Higher dose, shorter radiotherapy for Prostate Cancer

A new treatment approach for prostate cancer with higher radiotherapy doses over a shorter time works as well as current methods, but with fewer side effects according to a study. Cancer Research UK says the NHS needs to plan for the new approach that will also save it money.
The trial is reported in the journal Lancet Oncology and followed more than 3,200 men who were treated for prostate cancer between 2002 and 2011 at more than 70 UK centers.
The current standard radiotherapy schedule is 37 doses of 2 Gray (a measure of radiation) a day. This was compared with two alternative approaches, 19 doses of 3 Gray per day, and 20 doses of 3 Gray per day.
Five years later, the 20-dose schedule was no less effective than the current system.
The good news for men having prostate cancer treatment was that fewer but higher doses of intensity-modulated radiotherapy meant half the rate of side-effects than older NHS methods.

Clinical trials show success for new Cancer Treatment

Patients with advanced bladder, head and neck cancer, and classical Hodgkin lymphoma were among those whose lives were extended by immunotherapy.
Unlike surgery, radio or chemo, immunotherapy doesn’t directly target cancer cells. Instead, it retrains the immune system, which finds pathogens but doesn’t see cancer cells, to fight them.
Some cancer cells, for instance, multiply aggressively because they produce a signal called PD-L1 which deactivates the immune cells around them. Immunotherapy drugs called checkpoint inhibitors block that signal and free immune cells for the cancer-fighting cause.
In two trials of previously treated metastatic bladder cancer patients, the immunotherapy drugs atezolizumab (brand name Tecentriq), which was FDA approved last month, and nivolumab (brand name Opdivo), shrunk tumours by 30% in at least a fifth of patients.
On nivolumab, 45.6% of bladder cancer patients survived for at least a year, a follow-up study showed, “better than anything we’ve seen in the past”, according to oncologist Padmanee Sharma, who was involved in the trial.
Another checkpoint inhibitor called pembrolizumab (brand name Keytruda) was tested on heavily pre-treated patients with reoccurring or metastatic head and neck cancer.
In this study, 18% of 192 patients responded with either partial or full remission of tumours, and 65% of the responders continued to respond for 30 months. 

Brain Cancer treatment taps into sound waves

Brain cancer patients might benefit from an implantable ultrasound device that appears to enhance chemotherapy treatment. Researchers from the Pitie-Salpetriere Hospital in Paris and other French institutions tested the experimental device on 15 patients with recurrent glioblastoma, a particularly deadly brain cancer. When the so-called SonoCloud was activated, sound waves opened the blood-brain barrier, letting in more chemotherapy. While this blood-brain barrier protects the brain from toxins, "it means a challenge for treating brain diseases and disorders, as 99 percent of potential therapeutic drugs are blocked by it." "This is significant," said Dr. Ekokobe Fonkem, a neuro-oncologist at Baylor Scott and White's Vasicek Cancer Treatment Center, in Temple, Texas. "One of the reasons glioblastoma, which is one of the most aggressive forms of brain cancer, is very difficult to treat is because the blood-brain barrier prevents medications from getting across."

Tumor vaccine latest breakthrough in Cancer treatment

A step towards the revolutionary new cancer treatment has already been taken by researchers who tested it on three patients with melanoma, the deadliest form of skin cancer.
In each case, strong immune responses against the cancer were seen, although the early stage trial was not designed to measure the treatment’s effectiveness.The approach involves taking the genetic instructions for a specific cancer protein, encoded in a molecule of RNA, and using it to stimulate the immune system.
The RNA triggers the kind of immune response normally employed to see off viruses,
only in this case, the targets are cancer cells.
The German research raises the possibility of a vaccine that can be tailored for any kind of cancer, or even new versions of a disease that evolve as it progresses within the same patient.
‘This nano-medicine platform may give a strong boost to the vaccine field, and the results of forthcoming clinical studies will be of great interest.’

Hope for patients with hard-to-treat Breast Cancer

The team from Oxford University and the University of Nottingham found that using a drug called JQ1 can alter how cancer cells respond to hypoxia, or low oxygen, found in more than 50 per cent of breast tumors overall and most commonly in triple negative breast cancer, the form of the disease that is hardest to treat.
JQ1 works by stopping cancer cells adapting to the lack of oxygen. The study results showed that JQ1 slowed tumor growth and limited the number of blood vessels that were produced.
The study explains how the family of drugs to which JQ1 belongs works. Although this group of drugs, called bromodomain and extraterminal inhibitors or BETI, has been used to treat cancer before, this study sheds light on the role these drugs could play in hypoxia, which could prove vital for patients with hard-to-treat breast cancers.

