING ANY PARTICULAR FOOD/ MEDICATION/EXERCISE/OTHER REMEDIES.                                                                                                                                                                                                      PS- THOSE INTERESTED IN RECIPES ARE FREE TO VIEW MY BLOG-                                                                                           https://gseasyrecipes.blogspot.com/   

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Hypersensitivity to pain produced by early life stress gets worse by later stress exposure

Early-life stress such as childhood neglect and abuse is suspected to contribute to the development of chronic pain in adulthood, a new study has suggested.

Researchers  used an animal model of maternal neglect that stresses rat mothers by restricting nesting/bedding material.

These stressed rat mothers do not provide consistent levels of nurturing to their pups, i.e., the mothers are present but their care is unpredictable, resulting in increased levels of stress in the pups. The pups were otherwise not harmed or stressed.

Pups that had experienced this early-life stress showed increased reactivity to painful stimuli, particularly if they were exposed to a mild stress, an unpredictable unpleasant noise, as adults.

This enhanced muscle pain was related to both catecholamines, natural compounds in the body involved in the “fight-or-flight” response, and cytokines, molecules involved in the body’s inflammatory response system.

Interestingly, interventions that blocked the actions of the catecholamines and cytokines reduced the sensitivity to pain in the stressed pups.

Dr. said that while it has been recognized for some time that early life events can shift homeostatic balance, predisposing adults to the development of chronic pain, that this could be mediated by a peripheral mechanism, involving the interaction between immune and neuroendocrine stress axes suggests novel approaches to detecting individuals at risk as well as to treatment of chronic pain.

This study suggests a ‘two hit model’ for the risk for pain syndromes: an initial stressor that predisposes to increased reactivity to later stress. The authors implicate both stress response and inflammation systems in the body in the link between stress and pain, potentially pointing to new treatment mechanisms.

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