New compound shows potential for triple-negative Breast Cancer

Researchers at the University of Michigan have identified a promising new compound for targeting one of the most aggressive types of breast cancer.

The compound, currently called UM-164, goes after a kinase known to play a role in the growth and spread of triple-negative breast cancer. UM-164 blocks the kinase c-Src and inhibits another pathway, p38, involved in this subtype. The researchers also found that the compound had very few side effects in mice.
"Triple-negative breast cancer is in dire need of new drugs. The treatments that have dramatically improved breast cancer outcomes don't apply to patients with this type of disease," says senior study author Sofia Merajver, M.D., Ph.D., scientific director of the breast oncology program at the University of Michigan Comprehensive Cancer Center.
The U-M team took a different approach. While other c-Src inhibitors merely try to block the kinase, UM-164 binds to it and forces the kinase to turn off. Results of their study are published in Clinical Cancer Research.
"The reason our compound works is that we have a novel mechanism for binding the kinase. It has a response similar to removing the protein entirely from the cell, as opposed to only inhibiting the activity," says senior study author Matthew B. Soellner, Ph.D., assistant professor of medicinal chemistry at the University of Michigan.

Two companies to pay MassHealth $200k for misleading marketing of Cancer drug

Two pharmaceutical companies pay more than $200,000 to the state’s Medicaid program, settling claims they provided misleading marketing to physicians and health care providers about the effectiveness of a lung cancer drug, according to Attorney General Maura Healey’s office.
Genentech and OSI Pharmaceuticals, Inc., which was converted to a Delaware limited liability company, OSI Pharmaceuticals, LLC in 2011, manufactured, distributed, and marketed the drug Tarceva from 2006-2011.
The drug, which treats non-small cell lung cancer, was allegedly marketed and promoted to be effective in treating patients who were current or former smokers, according to the AG’s office. The treatment was not approved by the U.S. Food and Drug Administration, nor was there evidence by the company to support these claims, the AG’s office said.

New drug to fight Aggressive Bladder Cancer

A new drug that harnesses the immune system to attack tumors is highly effective against advanced bladder cancer, according to the results of an international clinical trial. Injections of the experimental agent Atezolizumab were found to shrink tumors by at least 30 percent and stall new tumor growth in 28 of 119 (or 24 percent of) patients. All had received the medication as their initial therapy for the disease. Part of a new class of drugs known as checkpoint inhibitors, atezolizumab, also known by its brand name, Tecentriq, was last month approved by the Food and Drug Administration based on recent research from a related clinical trial presented in 2015. "Our new study results argue that atezolizumab represents a major advance in the treatment of bladder cancer," says lead study investigator and medical oncologist Arjun Balar, MD, an assistant professor at NYU Langone Medical Center.
"Atezolizumab is the first therapy to be approved in more three decades for this disease, and it is the new standard of care for patients whose initial therapy with platinum-based chemotherapy drugs has failed," says Balar. "Indeed, it may be the only therapy some patients need."

Antibody-based therapy shows promise against Stomach Cancer

An experimental therapy based on immune-system antibodies is helping some people with advanced stomach cancer live longer, a new study finds.
The phase 2 clinical trial, involving 161 patients, focused on an antibody called IMAB362.
The median survival of people using the treatment plus standard chemotherapy was more than 13 months, compared with 8.4 months for those who received chemotherapy alone, the researchers reported. One specialist in gastric (stomach) cancer care believes therapeutic advances are sorely needed.
“Metastatic gastric cancer carries a poor prognosis and the treatment effectiveness of current chemotherapeutic agents leave a lot to be desired,” said Dr. David Bernstein, chief of hepatology at Northwell Health in Manhasset, N.Y.
The IMAB362 antibody employed in this new treatment targets a protein on cancer cells called claudin 18.2. German researchers found that study patients who had the highest levels of this protein in tumors prior to receiving the new treatment had an even longer median overall survival, at almost 17 months. IMAB362 is the first antibody to target claudin 18.2, which is also found in a number of other cancers, including pancreatic, lung, esophageal and ovarian tumors. Because of this, the same research team said it plans a phase 2 study of IMAB362 in patients with pancreatic cancers.
According to the researchers, a larger, phase 3 study in stomach cancer patients is scheduled to begin in early 2017.

Promising treatment for invasive Breast Cancer

Various antibodies such as trastuzumab and pertuzumab, which recognize the HER2 receptor, have been used in breast cancer therapy for many years now. However, these antibodies do not kill off the cancer cells. Instead, they render them dormant, and the cancer cells can become active again at any time.
The team led by Andreas Plückthun, Director of the Department of Biochemistry at the University of Zurich, involving postdoc Rastik Tamaskovic and PhD student Martin Schwill, has now found out why these antibodies merely slow tumor growth rather than killing off the cancer cells. The receptor HER2 uses several signaling pathways at the same time to inform the cell that it should grow and divide. But the antibodies available thus far only block one of those signaling pathways, while the others remain active. The most important of these open paths leads through the central hub called RAS. "It is this protein that is responsible for reactivating the growth signal emitted by the HER2 receptor. The antibodies lose effect and the cancer cells continue to proliferate." This is how Andreas Plückthun explains the mechanism, which has been understood in detail for the first time.
The UZH scientists have now discovered an astonishingly effective solution to switch off all signals emanating from HER2 in the cancer cells at the same time. They have designed a protein compound that binds itself simultaneously to two HER2 receptors in a targeted manner and changes their spatial structure. This "receptor bending" prevents any growth signals from being transmitted into the cell interior, and the cancer cells die off. Another advantage is the very selective effect of the substance, which ensures that the cancer cells are killed off efficiently but healthy body cells remain unharmed.

Enzyme with high potential for new Cancer treatment

A team of researchers from the Biology department at the TU Darmstadt has identified an enzyme that separates DNA replication from repair. This discovery could be of tremendous significance in the treatment of tumors. Biologists at the TU Darmstadt under Prof. Dr. Markus Löbrich and Dr. Julian Spies have collaborated with their colleagues at the University of California in Davis and identified a protein kinase called Nek1 that promotes the repair of DNA double-strand breaks and separates this repair from replication. Nek1 switches on the motor protein Rad54 only after the completion of replication in order to finalize the repair process. This is of physiological relevance because during replication, Rad54 possesses additional functions at the replication fork, and premature activation of Rad54 results in a major disturbance of the replication process. This discovery has a very high potential for use in the development of entirely new kinds of cancer treatments. Finding inhibitors that block the function of Nek1 would lead to a loss in the repair function. Tumor cells in particular would suffer from this loss of function in Nek1, since they experience a tremendous amount of DNA damage during their uncontrolled growth. The scientists suspect that the inhibition of Nek1 could be associated with an accumulation of unrepaired DNA damage in these cells that could cause the tumor cells to die. The team of researchers plans to continue to investigate these assumptions over the coming years.

'Trojan horse' Cancer-fighting injection sparks hope in human trials

German researchers presented a “Trojan horse” method of attacking cancer, sneaking virus impersonators into the human body which prompt an immune response that attacks tumors.
Tested in only three people so far, the treatment claims to be the latest advance in immunotherapy, which aims to rouse the body’s own immune system against disease.
Made in the lab, the Trojan horse is composed of nanoparticles containing cancer RNA, a form of genetic coding, enclosed by a fatty acid membrane.
The particles are injected into patients to simulate a viral infection, and infiltrate specialised immune cells. These dendritic cells decode the RNA embedded in the nanoparticles, triggering, in turn, the production of cancer antigens. The new treatment is called an RNA vaccine, it works just like a preventive vaccine by mimicking an infectious agent and training the body to respond to it.
If further trials find the therapy works, they added, the method could help pave the way to a treatment for all cancer types.

One gene, protein suppresses Cancer tumor formation

Pten (short for phosphatase and tensin homolog) is a tumor suppressor that is defective in about 20-25 percent of all patients with cancers. Mayo Clinic researchers now have discovered that Pten safeguards against tumor formation by keeping chromosome numbers intact when a cell splits into two daughter cells. In this study, the last three amino acids of the Pten protein, which are often missing in human cancers, were found to be critical. Pten is the most prominent human tumor suppressor after p53. The current thinking is that Pten's phosphatase activity counteracts PI3 kinase activity. Loss of this function causes tumor formation through uncontrolled stimulation of AKT, an enzyme that stimulates cell proliferation and survival and is often hyperactive in human tumors. "We found that Pten localizes to mitotic spindle poles to recruit the 'motor' protein EG5, which moves the poles apart to form a perfectly symmetrical bipolar spindle that accurately separates duplicated chromosomes," says senior author Jan van Deursen, Ph.D., a molecular biologist and cancer researcher at Mayo Clinic. The research team further found that the recruitment process involves Dlg1, an Eg5-binding protein that docks to the last three Pten amino acids at spindles poles. Importantly, mutant mice lacking these amino acids have abnormal chromosome numbers and form tumors at high frequency. The researchers say these new findings predict that a large proportion of Pten tumors will be hypersensitive to Eg5-inhibiting drugs, providing new opportunities for targeted cancer therapy.

Cancer survivors, a growing population

Cancer survivors in the United States reached record numbers this year, 15.5 million, and the American Cancer Society predicts they'll total more than 20 million in another decade.

But along with these success stories comes a growing demand for medical, emotional and psychological support to aid survivors' long-term recovery, according to a new cancer society report. 

"Many cancer survivors have to cope with long-term physical and psychological effects of their cancer treatment," said lead researcher Kimberly Miller, an American Cancer Society epidemiologist. "It's important for the public health community to have a better understanding of the current and future needs of these survivors."

Although cancer rates are declining for men and stable for women, survival numbers are up because of improved detection and treatment, as well as a growing and aging population, the study authors explained.

According to the report, nearly half of survivors are 70 and older, and 56 percent were diagnosed within the past 10 years. One-third were diagnosed less than five years ago.

"A lot of people go to their primary care physician after completing treatment for information, and that's an area where physicians may need more education and support," Miller said.

Primary doctors can help survivors with cancer screening and encourage good habits, such as quitting smoking, eating a healthy diet and exercising. In addition, they can make referrals to mental health experts if a patient is psychologically distressed. "They just need the tools to manage care efficiently," Miller said.

While most patients fare well emotionally, fears of cancer returning or a new cancer developing are common. Family and friends may find that many cancer survivors have "unmet psychosocial and medical needs," the study authors explained.

Statins could be valuable addition to Breast Cancer treatment

Scientists have raised the possibility of using statins, drugs used for reducing cholesterol, to stop some breast cancer tumors returning.
The most common form of breast cancer uses oestrogen to grow. Drugs such as tamoxifen and aromatase inhibitors cut off the supply of oestrogen, reducing the chances that the cancer will return after surgery. Research has shown that some early breast cancer tumours can produce a molecule made from cholesterol called 25-hydroxycholesterol (25-HC). It can mimic oestrogen and encourage tumors to grow.The scientists grew cancer cells in the lab in the absence of oestrogen and found they produced an alternative fuel, in the form of the cholesterol molecule. They then interfered with production of the molecule and found it slowed the cancer cells’ growth by between 30% and 50%. “This study breaks new ground in uncovering how some breast cancers continue to survive without oestrogen and suggests that women could benefit from adding statins to standard anti-hormone treatments. But this is early research and greater clinical evidence is now needed to understand the potential risks and benefits of this approach.”“This early study raises an interesting question of whether cholesterol-reducing treatment, such as statins, could help lower the chances of breast cancer returning for some women who have developed a resistance to hormone therapy.”

Brain Cancer treatment shows promise in early trial

An experimental viral treatment may extend the lives of patients with a hard-to-treat brain cancer, researchers say.
For the phase 1 study, patients with recurrent glioblastoma, the most common and aggressive brain tumor, were injected with an engineered virus.
Survival was 13.6 months among 43 patients treated with the viral therapy, compared with 7.1 months for patients who did not receive the new therapy, according to the study.
"For the first time, this clinical data shows that this treatment, used in combination with an antifungal drug, kills cancer cells and appears to activate the immune system against them while sparing healthy cells," said study co-leader Dr. Timothy Cloughesy. He is director of the neuro-oncology program at the University of California, Los Angeles.
"This approach also has potential in additional types of the disease, such as metastatic colorectal and breast cancers."
Here's how the treatment works: Injectable Toca 511 infects actively dividing cancer cells and delivers a gene for an enzyme called cytosine deaminase to the cancer cells. Inside the tumor, Toca 511 programs the cancer cells to make cytosine deaminase to set them up for the second step of the treatment.
In that next phase, the patient takes the antifungal drug Toca FC. The genetic changes triggered by Toca 511 cause the cancer cells to convert Toca FC into the anticancer drug 5-fluorouracil (5-FU).
This leads to the targeted death of infected cancer cells and cells that help tumors hide from the immune system, while leaving healthy cells unharmed, the researchers explained.
These are the first published clinical trial results of this new type of modified virus known as a retroviral replicating vector (RRV)